AIM:To determine whether lectin-like ox-LDL receptor(LOX-1)regulates adhesion molecules expression and neutrophil infiltration in Aspergillus fumigatus(A.fumigatus)keratitis of C57 BL/6 mice.METHODS:C57 BL/6 mice were...AIM:To determine whether lectin-like ox-LDL receptor(LOX-1)regulates adhesion molecules expression and neutrophil infiltration in Aspergillus fumigatus(A.fumigatus)keratitis of C57 BL/6 mice.METHODS:C57 BL/6 mice were pretreated with a neutralizing antibody to LOX-1(5μg/5μL)or control nonspecific IgG(5μg/5μL),LOX-1 inhibitor Poly-I(2μg/5μL)or PBS by subconjunctival injection.Fungal keratitis(FK)mouse models of C57 BL/6 mice were established by scraping corneal central epithelium,smearing A.fumigatus on the corneal surface and covering the eye with contact lenses.The corneal response to infection was assessed via clinical score.The mRNA levels of the adhesion molecules intercellular cell adhesion molecule-1(ICAM-1),vascular cell adhesion molecule-1(VCAM-1),P-selectin and E-selectin were tested in control and infected corneas by reverse transcriptionpolymerase chain reaction(RT-PCR).The protein levels of ICAM-1 were evaluated by immunofluorescence(IF)and Western blot.Neutrophils were extracted from the abdominal cavity of C57 BL/6 mice followed by pretreatment using antibody to LOX-1(10μg/mL)or control nonspecific IgG(10μg/mL),the Poly-I(4μg/mL)or PBS.The cells were then stimulated with A.fumigatus and tested mRNA and protein levels of lymphocyte function-associated antigen-1(LFA-1)using RT-PCR and Western blot.IF and myeloperoxidase(MPO)assays were used to assess neutrophil infiltration in mice corneas.RESULTS:Pretreatment of LOX-1 antibody or the Poly-I reduced the degree of inflammation of cornea and decreased the clinical FK score compared with pretreatment of IgG or PBS(both P<0.01).And these pretreatment also displayed an obvious decline in the mRNA levels of ICAM-1,VCAM-1,P-selectin,E-selectin and LFA-1 expression compared with control groups(all P<0.01).Furthermore,pretreated with LOX-1 antibody or Poly-I,the protein levels of ICAM-1 and LFA-1 also decreased compared with control groups(all P<0.05).Neutrophil infiltration in the cornea was significantly reduced after pretreatment of LOX-1 antibody or Poly-I compared with control groups by IF and MPO assays(both P<0.01).CONCLUSION:Inhibition of LOX-1 can decrease the expression of adhesion molecules and reduce neutrophil infiltration in A.fumigatus infected corneas of C57 BL/6 mice.展开更多
Objective: To detect mRNA levels and expression ofCD44, CD54, CD29 and E-cadherin (E-cad) and to discuss their relationship with formation and drug resistance ofovarian cancer SKOV3ip1 multicellular aggregates.Methods...Objective: To detect mRNA levels and expression ofCD44, CD54, CD29 and E-cadherin (E-cad) and to discuss their relationship with formation and drug resistance ofovarian cancer SKOV3ip1 multicellular aggregates.Methods: Liquid overlay system was employed to obtainmulticellular aggregates. mRNA levels and expression ofCD44, CD54, CD29 and E-cad were investigated with RTPCR and flow cytometry (FCM) respectively. Results:Compared with monolayer cells, RT-PCR results showed a decrease in CD44 mRNA level by 0.626-fold and a decrease in CD29 mRNA level by 0.792-fold in multicellularaggregates. However, an increase in CD54 mRNA level by 1.815-fold and an increase in E-cadherin mRNA level by1.344-fold were found in multicellular aggregates. Theresults revealed the downregulation of CD44 and CD29 and the upregulation of CD54 and E-cad genes activity. CD44 expression in monolayer cells and multicellular aggregates were 75.995?.046 and 50.700?.351 (%) respectively andthere was a significant decrease in multicellular aggregates (P=0.001). Compared with control cells, no expression of CD54 was detected in monolayer cells (P=0.563) but markedly elevated CD54 expression was detected in multicellular aggregates (15.780?.217) (%) (P<0.01). High expression of CD29 was seen in monolayer cells and also in multicellular aggregates with positive rates of 96.290+1.201 (%) and 92.494?.055 (%). However, the expression of CD29 in multicellular aggregates was significantly reduced (P=0.014). Also no expression of E-cadherin was found in monolayer cells compared with control cells (4.490?.283) (%) (P=0.65) while significantly increased expression in aggregates cells (17.258?5.572) (%) (P=0.003) was observed. Conclusion: Significant differences in mRNA levels and expression of CD44, CD54, CD29 and E-cadherin clearly exist between monolayer cells and multicellular aggregates, which may be associated with the formation of multicellular aggregates and its drug resistance.展开更多
During development and regeneration,axonal growth depends on a rapid response to extracellular growth and guidance molecules.One mechanism underlying this rapid response is local protein synthesis(Jung et al.,2012)....During development and regeneration,axonal growth depends on a rapid response to extracellular growth and guidance molecules.One mechanism underlying this rapid response is local protein synthesis(Jung et al.,2012).Local protein synthesis is a highly tuned,展开更多
Regulation of the adhesion molecules expression by cytokine in vascular endothelial cells was investigated. Human umbilical vein endothelial cells (HUVEC) were stimulated with cytokines, TNF α (1-250 U/ml) or IL 1...Regulation of the adhesion molecules expression by cytokine in vascular endothelial cells was investigated. Human umbilical vein endothelial cells (HUVEC) were stimulated with cytokines, TNF α (1-250 U/ml) or IL 1β (0.1-50 U/ml) for 24 h. HUVEC were also cultured with cytokines, TNF α (100 U/ml) or IL 1β (10 U/ml), for 4-72 h, cell surface expression of adhesion molecules (ICAM 1 and VCAM 1) were detected and quantitated by immunocytochemical methods and computerized imaging analysis technique. Adhesion molecules expression were up regulated by TNF α, IL 1β in a concentration and time dependent manner. Some significant differences were observed between the effects of cytokines on the ICAM 1 and on VCAM 1 expression. Cytokines might directly induce the expression of ICAM 1 and VCAM 1 in vascular endothelial cells. Our observations indicate differential functions of the two adhesion molecules during the evolution of inflammatory responses in stroke.展开更多
The expression of nerve cell adhesion molecule L1 in the neuronal growth cone of the central nervous system is strongly associated with the direction of growth of the axon, but its role in the regeneration of the peri...The expression of nerve cell adhesion molecule L1 in the neuronal growth cone of the central nervous system is strongly associated with the direction of growth of the axon, but its role in the regeneration of the peripheral nerve is still unknown. This study explored the problem in a femoral nerve section model in rats. L1 and semaphorin 3A m RNA and protein expressions were measured over the 4-week recovery period. Quantitative polymerase chain reaction showed that nerve cell adhesion molecule L1 expression was higher in the sensory nerves than in motor nerves at 2 weeks after injury, but vice versa for the expression of semaphorin 3A. Western blot assay results demonstrated that nerve cell adhesion molecule L1 expression was higher in motor nerves than in the sensory nerves at the proximal end after injury, but its expression was greater in the sensory nerves at 2 weeks. Semaphorin 3A expression was higher in the motor nerves than in the sensory nerves at 3 days and 1 week after injury. Nerve cell adhesion molecule L1 and semaphorin 3A expressions at the distal end were higher in the motor nerves than in the sensory nerves at 3 days, 1 and 2 weeks. Immunohistochemical staining results showed that nerve cell adhesion molecule L1 expression at the proximal end was greater in the sensory nerves than in the motor nerves; semaphorin 3A expression was higher in the motor nerves than in the sensory nerves at 2 weeks after injury. Taken together, these results indicated that nerve cell adhesion molecules L1 and semaphorin 3A exhibited different expression patterns at the proximal and distal ends of sensory and motor nerves, and play a coordinating role in neural chemotaxis regeneration.展开更多
To investigate whether peroxisome proliferators-activated receptor-γ (PPARγ) ligand Troglitazone can reduce endothelial injury and activation during storage of harvested saphenous vein grafts. Segments of human sa...To investigate whether peroxisome proliferators-activated receptor-γ (PPARγ) ligand Troglitazone can reduce endothelial injury and activation during storage of harvested saphenous vein grafts. Segments of human saphenous vein graft were collected from 9 patients undergoing coronary bypass surgery and then divided into two equal parts of control and test specimens, were stored in ei- ther heparinized blood (control group) or heparinized blood containing 20 μmol/L troglitazone (test group) for 1 h at room temperature. Tissue distribution and protein expression of VCAM-I, ICAM-I, and endothelial nitric oxide synthase (eNOS) were compared using immunohistochemistry and Western blot analysis. Myeloperoxidase (MPO) activity, a marker of neutrophil sequestration in human saphenous vein grafts, was also measured in each group. The expression of ICAM-1 (753±132 versus 7201±934; P〈0.01) , VCAM-1 (3731±294 versus 8292±793; P〈0.01), and MPO activity (1.52±0.42 U/g, 5.04±1.26 U/g P〈0.01) were significantly lower in test group. In contract, eNOS expression (7983±834 versus 3989±1008; P〈0.01) was significantly higher in test group. PPARγ ligand troglitazone might reduce endothelial injury during the storage period of human saphenous vein grafts.展开更多
Objective To observe the changes of serum soluble intercellular adhesion moiecuie type-1(ICAM-1) and E-selectin in patients with acute myocardial inlarction (AMI) receiving reperfusiontherapy. Methods Peripheral venou...Objective To observe the changes of serum soluble intercellular adhesion moiecuie type-1(ICAM-1) and E-selectin in patients with acute myocardial inlarction (AMI) receiving reperfusiontherapy. Methods Peripheral venous blood samples were taken from 21 patients with AMI before and4,8,12,24,48,72h after thrombolytic treatment or direct percutaneous transluminal coronary angioplasty (PTCA).Blood samples from 16 control subjects were drawn for one time. Serum concentration of ICAM-1 and E-selectinwas determined by double antibodies sandwich enzyme-linked immunosorbent assay. Results Serum levels ofICAM-1 and E-selectin were higher in patients with AMI than those in controls. Sixteen patients with AMIand successful roperfusion therapy had signifcantly reduction in serum concentration of ICAM-1 and E-selectinat 24 and 48h, but had a peak at 4h. The remaining live patients who failed in mperfusion theropy didn’t show anysignificant changes in these values. Conclusion The serum concentration of ICAM-1 and E-selectin waselevated significantly in patients with AMI Successful reperfusion therapy can reduce the increased serumconcentration.展开更多
Adhesion molecules mediate cell-to-cell and cell-to-extracellular matrix interactions and transmit mechanical and chemical signals among them.Various mechanisms deregulate adhesion molecules in cancer,enabling tumor c...Adhesion molecules mediate cell-to-cell and cell-to-extracellular matrix interactions and transmit mechanical and chemical signals among them.Various mechanisms deregulate adhesion molecules in cancer,enabling tumor cells to proliferate without restraint,invade through tissue boundaries,escape from immune surveillance,and survive in the tumor microenvironment.Recent studies have revealed that adhesion molecules also drive angiogenesis,reshape metabolism,and are involved in stem cell self-renewal.In this review,we summarize the functions and mechanisms of adhesion molecules in cancer and the tumor microenvironment,as well as the therapeutic strategies targeting adhesion molecules.These studies have implications for furthering our understanding of adhesion molecules in cancer and providing a paradigm for exploring novel therapeutic approaches.展开更多
ObjectiveTo examine the gene and protein expression of CD11b, L selectin and CD45, and the relationship between their expression and leukocytopenia during a hemodialysis session Methods Ten maintenance hemodialysis...ObjectiveTo examine the gene and protein expression of CD11b, L selectin and CD45, and the relationship between their expression and leukocytopenia during a hemodialysis session Methods Ten maintenance hemodialysis patients, 20 uremic non dialysis patients and 10 healthy volunteers were included in this study The mRNA expression of CD11b, L selectin and CD45 in peripheral blood mononuclear cells was detected by RT PCR, while cell surface expression of these molecules on monocytes was detected by flow cytometry and leukocyte number was counted manually Results After the start of dialysis, both mRNA expression and cell surface expression of CD11b increased rapidly, while those of L selectin and leukocyte number fell The mRNA expression of CD45 first decreased and the cell surface expression increased, followed by a return to pre dialysis levels, by the end of dialysis Conclusions Hemodialysis using a cuprophane membrane can induce rapid upregulation of CD11b and down regulation of L selectin, which might influence the normal adhesion and anti inflammatory response of leukocytes In this process CD45 may play a role in regulating and/or transducing activation signal展开更多
To study the changes of adhesion molecules' expressions during the recombinant h u man granulocyte colony stimulating factor (rhG CSF) mobilization in periphera l blood stem cell transplantation (PBSCT), and to...To study the changes of adhesion molecules' expressions during the recombinant h u man granulocyte colony stimulating factor (rhG CSF) mobilization in periphera l blood stem cell transplantation (PBSCT), and to confirm the influence of rhG CSF on hematopoietic stem cells, which are proposed to guide mobilization in PBS CT Methods Mice were injected subcutaneously with diluted rhG CSF or normal saline for 7 d ays The blood Sca 1 + stem cell count and bone marrow (BM) nucleated cell co unt were enumerated The expressions of CD49d and CD44 and the adhesive ability of mononuclear cells to bone marrow matrix (fibronectin) were examined by flow c ytometry and 51 Cr adhesive assay, respectively Results The mobilizing effect of rhG CSF on mice was the same as on humans The number of Sca 1 + cells in peripheral blood reached the peak on the seventh day, the BM nucleated cell count was reduced, and the expressions of CD49d and the cells ' adhesive ability in BM and PB declined Conclusions rhG CSF can reduce some cell adhesion molecules' expressions and the adhesive a bility of hematopoietic stem cells to BM matrix, therefore mobilizing hematopoie tic stem cells (HSC) from the BM to the peripheral blood展开更多
BACKGROUND: Transplantation of bone marrow-derived mesenchymal stem cells (BMSCs) improves motor functional recovery, but the mechanisms remain unclear. OBJECTIVE: To investigate expression of growth-associated pr...BACKGROUND: Transplantation of bone marrow-derived mesenchymal stem cells (BMSCs) improves motor functional recovery, but the mechanisms remain unclear. OBJECTIVE: To investigate expression of growth-associated protein 43 (GAP-43) and neural cell adhesion molecule following BMSC transplantation to the lateral ventricle in rats with acute focal cerebral ischemic brain damage. DESIGN, TIME AND SETTING: A randomized, controlled, animal experiment using immunohistochemistry was performed at the laboratories of Department of Neurology, Renmin Hospital of Wuhan University and Doctoral Scientific Research Work Station of C-BONS PHARMA, Hubei Province, China, from January 2007 to December 2008. MATERIALS: Monoclonal mouse anti-rat 5-bromo-2-deoxyuridine and neural cell adhesion molecule antibodies were purchased from Sigma, USA; monoclonal mouse anti-rat GAP-43 antibody was purchased from Wuhan Boster, China. METHODS: Rat models of right middle cerebral artery occlusion were established using the thread method. At 1 day after middle cerebral artery occlusion, 20μL culture solution, containing 5×10^5 BMSCs, was transplanted to the left lateral ventricle using micro-injection. MAIN OUTCOME MEASURES: Scores of neurological impairment were measured to assess neural function. Expression of GAP-43 and neural cell adhesion molecule at the lesion areas was examined by immunohistochemistry. RESULTS: GAP-43 and neural cell adhesion molecule expression was low in brain tissues of the sham-operated group, but expression increased at the ischemic boundary (P 〈 0.05). Transplantation of BMSCs further enhanced expression of GAP-43 and neural cell adhesion molecule (P 〈 0.05) and remarkably improved neurological impairment of ischemic rats (P 〈 0.05). CONCLUSION: BMSC transplantation promoted neurological recovery in rats by upregulating expression of GAP-43 and neural cell adhesion molecule.展开更多
The increased vascular infl ammation is a key event in the development of atherosclerotic lesions.Antrodia cinnamomea has been shown to promote anticancerogenic activity through decreasing infl ammation.However,the po...The increased vascular infl ammation is a key event in the development of atherosclerotic lesions.Antrodia cinnamomea has been shown to promote anticancerogenic activity through decreasing infl ammation.However,the potential role of A.cinnamomea in cardiovascular diseases remains unexplored.Herein,using carotid arterial ligation models,we found that ethanol extract from A.cinnamomea(EEAC)signifi cantly inhibited neointimal hyperplasia in a dose-dependent manner,accompanied with the reduced expression of activated p65 and infl ammatory cytokines.We also show that EEAC ameliorated TNF-α-induced phosphorylation of p65 and pro-infl ammatory cytokine expression in both vascular smooth muscle cells(VSMCs)and macrophages in vitro.Mechanistically,EEAC suppressed expression levels of intercellular adhesion molecule-1(ICAM-1)and vascular cell adhesion molecule(VCAM-1)in VSMCs,which attenuates the ability of monocytes/macrophages adhesion to VSMCs.Furthermore,the expression level of these adhesion molecules and infi ltration of monocytes/macrophages were also decreased in neointimal VSMCs of arteries pretreated with EEAC.Altogether,our results reveal a novel function of A.cinnamomea in suppressing vascular infl ammation upon ligation injury during neointimal formation,likely through inhibition of infl ammatory cell infi ltration via downregulating the adhesion molecules in VSMCs.Thus,A.cinnamomea may offer a pharmacological therapy to slow down disease progression in patients with vascular injury.展开更多
The formation of nerve bundles,which is partially regulated by neural cell adhesion molecule 1(NCAM1),is important for neural network organization during peripheral nerve regeneration.However,little is known about how...The formation of nerve bundles,which is partially regulated by neural cell adhesion molecule 1(NCAM1),is important for neural network organization during peripheral nerve regeneration.However,little is known about how the extracellular matrix(ECM)microenvironment affects this process.Here,we seeded dorsal root ganglion tissue blocks on different ECM substrates of peripheral nerve ECM-derived matrixgel,Matrigel,laminin 521,collagen I,and collagen IV,and observed well-aligned axon bundles growing in the peripheral nerve ECM-derived environment.We confirmed that NCAM1 is necessary but not sufficient to trigger this phenomenon.A protein interaction assay identified collagen VI as an extracellular partner of NCAM1 in the regulation of axonal fasciculation.Collagen VI interacted with NCAM1 by directly binding to the FNIII domain,thereby increasing the stability of NCAM1 at the axolemma.Our in vivo experiments on a rat sciatic nerve defect model also demonstrated orderly nerve bundle regeneration with improved projection accuracy and functional recovery after treatment with 10 mg/m L Matrigel and 20μg/m L collagen VI.These findings suggest that the collagen VI-NCAM1 pathway plays a regulatory role in nerve bundle formation.This study was approved by the Animal Ethics Committee of Guangzhou Medical University(approval No.GY2019048)on April 30,2019.展开更多
AIM:To investigate the impact of polysialylated neural cell adhesion molecule(PSA-NCAM)on the survival of retinal ganglion cells(RGCs)in the experimentally induced diabetes in mice.METHODS:Diabetes was induced i...AIM:To investigate the impact of polysialylated neural cell adhesion molecule(PSA-NCAM)on the survival of retinal ganglion cells(RGCs)in the experimentally induced diabetes in mice.METHODS:Diabetes was induced in 2.5 months old Swiss Webster mice by intraperitoneal injection of streptozotocin(STZ,90 mg/kg)once daily for two consecutive days.Examination of the proteins of interest in the retinas from diabetic mice at 2mo after diabetes induction was performed using immunohistochemistry and Western blot analysis.RGCs were counted in the wholemounted retinas,and Brn3a marker was used.RESULTS:Examination of retinas from diabetic mice at 2mo after diabetes induction revealed a considerable reduction in RGC density.Our experiments also demonstrated a redistribution of PSA-NCAM in the retina of diabetic animals.PSA-NCAM immunoreactivity was diminished in the inner part of the retina where RGCs were located.In contrast,an enhanced PSA-NCAM immunoreactivity was detected in the outer layers of the retina.PSA-NCAM signal was co-localized with glial fibrillary acidic protein immunoreactivity in the Müller cell branches.Previous studies have shown that matrix metalloproteinase-9(MMP-9)is responsible for the reduction in PSA-NCAM levels in neuronal cells.The reduced levels of PSA-NCAM in inner layers(nerve fiber layer,ganglion cell layer)were accompanied by the increased expression of MMP-9.In contrast,in the outer retinal layers,the expression of MMP-9 was much less pronounced.CONCLUSION:MMP-9 induces PSA-NCAM shedding in the inner part of the retina and the decreased level of PSA-NCAM in the inner part of the retina might be,at least in part,responsible for the loss of RGCs in diabetic mice.展开更多
BACKGROUND: Animal studies have confirmed that hyperbaric oxygen (HBO) therapy can reduce matrix metalloproteinase activity and blood brain barrier permeability, thereby exhibiting neuroprotective effects. However,...BACKGROUND: Animal studies have confirmed that hyperbaric oxygen (HBO) therapy can reduce matrix metalloproteinase activity and blood brain barrier permeability, thereby exhibiting neuroprotective effects. However, at present, consensus does not exist in terms of its clinical efficacy. OBJECTIVE: To validate the significance of changes in serum cellular adhesion molecule and MMP-9 levels in patients with cerebral infarction following HBO therapy. DESIGN, TIME AND SETTING: This randomized, controlled, neurobiochemical study was performed at the Department of Neurology, Affiliated Hospital of Qingdao University Medical College between December 2002 and March 2006. PARTICIPANTS: A total of 112 patients with acute cerebral infarction of internal carotid artery, comprising 64 males and 48 females, averaging (67 ±11) years, were recruited and randomized to a HBO group (n = 50) and a routine treatment group (n = 62). An additional 30 gender- and age-matched normal subjects, consisting of 17 males and 13 females, averaging (63 ± 9) years, were enrolled as control subjects. METHODS: The routine treatment group received routine drug treatment and rehabilitation exercise. HBO treatment was additionally performed in the HBO group, once a day, for a total of 10 days. MAIN OUTCOME MEASURES: Serum levels of soluble intercellular adhesion molecule, soluble vascular cell adhesion molecule, soluble E-selectin, and matrix metalloproteinase-9 were detected by enzyme linked immunosorbent assay. RESULTS: Upon admission, serum levels of soluble intercellular adhesion molecule, soluble vascular cell adhesion molecule, soluble E-selectin, and matrix metalloproteinase-9 were significantly increased in patients with cerebral infarction, compared with control subjects (P 〈 0.01). Following HBO and routine treatments, serum levels of the above-mentioned indices were significantly reduced in the HBO and routine treatment groups (P 〈 0.01). Moreover, greater efficacy was observed in the HBO group, compared with the routine treatment group (P 〈 0.05 or P 〈 0.01). CONCLUSION: Intergroup comparison and case-control results indicated that HBO noticeably reduced serum levels of soluble intercellular adhesion molecule, soluble vascular cell adhesion molecule, soluble E-selectin, and matrix metalloproteinase-9.展开更多
BACKGROUND: Learning and memory damage is one of the most permanent and the severest symptoms of traumatic brain injury; it can seriously influence the normal life and work of patients. Some research has demonstrated...BACKGROUND: Learning and memory damage is one of the most permanent and the severest symptoms of traumatic brain injury; it can seriously influence the normal life and work of patients. Some research has demonstrated that cognitive disorder is closely related to nicotine cholinergic receptors, N-methyl-D aspartate receptors, neural cell adhesion molecule, and brain-derived neurotrophic factor. OBJECTIVE: To summarize the cognitive disorder and changes in nicotine cholinergic receptors, N-methyl-D aspartate receptors, neural cell adhesion molecule, and brain-derived neurotrophic factor following brain injury. RETRIEVAL STRATEGY: A computer-based online search was conducted in PUBMED for English language publications containing the key words "brain injured, cognitive handicap, acetylcholine, N-methyl-D aspartate receptors, neural cell adhesion molecule, brain-derived neurotrophic factor" from January 2000 to December 2007. There were 44 papers in total. Inclusion criteria: ① articles about changes in nicotine cholinergic receptors, N-methyl-D aspartate receptors, neural cell adhesion molecule, and brain-derived neurotrophic factor following brain injury; ② articles in the same researching circle published in authoritative journals or recently published. Exclusion criteria: duplicated articles. LITERATURE EVALUATION: References were mainly derived from research on changes in these four factors following brain injury. The 20 included papers were clinical or basic experimental studies. DATA SYNTHESIS: After craniocerebral injury, changes in these four factors in brain were similar to those during recovery from cognitive disorder, to a certain degree. Some data have indicated that activation of nicotine cholinergic receptors, N-methyl-D aspartate receptors, neural cell adhesion molecule, and brain-derived neurotrophic factor could greatly improve cognitive disorder following brain injury. However, there are still a lot of questions remaining; for example, how do these factors change at different time points after brain injury, and what is the relationship between associated factors and cognitive disorder. CONCLUSION: It is necessary to comprehensively study some associated factors, to analyze their changes and their relationship with cognitive disorder following brain injury, and to investigate their effects at different time points after brain injury.展开更多
Objective:Lymphatic endothelial cell(LEC)proliferation is essential for lymphangiogenesis.Hypoxia induces lymphangiogenesis,but it directly inhibits LEC proliferation and the underlying mechanisms have not been fully ...Objective:Lymphatic endothelial cell(LEC)proliferation is essential for lymphangiogenesis.Hypoxia induces lymphangiogenesis,but it directly inhibits LEC proliferation and the underlying mechanisms have not been fully understood.The aim of this study was to investigate the role of carcinoembryonic antigen-related cell adhesion molecule 1(CEACAM1)in hypoxia-repressed LEC proliferation.Methods:Human dermal lymphatic endothelial cells(HDLECs)were cultured under normoxic or hypoxic conditions,and cell proliferation was determined using MTT or CCK-8 assays.CEACAM1 expression was silenced by siRNA transfection.Activation of mitogen-activated protein kinases(MAPKs)was examined by Western blotting and blocked by specific inhibitors.Results:Under hypoxia,HDLECs proliferation was suppressed and CEACAM1 expression was downregulated.Silence of CEACAM1 in normoxia inhibited HDLECs proliferation and did not further decrease proliferation in HDLECs in response to hypoxia,suggesting that CEACAM1 may mediate hypoxia-induced inhibition of HDLECs proliferation.In addition,silence of CEACAM1 increased phosphorylation of MAPK molecules:extracellular signal-regulated kinase(ERK),p38 MAPK and Jun N-terminal kinase(JNK)in HDLECs.However,only inhibition of the JNK pathway rescued the reduction of HDLEC proliferation induced by CEACAM1 silence.Conclusion:Our results suggested that hypoxia downregulates CEACAM1 expression by activation of the JNK pathway,leading to inhibition of HDLEC proliferation.These findings may help to understand the mechanisms of LEC-specific response to hypoxia and develop novel therapies for pathological lymphangiogenesis.展开更多
This study examined the expression of cell adhesion molecule 1 (CADM1) in pancreatic cancer and the possible mechanism. The expression of CADM 1 was detected by immunohistochemistry in tissues of pancreatic cancer, ...This study examined the expression of cell adhesion molecule 1 (CADM1) in pancreatic cancer and the possible mechanism. The expression of CADM 1 was detected by immunohistochemistry in tissues of pancreatic cancer, pancreatitis, and normal pancreas. The plasmid pcDNA3.1-Hy- gro(+)/CADM1 was transfected into PANC-1 cells (a pancreatic cancer cell line). The expression of CADM1 in the transfected cells was determined by RT-PCR and Western blotting. Cell growth was measured by the MTT method and cell apoptosis by flow cytometry. The results showed that CADM1 was weakly expressed in tissues of pancreatic cancer in contrast to its high expression in normal pancreatic and pancreatitis tissues. The expression level of CADM in pancreatic caner was intensely correlated with the differentiation degree, lymph node metastasis and TNM stages. The growth of CADMl-transfected PANC-1 cells was significantly suppressed in vitro by a G1 cell cycle arrest and apoptosis occurrence. It was concluded that re-expression of CADM1 inhibits the growth of pancreatic cancer cells and induces their apoptosis in vitro. As a tumor suppressor gene, CADM1 plays an important role in the occurrence, progression and metastasis of pancreatic cancer.展开更多
基金Supported by the National Natural Science Foundation of China(No.81870632,No.81470609,No.81700800,No.81800800)the Key Research Project Foundation of Shandong Province(No.2019GSF107022)。
文摘AIM:To determine whether lectin-like ox-LDL receptor(LOX-1)regulates adhesion molecules expression and neutrophil infiltration in Aspergillus fumigatus(A.fumigatus)keratitis of C57 BL/6 mice.METHODS:C57 BL/6 mice were pretreated with a neutralizing antibody to LOX-1(5μg/5μL)or control nonspecific IgG(5μg/5μL),LOX-1 inhibitor Poly-I(2μg/5μL)or PBS by subconjunctival injection.Fungal keratitis(FK)mouse models of C57 BL/6 mice were established by scraping corneal central epithelium,smearing A.fumigatus on the corneal surface and covering the eye with contact lenses.The corneal response to infection was assessed via clinical score.The mRNA levels of the adhesion molecules intercellular cell adhesion molecule-1(ICAM-1),vascular cell adhesion molecule-1(VCAM-1),P-selectin and E-selectin were tested in control and infected corneas by reverse transcriptionpolymerase chain reaction(RT-PCR).The protein levels of ICAM-1 were evaluated by immunofluorescence(IF)and Western blot.Neutrophils were extracted from the abdominal cavity of C57 BL/6 mice followed by pretreatment using antibody to LOX-1(10μg/mL)or control nonspecific IgG(10μg/mL),the Poly-I(4μg/mL)or PBS.The cells were then stimulated with A.fumigatus and tested mRNA and protein levels of lymphocyte function-associated antigen-1(LFA-1)using RT-PCR and Western blot.IF and myeloperoxidase(MPO)assays were used to assess neutrophil infiltration in mice corneas.RESULTS:Pretreatment of LOX-1 antibody or the Poly-I reduced the degree of inflammation of cornea and decreased the clinical FK score compared with pretreatment of IgG or PBS(both P<0.01).And these pretreatment also displayed an obvious decline in the mRNA levels of ICAM-1,VCAM-1,P-selectin,E-selectin and LFA-1 expression compared with control groups(all P<0.01).Furthermore,pretreated with LOX-1 antibody or Poly-I,the protein levels of ICAM-1 and LFA-1 also decreased compared with control groups(all P<0.05).Neutrophil infiltration in the cornea was significantly reduced after pretreatment of LOX-1 antibody or Poly-I compared with control groups by IF and MPO assays(both P<0.01).CONCLUSION:Inhibition of LOX-1 can decrease the expression of adhesion molecules and reduce neutrophil infiltration in A.fumigatus infected corneas of C57 BL/6 mice.
基金This work was supported by the National Natural Science Foundation of China (No. 30000177).
文摘Objective: To detect mRNA levels and expression ofCD44, CD54, CD29 and E-cadherin (E-cad) and to discuss their relationship with formation and drug resistance ofovarian cancer SKOV3ip1 multicellular aggregates.Methods: Liquid overlay system was employed to obtainmulticellular aggregates. mRNA levels and expression ofCD44, CD54, CD29 and E-cad were investigated with RTPCR and flow cytometry (FCM) respectively. Results:Compared with monolayer cells, RT-PCR results showed a decrease in CD44 mRNA level by 0.626-fold and a decrease in CD29 mRNA level by 0.792-fold in multicellularaggregates. However, an increase in CD54 mRNA level by 1.815-fold and an increase in E-cadherin mRNA level by1.344-fold were found in multicellular aggregates. Theresults revealed the downregulation of CD44 and CD29 and the upregulation of CD54 and E-cad genes activity. CD44 expression in monolayer cells and multicellular aggregates were 75.995?.046 and 50.700?.351 (%) respectively andthere was a significant decrease in multicellular aggregates (P=0.001). Compared with control cells, no expression of CD54 was detected in monolayer cells (P=0.563) but markedly elevated CD54 expression was detected in multicellular aggregates (15.780?.217) (%) (P<0.01). High expression of CD29 was seen in monolayer cells and also in multicellular aggregates with positive rates of 96.290+1.201 (%) and 92.494?.055 (%). However, the expression of CD29 in multicellular aggregates was significantly reduced (P=0.014). Also no expression of E-cadherin was found in monolayer cells compared with control cells (4.490?.283) (%) (P=0.65) while significantly increased expression in aggregates cells (17.258?5.572) (%) (P=0.003) was observed. Conclusion: Significant differences in mRNA levels and expression of CD44, CD54, CD29 and E-cadherin clearly exist between monolayer cells and multicellular aggregates, which may be associated with the formation of multicellular aggregates and its drug resistance.
基金supported by a Jérome Lejeune Foundation award and a Kent State University Innovation Research Seed Award to KW
文摘During development and regeneration,axonal growth depends on a rapid response to extracellular growth and guidance molecules.One mechanism underlying this rapid response is local protein synthesis(Jung et al.,2012).Local protein synthesis is a highly tuned,
文摘Regulation of the adhesion molecules expression by cytokine in vascular endothelial cells was investigated. Human umbilical vein endothelial cells (HUVEC) were stimulated with cytokines, TNF α (1-250 U/ml) or IL 1β (0.1-50 U/ml) for 24 h. HUVEC were also cultured with cytokines, TNF α (100 U/ml) or IL 1β (10 U/ml), for 4-72 h, cell surface expression of adhesion molecules (ICAM 1 and VCAM 1) were detected and quantitated by immunocytochemical methods and computerized imaging analysis technique. Adhesion molecules expression were up regulated by TNF α, IL 1β in a concentration and time dependent manner. Some significant differences were observed between the effects of cytokines on the ICAM 1 and on VCAM 1 expression. Cytokines might directly induce the expression of ICAM 1 and VCAM 1 in vascular endothelial cells. Our observations indicate differential functions of the two adhesion molecules during the evolution of inflammatory responses in stroke.
基金supported by the National Natural Science Foundation of China,No.81371389,31500927,31300942,81201017the Collegiate Natural Science Foundation of Jiangsu Province of China,No.13KJB180018the Natural Science Foundation of Nantong University of China,No.14ZY013
文摘The expression of nerve cell adhesion molecule L1 in the neuronal growth cone of the central nervous system is strongly associated with the direction of growth of the axon, but its role in the regeneration of the peripheral nerve is still unknown. This study explored the problem in a femoral nerve section model in rats. L1 and semaphorin 3A m RNA and protein expressions were measured over the 4-week recovery period. Quantitative polymerase chain reaction showed that nerve cell adhesion molecule L1 expression was higher in the sensory nerves than in motor nerves at 2 weeks after injury, but vice versa for the expression of semaphorin 3A. Western blot assay results demonstrated that nerve cell adhesion molecule L1 expression was higher in motor nerves than in the sensory nerves at the proximal end after injury, but its expression was greater in the sensory nerves at 2 weeks. Semaphorin 3A expression was higher in the motor nerves than in the sensory nerves at 3 days and 1 week after injury. Nerve cell adhesion molecule L1 and semaphorin 3A expressions at the distal end were higher in the motor nerves than in the sensory nerves at 3 days, 1 and 2 weeks. Immunohistochemical staining results showed that nerve cell adhesion molecule L1 expression at the proximal end was greater in the sensory nerves than in the motor nerves; semaphorin 3A expression was higher in the motor nerves than in the sensory nerves at 2 weeks after injury. Taken together, these results indicated that nerve cell adhesion molecules L1 and semaphorin 3A exhibited different expression patterns at the proximal and distal ends of sensory and motor nerves, and play a coordinating role in neural chemotaxis regeneration.
基金the Health Min-istry of Hubei Province (JX2B16).
文摘To investigate whether peroxisome proliferators-activated receptor-γ (PPARγ) ligand Troglitazone can reduce endothelial injury and activation during storage of harvested saphenous vein grafts. Segments of human saphenous vein graft were collected from 9 patients undergoing coronary bypass surgery and then divided into two equal parts of control and test specimens, were stored in ei- ther heparinized blood (control group) or heparinized blood containing 20 μmol/L troglitazone (test group) for 1 h at room temperature. Tissue distribution and protein expression of VCAM-I, ICAM-I, and endothelial nitric oxide synthase (eNOS) were compared using immunohistochemistry and Western blot analysis. Myeloperoxidase (MPO) activity, a marker of neutrophil sequestration in human saphenous vein grafts, was also measured in each group. The expression of ICAM-1 (753±132 versus 7201±934; P〈0.01) , VCAM-1 (3731±294 versus 8292±793; P〈0.01), and MPO activity (1.52±0.42 U/g, 5.04±1.26 U/g P〈0.01) were significantly lower in test group. In contract, eNOS expression (7983±834 versus 3989±1008; P〈0.01) was significantly higher in test group. PPARγ ligand troglitazone might reduce endothelial injury during the storage period of human saphenous vein grafts.
文摘Objective To observe the changes of serum soluble intercellular adhesion moiecuie type-1(ICAM-1) and E-selectin in patients with acute myocardial inlarction (AMI) receiving reperfusiontherapy. Methods Peripheral venous blood samples were taken from 21 patients with AMI before and4,8,12,24,48,72h after thrombolytic treatment or direct percutaneous transluminal coronary angioplasty (PTCA).Blood samples from 16 control subjects were drawn for one time. Serum concentration of ICAM-1 and E-selectinwas determined by double antibodies sandwich enzyme-linked immunosorbent assay. Results Serum levels ofICAM-1 and E-selectin were higher in patients with AMI than those in controls. Sixteen patients with AMIand successful roperfusion therapy had signifcantly reduction in serum concentration of ICAM-1 and E-selectinat 24 and 48h, but had a peak at 4h. The remaining live patients who failed in mperfusion theropy didn’t show anysignificant changes in these values. Conclusion The serum concentration of ICAM-1 and E-selectin waselevated significantly in patients with AMI Successful reperfusion therapy can reduce the increased serumconcentration.
基金supported by the National Natural Science Foundation of China(82203163)the Natural Science Foundation of Hunan Province(2022JJ40660)+1 种基金the Natural Science Foundation of Changsha(kq2202123)the Young Elite Scientists Sponsorship Program by CAST(2022QNRC001)。
文摘Adhesion molecules mediate cell-to-cell and cell-to-extracellular matrix interactions and transmit mechanical and chemical signals among them.Various mechanisms deregulate adhesion molecules in cancer,enabling tumor cells to proliferate without restraint,invade through tissue boundaries,escape from immune surveillance,and survive in the tumor microenvironment.Recent studies have revealed that adhesion molecules also drive angiogenesis,reshape metabolism,and are involved in stem cell self-renewal.In this review,we summarize the functions and mechanisms of adhesion molecules in cancer and the tumor microenvironment,as well as the therapeutic strategies targeting adhesion molecules.These studies have implications for furthering our understanding of adhesion molecules in cancer and providing a paradigm for exploring novel therapeutic approaches.
文摘ObjectiveTo examine the gene and protein expression of CD11b, L selectin and CD45, and the relationship between their expression and leukocytopenia during a hemodialysis session Methods Ten maintenance hemodialysis patients, 20 uremic non dialysis patients and 10 healthy volunteers were included in this study The mRNA expression of CD11b, L selectin and CD45 in peripheral blood mononuclear cells was detected by RT PCR, while cell surface expression of these molecules on monocytes was detected by flow cytometry and leukocyte number was counted manually Results After the start of dialysis, both mRNA expression and cell surface expression of CD11b increased rapidly, while those of L selectin and leukocyte number fell The mRNA expression of CD45 first decreased and the cell surface expression increased, followed by a return to pre dialysis levels, by the end of dialysis Conclusions Hemodialysis using a cuprophane membrane can induce rapid upregulation of CD11b and down regulation of L selectin, which might influence the normal adhesion and anti inflammatory response of leukocytes In this process CD45 may play a role in regulating and/or transducing activation signal
基金ThisstudywassupportedbyShanghaiScience TechnologyDevelopingFoundationofChina (No .9741 1 90 0 6)
文摘To study the changes of adhesion molecules' expressions during the recombinant h u man granulocyte colony stimulating factor (rhG CSF) mobilization in periphera l blood stem cell transplantation (PBSCT), and to confirm the influence of rhG CSF on hematopoietic stem cells, which are proposed to guide mobilization in PBS CT Methods Mice were injected subcutaneously with diluted rhG CSF or normal saline for 7 d ays The blood Sca 1 + stem cell count and bone marrow (BM) nucleated cell co unt were enumerated The expressions of CD49d and CD44 and the adhesive ability of mononuclear cells to bone marrow matrix (fibronectin) were examined by flow c ytometry and 51 Cr adhesive assay, respectively Results The mobilizing effect of rhG CSF on mice was the same as on humans The number of Sca 1 + cells in peripheral blood reached the peak on the seventh day, the BM nucleated cell count was reduced, and the expressions of CD49d and the cells ' adhesive ability in BM and PB declined Conclusions rhG CSF can reduce some cell adhesion molecules' expressions and the adhesive a bility of hematopoietic stem cells to BM matrix, therefore mobilizing hematopoie tic stem cells (HSC) from the BM to the peripheral blood
基金This study was supported by grants from the National Natural Science Foundation of China (39970340) Scientific Found of the Chinese Ministry of Health (98 2 283) and Natural Science Foundation of Shanghai (02ZB14041and 034119916)
文摘BACKGROUND: Transplantation of bone marrow-derived mesenchymal stem cells (BMSCs) improves motor functional recovery, but the mechanisms remain unclear. OBJECTIVE: To investigate expression of growth-associated protein 43 (GAP-43) and neural cell adhesion molecule following BMSC transplantation to the lateral ventricle in rats with acute focal cerebral ischemic brain damage. DESIGN, TIME AND SETTING: A randomized, controlled, animal experiment using immunohistochemistry was performed at the laboratories of Department of Neurology, Renmin Hospital of Wuhan University and Doctoral Scientific Research Work Station of C-BONS PHARMA, Hubei Province, China, from January 2007 to December 2008. MATERIALS: Monoclonal mouse anti-rat 5-bromo-2-deoxyuridine and neural cell adhesion molecule antibodies were purchased from Sigma, USA; monoclonal mouse anti-rat GAP-43 antibody was purchased from Wuhan Boster, China. METHODS: Rat models of right middle cerebral artery occlusion were established using the thread method. At 1 day after middle cerebral artery occlusion, 20μL culture solution, containing 5×10^5 BMSCs, was transplanted to the left lateral ventricle using micro-injection. MAIN OUTCOME MEASURES: Scores of neurological impairment were measured to assess neural function. Expression of GAP-43 and neural cell adhesion molecule at the lesion areas was examined by immunohistochemistry. RESULTS: GAP-43 and neural cell adhesion molecule expression was low in brain tissues of the sham-operated group, but expression increased at the ischemic boundary (P 〈 0.05). Transplantation of BMSCs further enhanced expression of GAP-43 and neural cell adhesion molecule (P 〈 0.05) and remarkably improved neurological impairment of ischemic rats (P 〈 0.05). CONCLUSION: BMSC transplantation promoted neurological recovery in rats by upregulating expression of GAP-43 and neural cell adhesion molecule.
基金This work was supported by the National Key Research Project of China(2019YFC1606400)Major Public Welfare Projects in Henan Province(201300110200)+4 种基金National Key Research Project of Hebei Province(20375502D)Natural Science Foundation of Hebei Province(H2019206212)High-level Talent Funding Project of Hebei Province(A201905006)Fund of National R&D Center for Edible Fungus Processing Technology,Henan University(20200109)the Open Fund from Beijing Advanced Innovation Center for Food Nutrition and Human Health(20182025).
文摘The increased vascular infl ammation is a key event in the development of atherosclerotic lesions.Antrodia cinnamomea has been shown to promote anticancerogenic activity through decreasing infl ammation.However,the potential role of A.cinnamomea in cardiovascular diseases remains unexplored.Herein,using carotid arterial ligation models,we found that ethanol extract from A.cinnamomea(EEAC)signifi cantly inhibited neointimal hyperplasia in a dose-dependent manner,accompanied with the reduced expression of activated p65 and infl ammatory cytokines.We also show that EEAC ameliorated TNF-α-induced phosphorylation of p65 and pro-infl ammatory cytokine expression in both vascular smooth muscle cells(VSMCs)and macrophages in vitro.Mechanistically,EEAC suppressed expression levels of intercellular adhesion molecule-1(ICAM-1)and vascular cell adhesion molecule(VCAM-1)in VSMCs,which attenuates the ability of monocytes/macrophages adhesion to VSMCs.Furthermore,the expression level of these adhesion molecules and infi ltration of monocytes/macrophages were also decreased in neointimal VSMCs of arteries pretreated with EEAC.Altogether,our results reveal a novel function of A.cinnamomea in suppressing vascular infl ammation upon ligation injury during neointimal formation,likely through inhibition of infl ammatory cell infi ltration via downregulating the adhesion molecules in VSMCs.Thus,A.cinnamomea may offer a pharmacological therapy to slow down disease progression in patients with vascular injury.
基金supported by the National Natural Science Foundation of China,No.31800892(to JLZ)the Natural Science Foundation of Guangdong Province of China,No.2018A030310254(to YY)a grant from Guangzhou Medical University Start-up Project of China,No.B195002002048(to JLZ)。
文摘The formation of nerve bundles,which is partially regulated by neural cell adhesion molecule 1(NCAM1),is important for neural network organization during peripheral nerve regeneration.However,little is known about how the extracellular matrix(ECM)microenvironment affects this process.Here,we seeded dorsal root ganglion tissue blocks on different ECM substrates of peripheral nerve ECM-derived matrixgel,Matrigel,laminin 521,collagen I,and collagen IV,and observed well-aligned axon bundles growing in the peripheral nerve ECM-derived environment.We confirmed that NCAM1 is necessary but not sufficient to trigger this phenomenon.A protein interaction assay identified collagen VI as an extracellular partner of NCAM1 in the regulation of axonal fasciculation.Collagen VI interacted with NCAM1 by directly binding to the FNIII domain,thereby increasing the stability of NCAM1 at the axolemma.Our in vivo experiments on a rat sciatic nerve defect model also demonstrated orderly nerve bundle regeneration with improved projection accuracy and functional recovery after treatment with 10 mg/m L Matrigel and 20μg/m L collagen VI.These findings suggest that the collagen VI-NCAM1 pathway plays a regulatory role in nerve bundle formation.This study was approved by the Animal Ethics Committee of Guangzhou Medical University(approval No.GY2019048)on April 30,2019.
基金Supported by the Estonian Science Council Grant(Institutional research founding)IUT2-3
文摘AIM:To investigate the impact of polysialylated neural cell adhesion molecule(PSA-NCAM)on the survival of retinal ganglion cells(RGCs)in the experimentally induced diabetes in mice.METHODS:Diabetes was induced in 2.5 months old Swiss Webster mice by intraperitoneal injection of streptozotocin(STZ,90 mg/kg)once daily for two consecutive days.Examination of the proteins of interest in the retinas from diabetic mice at 2mo after diabetes induction was performed using immunohistochemistry and Western blot analysis.RGCs were counted in the wholemounted retinas,and Brn3a marker was used.RESULTS:Examination of retinas from diabetic mice at 2mo after diabetes induction revealed a considerable reduction in RGC density.Our experiments also demonstrated a redistribution of PSA-NCAM in the retina of diabetic animals.PSA-NCAM immunoreactivity was diminished in the inner part of the retina where RGCs were located.In contrast,an enhanced PSA-NCAM immunoreactivity was detected in the outer layers of the retina.PSA-NCAM signal was co-localized with glial fibrillary acidic protein immunoreactivity in the Müller cell branches.Previous studies have shown that matrix metalloproteinase-9(MMP-9)is responsible for the reduction in PSA-NCAM levels in neuronal cells.The reduced levels of PSA-NCAM in inner layers(nerve fiber layer,ganglion cell layer)were accompanied by the increased expression of MMP-9.In contrast,in the outer retinal layers,the expression of MMP-9 was much less pronounced.CONCLUSION:MMP-9 induces PSA-NCAM shedding in the inner part of the retina and the decreased level of PSA-NCAM in the inner part of the retina might be,at least in part,responsible for the loss of RGCs in diabetic mice.
文摘BACKGROUND: Animal studies have confirmed that hyperbaric oxygen (HBO) therapy can reduce matrix metalloproteinase activity and blood brain barrier permeability, thereby exhibiting neuroprotective effects. However, at present, consensus does not exist in terms of its clinical efficacy. OBJECTIVE: To validate the significance of changes in serum cellular adhesion molecule and MMP-9 levels in patients with cerebral infarction following HBO therapy. DESIGN, TIME AND SETTING: This randomized, controlled, neurobiochemical study was performed at the Department of Neurology, Affiliated Hospital of Qingdao University Medical College between December 2002 and March 2006. PARTICIPANTS: A total of 112 patients with acute cerebral infarction of internal carotid artery, comprising 64 males and 48 females, averaging (67 ±11) years, were recruited and randomized to a HBO group (n = 50) and a routine treatment group (n = 62). An additional 30 gender- and age-matched normal subjects, consisting of 17 males and 13 females, averaging (63 ± 9) years, were enrolled as control subjects. METHODS: The routine treatment group received routine drug treatment and rehabilitation exercise. HBO treatment was additionally performed in the HBO group, once a day, for a total of 10 days. MAIN OUTCOME MEASURES: Serum levels of soluble intercellular adhesion molecule, soluble vascular cell adhesion molecule, soluble E-selectin, and matrix metalloproteinase-9 were detected by enzyme linked immunosorbent assay. RESULTS: Upon admission, serum levels of soluble intercellular adhesion molecule, soluble vascular cell adhesion molecule, soluble E-selectin, and matrix metalloproteinase-9 were significantly increased in patients with cerebral infarction, compared with control subjects (P 〈 0.01). Following HBO and routine treatments, serum levels of the above-mentioned indices were significantly reduced in the HBO and routine treatment groups (P 〈 0.01). Moreover, greater efficacy was observed in the HBO group, compared with the routine treatment group (P 〈 0.05 or P 〈 0.01). CONCLUSION: Intergroup comparison and case-control results indicated that HBO noticeably reduced serum levels of soluble intercellular adhesion molecule, soluble vascular cell adhesion molecule, soluble E-selectin, and matrix metalloproteinase-9.
基金the grantsfrom Fujian Science and Technology Bureau, No.2006Y0012
文摘BACKGROUND: Learning and memory damage is one of the most permanent and the severest symptoms of traumatic brain injury; it can seriously influence the normal life and work of patients. Some research has demonstrated that cognitive disorder is closely related to nicotine cholinergic receptors, N-methyl-D aspartate receptors, neural cell adhesion molecule, and brain-derived neurotrophic factor. OBJECTIVE: To summarize the cognitive disorder and changes in nicotine cholinergic receptors, N-methyl-D aspartate receptors, neural cell adhesion molecule, and brain-derived neurotrophic factor following brain injury. RETRIEVAL STRATEGY: A computer-based online search was conducted in PUBMED for English language publications containing the key words "brain injured, cognitive handicap, acetylcholine, N-methyl-D aspartate receptors, neural cell adhesion molecule, brain-derived neurotrophic factor" from January 2000 to December 2007. There were 44 papers in total. Inclusion criteria: ① articles about changes in nicotine cholinergic receptors, N-methyl-D aspartate receptors, neural cell adhesion molecule, and brain-derived neurotrophic factor following brain injury; ② articles in the same researching circle published in authoritative journals or recently published. Exclusion criteria: duplicated articles. LITERATURE EVALUATION: References were mainly derived from research on changes in these four factors following brain injury. The 20 included papers were clinical or basic experimental studies. DATA SYNTHESIS: After craniocerebral injury, changes in these four factors in brain were similar to those during recovery from cognitive disorder, to a certain degree. Some data have indicated that activation of nicotine cholinergic receptors, N-methyl-D aspartate receptors, neural cell adhesion molecule, and brain-derived neurotrophic factor could greatly improve cognitive disorder following brain injury. However, there are still a lot of questions remaining; for example, how do these factors change at different time points after brain injury, and what is the relationship between associated factors and cognitive disorder. CONCLUSION: It is necessary to comprehensively study some associated factors, to analyze their changes and their relationship with cognitive disorder following brain injury, and to investigate their effects at different time points after brain injury.
基金supported by grants from the National Natural Science Foundation of China(No.81873473 and No.91939110)Academic Promotion Program of Shandong First Medical University(No.2019QL014)Shandong Taishan Scholarship(Ju Liu).
文摘Objective:Lymphatic endothelial cell(LEC)proliferation is essential for lymphangiogenesis.Hypoxia induces lymphangiogenesis,but it directly inhibits LEC proliferation and the underlying mechanisms have not been fully understood.The aim of this study was to investigate the role of carcinoembryonic antigen-related cell adhesion molecule 1(CEACAM1)in hypoxia-repressed LEC proliferation.Methods:Human dermal lymphatic endothelial cells(HDLECs)were cultured under normoxic or hypoxic conditions,and cell proliferation was determined using MTT or CCK-8 assays.CEACAM1 expression was silenced by siRNA transfection.Activation of mitogen-activated protein kinases(MAPKs)was examined by Western blotting and blocked by specific inhibitors.Results:Under hypoxia,HDLECs proliferation was suppressed and CEACAM1 expression was downregulated.Silence of CEACAM1 in normoxia inhibited HDLECs proliferation and did not further decrease proliferation in HDLECs in response to hypoxia,suggesting that CEACAM1 may mediate hypoxia-induced inhibition of HDLECs proliferation.In addition,silence of CEACAM1 increased phosphorylation of MAPK molecules:extracellular signal-regulated kinase(ERK),p38 MAPK and Jun N-terminal kinase(JNK)in HDLECs.However,only inhibition of the JNK pathway rescued the reduction of HDLEC proliferation induced by CEACAM1 silence.Conclusion:Our results suggested that hypoxia downregulates CEACAM1 expression by activation of the JNK pathway,leading to inhibition of HDLEC proliferation.These findings may help to understand the mechanisms of LEC-specific response to hypoxia and develop novel therapies for pathological lymphangiogenesis.
文摘This study examined the expression of cell adhesion molecule 1 (CADM1) in pancreatic cancer and the possible mechanism. The expression of CADM 1 was detected by immunohistochemistry in tissues of pancreatic cancer, pancreatitis, and normal pancreas. The plasmid pcDNA3.1-Hy- gro(+)/CADM1 was transfected into PANC-1 cells (a pancreatic cancer cell line). The expression of CADM1 in the transfected cells was determined by RT-PCR and Western blotting. Cell growth was measured by the MTT method and cell apoptosis by flow cytometry. The results showed that CADM1 was weakly expressed in tissues of pancreatic cancer in contrast to its high expression in normal pancreatic and pancreatitis tissues. The expression level of CADM in pancreatic caner was intensely correlated with the differentiation degree, lymph node metastasis and TNM stages. The growth of CADMl-transfected PANC-1 cells was significantly suppressed in vitro by a G1 cell cycle arrest and apoptosis occurrence. It was concluded that re-expression of CADM1 inhibits the growth of pancreatic cancer cells and induces their apoptosis in vitro. As a tumor suppressor gene, CADM1 plays an important role in the occurrence, progression and metastasis of pancreatic cancer.