期刊文献+
共找到16篇文章
< 1 >
每页显示 20 50 100
Transcriptome analysis of adherens junction pathway-related genes after peripheral nerve injury 被引量:3
1
作者 Sheng Yi Xing-Hui Wang Ling-Yan Xing 《Neural Regeneration Research》 SCIE CAS CSCD 2018年第10期1804-1810,共7页
The neural regeneration process is driven by a wide range of molecules and pathways. Adherens junctions are critical cellular junctions for the integrity of peripheral nerves. However, few studies have systematically ... The neural regeneration process is driven by a wide range of molecules and pathways. Adherens junctions are critical cellular junctions for the integrity of peripheral nerves. However, few studies have systematically characterized the transcript changes in the adherens junction pathway following injury. In this study, a rat model of sciatic nerve crush injury was established by forceps. Deep sequencing data were analyzed using comprehensive transcriptome analysis at 0, 1, 4, 7, and 14 days after injury. Results showed that most individual molecules in the adherens junctions were either upregulated or downregulated after nerve injury. The m RNA expression of ARPC1 B, ARPC3, TUBA8, TUBA1 C, CTNNA2, ACTN3, MET, HGF, NME1 and ARF6, which are involved in the adherens junction pathway and in remodeling of adherens junctions, was analyzed using quantitative real-time polymerase chain reaction. Most of these genes were upregulated in the sciatic nerve stump following peripheral nerve injury, except for CTNNA2, which was downregulated. Our findings reveal the dynamic changes of key molecules in adherens junctions and in remodeling of adherens junctions. These key genes provide a reference for the selection of clinical therapeutic targets for peripheral nerve injury. 展开更多
关键词 peripheral nerve regeneration crushed sciatic nerve RNA-SEQ adherens junctions remodeling of adherens junctions Venn diagram ingenuity pathway analysis differentially expressed genes comprehensive transcript analysis transcriptomics heatmap neural regeneration
下载PDF
The tumor suppressor CYLD controls epithelial morphogenesis and homeostasis by regulating mitotic spindle behavior and adherens junction assembly 被引量:1
2
作者 Wei Xie Yunfan Yang +5 位作者 Siqi Gao Ting Song Yuhan Wu Dengwen Li Min Liu Jun Zhou 《Journal of Genetics and Genomics》 SCIE CAS CSCD 2017年第7期343-353,共11页
Epithelial morphogenesis and homeostasis are essential for animal development and tissue regeneration, and epithelial disorganization is associated with developmental disorders and tumorigenesis. However, the molecula... Epithelial morphogenesis and homeostasis are essential for animal development and tissue regeneration, and epithelial disorganization is associated with developmental disorders and tumorigenesis. However, the molecular mechanisms that contribute to the morphogenesis and homeostasis of the epithelium remain elusive. Herein, we report a novel role for the cylindromatosis (CYLD) tumor suppressor in these events. Our results show that CYLD depletion disrupts epithelial organization in both Drosophila egg chambers and mouse skin and intestinal epithelia. Microscopic analysis of proliferating cells in mouse epithelial tissues and cultured organoids reveals that loss of CYLD synergizes with tumor-promoting agents to cause the misorientation of the mitotic spindle. Mechanistic studies show that CYLD accu- mulates at the cell cortex in epithelial tissues and cultured ceils, where it promotes the formation of epithelial adherens junctions through the modulation of microtuhule dynamics. These data suggest that CYLD controls epithelial morphogenesis and homeostasis by modulating the assembly of adherens junctions and ensuring proper orientation of the mitotic spindle. Our findings thus provide novel insight into the role of CYLD in development, tissue homeostasis, and tumorigenesis. 展开更多
关键词 EPITHELIUM CYLD Mitotic spindle Cell cortex adherens junction
原文传递
The complex of Fas-associated factor 1 with Hsp70 stabilizes the adherens junction integrity by suppressing RhoA activation 被引量:1
3
作者 Soonhwa Song Joon Kyu Park +7 位作者 Sang Chui Shin Jae-Jin Lee Seung Kon Hong In-Kang Song Bokyung Kim Eun Joo Song Kong-Joo Lee Eunice EunKyeong Kim 《Journal of Molecular Cell Biology》 SCIE CAS CSCD 2022年第6期14-29,共16页
Fas-associated factor 1 (FAF1) is a scaffolding protein that plays multiple functions, and dysregulation of FAF1 is associated withmany types of diseases such as cancers. FAF1 contains multiple ubiquitin-related domai... Fas-associated factor 1 (FAF1) is a scaffolding protein that plays multiple functions, and dysregulation of FAF1 is associated withmany types of diseases such as cancers. FAF1 contains multiple ubiquitin-related domains (UBA, UBL1, UBL2, UAS, and UBX), eachdomain interacting with a specific partner. In particular, the interaction of UBL1 with heat shock protein 70 (Hsp70) is associatedwith tumor formation, although the molecular understanding remains unknown. In this study, the structural analysis revealed thatHis160 of FAF1 is important for its interaction with Hsp70. The association of Hsp70 with FAF1 is required for the interaction withIQGAP1. FAF1 negatively regulates RhoA activation by FAF1–Hsp70 complex formation, which then interacts with IQGAP1. Thesesteps play a key role in maintaining the stability of cell-to-cell junction. We conclude that FAF1 plays a critical role in the structureand function of adherens junction during tissue homeostasis and morphogenesis by suppressing RhoA activation, which induces theactivation of Rho-associated protein kinase, phosphorylation of myosin light chain, formation of actin stress fiber, and disruptionof adherens junction. In addition, depletion of FAF1 increased collective invasion in a 3D spheroid cell culture. These results provideinsightinto how the FAF1–Hsp70 complex acts as a novelregulator ofthe adherens junction integrity. The complex can be a potentialtherapeutic target to inhibit tumorigenesis and metastasis. 展开更多
关键词 human Fas-associated factor 1(FAF1) heat shock protein 70(Hsp70) adherens junction RhoA activation IQGAP1 X-ray crystallography FAF1–Hsp70 complex
原文传递
Beneficial effects of nutritional supplements on intestinal epithelial barrier functions in experimental colitis models in vivo 被引量:6
4
作者 Hilda Vargas-Robles Karla Fabiola Castro-Ochoa +1 位作者 Alí Francisco Citalán-Madrid Michael Schnoor 《World Journal of Gastroenterology》 SCIE CAS 2019年第30期4181-4198,共18页
Acute and chronic colitis affect a huge proportion of the population world-wide.The etiology of colitis cases can be manifold,and diet can significantly affect onset and outcome of colitis.While many forms of acute co... Acute and chronic colitis affect a huge proportion of the population world-wide.The etiology of colitis cases can be manifold,and diet can significantly affect onset and outcome of colitis.While many forms of acute colitis are easily treatable,chronic forms of colitis such as ulcerative colitis and Crohn’s disease(summarized as inflammatory bowel diseases)are multifactorial with poorly understood pathogenesis.Inflammatory bowel diseases are characterized by exacerbated immune responses causing epithelial dysfunction and bacterial translocation.There is no cure and therapies aim at reducing inflammation and restoring intestinal barrier function.Unfortunately,most drugs can have severe side effects.Changes in diet and inclusion of nutritional supplements have been extensively studied in cell culture and animal models,and some supplements have shown promising results in clinical studies.Most of these nutritional supplements including vitamins,fatty acids and phytochemicals reduce oxidative stress and inflammation and have shown beneficial effects during experimental colitis in rodents induced by dextran sulphate sodium or 2,4,6-trinitrobenzene sulfonic acid,which remain the gold standard in pre-clinical colitis research.Here,we summarize the mechanisms through which such nutritional supplements contribute to epithelial barrier stabilization. 展开更多
关键词 Colitis DEXTRAN sulphate sodium 2 4 6-trinitrobenzene sulfonic acid Tight JUNCTION adherens JUNCTION PHYTOCHEMICALS BUTYRATE VITAMINS Short chain fatty acids MICRONUTRIENTS
下载PDF
Orchestration of occludins, claudins, catenins and cadherins as players involved in maintenance of the blood-epididymal barrier in animals and humans 被引量:3
5
作者 Daniel G. Cyr Mary Gregory +3 位作者 Evemie Dube Julie Dufresne Peter T. K. Chan Louis Hermo 《Asian Journal of Andrology》 SCIE CAS CSCD 2007年第4期463-475,共13页
Although spermatozoa are formed during spermatogenesis in the testis, testicular spermatozoa are immature and cannot swim or fertilize. These critical spermatozoal functions are acquired in the epididymis where a spec... Although spermatozoa are formed during spermatogenesis in the testis, testicular spermatozoa are immature and cannot swim or fertilize. These critical spermatozoal functions are acquired in the epididymis where a specific luminal environment is created by the blood-epididymal barrier; proteins secreted by epididymal principal cells bind to maturing spermatozoa and regulate the maturational process of the spermatozoa. In the epididymis, epithelial cell-cell interactions are mediated by adhering junctions, necessary for cell adhesion, and by tight junctions, which form the blood-epididymal barrier. The regulation of these cellular junctions is thought to represent a key determinant in the process of sperm maturation within the epididymis. Tight junctions between adjacent principal cells permit the formation of a specific microenvironment in the lumen of the epididymis that is essential for sperm maturation. Although we have made significant progress in understanding epididymal function and the blood-epididymal barrier, using animal models, there is limited information on the human epididymis. If we are to understand the normal and pathological conditions attributable to human epididymal function, we must clearly establish the physiological, cellular and molecular regulation of the human epididymis, develop tools to characterize these functions and develop clinical strategies that will use epididymal functions to improve treatment of infertility. (Asian J Androl 2007 July; 9: 463- 475) 展开更多
关键词 CLAUDINS CADHERINS CATENINS human rat mouse tight junction adherens junction
下载PDF
Genetic factors for nerve susceptibility to injuries – lessons from PMP22 deficiency 被引量:3
6
作者 Jun Li 《Neural Regeneration Research》 SCIE CAS CSCD 2014年第18期1661-1664,共4页
Genetic factors may be learnt from families with gene mutations that render nerve-injury sus- ceptibility even to ordinary physical activities. A typical example is hereditary neuropathy with liability to pressure pal... Genetic factors may be learnt from families with gene mutations that render nerve-injury sus- ceptibility even to ordinary physical activities. A typical example is hereditary neuropathy with liability to pressure palsies (HNPP). HNPP is caused by a heterozygous deletion of PMP22 gene. PMP22 deficiency disrupts myelin junctions (such as tight junction and adherens junctions), leading to abnormally increased myelin permeability that explains the nerve susceptibility to injury. This finding should motivate investigators to identify additional genetic factors contribut- ing to nerve vulnerability of injury. 展开更多
关键词 nerve injury peripheral myelin protein-22 PMP22 Charcot-Marie-Tooth disease MYELIN tight junction adherens junction action potential propagation myelin permeability
下载PDF
Alterations in cell adhesion proteins and cardiomyopathy 被引量:2
7
作者 Jifen Li 《World Journal of Cardiology》 CAS 2014年第5期304-313,共10页
Cell adhesive junction is specialized intercellular struc-ture composed of cell adhesion proteins. They are essential to connect adjacent heart muscle cell and make heart contraction effectively and properly. Clini-ca... Cell adhesive junction is specialized intercellular struc-ture composed of cell adhesion proteins. They are essential to connect adjacent heart muscle cell and make heart contraction effectively and properly. Clini-cal and genetic studies have revealed close relationship between cell adhesive proteins and the occurrence of various cardiomyopathies. Here we will review recent development on the disease phenotype, potential cel-lular and molecular mechanism related to cell adhesion molecules, with particular disease pathogenesis learned from genetic manipulated murine models. 展开更多
关键词 CARDIOMYOPATHY adherens junction DESMOSOME INTERCALATED DISC ARRHYTHMIA
下载PDF
Dynamic interplay between adhesion surfaces in carcinomas:Cell-cell and cell-matrix crosstalk 被引量:1
8
作者 Yvonne E Smith Sri HariKrishna Vellanki Ann M Hopkins 《World Journal of Biological Chemistry》 CAS 2016年第1期64-77,共14页
Cell-cell and cell-matrix signaling and communication between adhesion sites involve mechanisms which are required for cellular functions during normal development and homeostasis; however these cellular functions and... Cell-cell and cell-matrix signaling and communication between adhesion sites involve mechanisms which are required for cellular functions during normal development and homeostasis; however these cellular functions and mechanisms are often deregulated in cancer. Aberrant signaling at cell-cell and cell-matrix adhesion sites often involves downstream mediators including Rho GTPases and tyrosine kinases. This review discusses these molecules as putative mediators of cellular crosstalk between cell-cell and cell-matrix adhesion sites, in addition to their attractiveness as therapeutic targets in cancer. Interestingly, inter-junctional crosstalk mechanisms are frequently typified by the way in which bacterial and viral pathogens opportunistically infect or intoxicate mammalian cells. This review therefore also discusses the concept of learning from pathogen-host interaction studies to better understand coordinated communication between cell-cell and cell-matrix adhesion sites, in addition to highlighting the potential therapeutic usefulness of exploiting pathogens or their products to tap into inter-junctional crosstalk. Taken together, we feel that increased knowledge around mechanisms of cell-cell and cell-matrix adhesion site crosstalk and consequently a greater understanding of their therapeutic targeting offers a unique opportunity to contribute to the emerging molecular revolution in cancer biology. 展开更多
关键词 Cell-cell Cell-matrix ADHESION Cancer CROSSTALK Pathogens Epithelial Barrier function Tight JUNCTION CELL migration Apical junctional complex adherens JUNCTION ADHESION molecules Extracellular matrix Tyrosine kinases GTPases Rho
下载PDF
Soft Substrate Induces Endothelial Cell Inflammation and Disrupts Endothelium Integrity
9
作者 Yiling Tan Xiuli Mao Huanli Wang 《Journal of Biosciences and Medicines》 2021年第2期92-102,共11页
Atherosclerosis (AS) is the main cause of death and disability all over the world. A lot of efforts have been devoted to treat AS, among which tissue engineering blood vessel materials, including artificial blood vess... Atherosclerosis (AS) is the main cause of death and disability all over the world. A lot of efforts have been devoted to treat AS, among which tissue engineering blood vessel materials, including artificial blood vessels, stents and vascular patches, have brought hope to ameliorate the symptoms in AS patients. However, there remains a large percentage of implantation failure due to the incompatibility of the material with the body. AS is a multi-factor related disease, and chronic inflammation is a major event that involves with its pathogenesis and development. Since previous studies suggested that the stiffness of the blood vessel might affect the inflammatory conditions, in this paper, we investigate the mechanism of how substrate stiffness could affect the inflammation response of the endothelial cells (ECs). Polyacrylamide (PA) based hydrogels at different concentrations were used as the culture substrate for ECs. The mRNA expression level of VCAM-1 and ICAM-1 was determined by qRT-PCR. EC chemotactic effect was evaluated by the number of THP-1 adhered to EC monolayer. The protein levels of IκBα and NF-κB were determined by western blotting analysis. The expression and localization of the major adherens junctions (AJs) proteins, VE-cadherin and β-catenin, were evaluated by western blotting and immunofluorescence staining. Our results showed that ECs cultured on soft substrate (1 kPa) demonstrated more chemotactic effect and the amount of the monocytes adhered to them was higher than that on harder substrate (20 kPa, p < 0.05). Moreover, NF-κB signaling pathway in ECs on 1 kPa substrate was more activated compared to those on 20 kPa substrate, with the IκBα protein expression level in the cytoplasm decreasing and NF-κB translocating more into the nuclear. In addition, the AJs of the endothelial monolayer changed with the substrate stiffness. Compared with ECs on normal substrate (20 kPa), the protein expression level of β-catenin decreased (p < 0.05), and immunofluorescence staining of VE-cadherin and β-catenin showed the AJs between the ECs on soft substrate (1 kPa) were punctuated. Taken together, our results suggested the stiffness of the substrate was important in regulating inflammation of the ECs and the integrity of the cell-cell junction. Therefore, the stiffness of the tissue engineering blood vessel material should be considered as an important criterium to avoid EC inflammation. 展开更多
关键词 Substrate Stiffness Endothelial Cells INFLAMMATION adherens Junction
下载PDF
The P2Y<sub>2</sub>Receptor Interacts with VE-Cadherin and VEGF Receptor-2 to Regulate Rac1 Activity in Endothelial Cells
10
作者 Zhongji Liao Chen Cao +4 位作者 Jianjie Wang Virginia H. Huxley Olga Baker Gary A. Weisman Laurie Erb 《Journal of Biomedical Science and Engineering》 2014年第14期1105-1121,共17页
Vascular endothelial cadherin (VE-cadherin) mediates homophylic adhesion between endothelial cells and is an important regulator of angiogenesis, blood vessel permeability and leukocyte trafficking. Rac1, a member of ... Vascular endothelial cadherin (VE-cadherin) mediates homophylic adhesion between endothelial cells and is an important regulator of angiogenesis, blood vessel permeability and leukocyte trafficking. Rac1, a member of the Rho family of GTPases, controls VE-cadherin adhesion by acting downstream of several growth factors, including angiopoietin-1 and vascular endothelial growth factor (VEGF). Here we show that UTP-induced activation of the Gq protein-coupled P2Y2 nucleotide receptor (P2Y2R) in human coronary artery endothelial cells (HCAECs) activated Rac1 and caused a transient complex to form between P2Y2R, VE-cadherin and VEGF receptor-2 (VEGFR-2). Knockdown of VE-cadherin expression with siRNA did not affect UTP-induced activation of extracellular signal-regulated kinases 1/2 (ERK1/2) but led to a loss of UTP-induced Rac1 activation and tyrosine phosphorylation of p120 catenin, a cytoplasmic protein known to interact with VE- cadherin. Activation of the P2Y2R by UTP also caused a prolonged interaction between p120 catenin and vav2 (a guanine nucleotide exchange factor for Rac) that correlated with the kinetics of UTP-induced tyrosine phosphorylation of p120 catenin and VE-cadherin. Inhibitors of VEGFR-2 (SU1498) or Src (PP2) significantly diminished UTP-induced Rac1 activation, tyrosine phosphorylation of p120 catenin and VE-cadherin, and association of the P2Y2R with VE-cadherin and p120 catenin with vav2. These findings suggest that the P2Y2R uses Src and VEGFR-2 to mediate association of the P2Y2R with VE-cadherin complexes in endothelial adherens junctions to activate Rac1. 展开更多
关键词 VE-CADHERIN P2Y Receptors Rac ENDOTHELIUM adherens Junctions
下载PDF
Gα_s Relays Sphingosine-1-Phosphate Receptor 1 Signaling to Stabilize Vascular Endothelial-Cadherin at Endothelial Junctions to Control Mouse Embryonic Vascular Integrity 被引量:8
11
作者 Ximing Shao Ke Liu +6 位作者 Yi Fan Zhihao Ding Min Chen Minyan Zhu Lee S.Weinstein Hongchang Li Huashun Li 《Journal of Genetics and Genomics》 SCIE CAS CSCD 2015年第11期613-624,共12页
Sphingosine-1-phosphate receptor 1 (S1PR1), a G protein-coupled recep (GPCR). controls vasct stability by stabilizing vascular endothelial (VE)-cadherin junctional localization and inhibiting vascular endothelia... Sphingosine-1-phosphate receptor 1 (S1PR1), a G protein-coupled recep (GPCR). controls vasct stability by stabilizing vascular endothelial (VE)-cadherin junctional localization and inhibiting vascular endothelial growth factor receptor 2(VEGFR2) signaling. However, the molecular mechanisms that link S1PR1 signaling to intracellular effectors remain unknown.In this study,we demonstrate that the heterotrimeric G protein subfamily member Gαs, encoded by GNAS,acts as a relay mediator of S1PR1 signaling to control vascular integrity by stabilizing VE-cadherin at endothelial junctions. The endothelial cell -spectific deletion of Gαs in mice causes early embryonic lethality with massive hemorrhage and a disorganized Vaseuiature.The immunostaining results revealed that Gαs deletion remarkably reduces the junctional localization of VE-cadherin, whereas the mull cell coverage of the vessels is not impaired.In addition, we found-that Gαs depletion blocks the S1PR1-activation induced VE-cadherin stabilization at junctons,supporting that Gαs acts downstream of S1PR1 signaling ThuS, our results demonstrate that Gαs is an essential mediator to relay S1PR1 signaling and maintain vascular integrity. 展开更多
关键词 Gαs VE-eadherin S1PR1 signaling adherens junctions vascular integrity
原文传递
Role of Glutamine in the Mediation of E-cadherin, p120-catenin and Inflammation in Ventilator-induced Lung Injury 被引量:8
12
作者 Jian-Lei Qiu Bai-Ling Song +2 位作者 Yu-Juan Wang Fu-Tao Zhang Yue-Lan Wang 《Chinese Medical Journal》 SCIE CAS CSCD 2018年第7期804-812,共9页
Background: Ventilator-induced lung injury (VILI) is commonly associated with barrier dysfunction and inflammation reaction. Glutamine could ameliorate VILI, but its role has not been fully elucidated, This study e... Background: Ventilator-induced lung injury (VILI) is commonly associated with barrier dysfunction and inflammation reaction. Glutamine could ameliorate VILI, but its role has not been fully elucidated, This study examined the relationship between inflammatory cytokines (interleukin JILl-6, tumor necrosis factor [TNF]-α, and IL-10) and adherens junctions (E-cadherin, p 120-catenin), which were ameliorated by glutamine in VILI, both in vitro and in vivo. Methods: For the in vivo study, 30 healthy C57BL/6 mice weighing 25-30 g were randomly divided into five groups with random number table (n = 6 in each group): control (Group C); low tidal volume (Group L); low tidal volume + glutamine (Group L + G); high tidal volume (Group H); and high tidal volume + glutamine (Group H + G). Mice in all groups, except Group C, underwent mechanical ventilation for 4 h. For the in vitro study, mouse lung epithelial 12 (MLE- 12) cells pretreated with glutamine underwent cyclic stretching at 20% for 4 h. Cell lysate and lung tissue were obtained to detect the junction proteins, inflammatory cytokines, and lung pathological changes by the Western blotting, cytokine assay, hematoxylin and eosin staining, and immunofluorescence. Results: In vivo, compared with Group C, total cell counts (t= -28.182, P 〈 0.01), the percentage of neutrophils (t = -28.095, P 〈 0.01), IL-6 (t = -28.296, P 〈 0.01 ), and TNF-α(t = - 19.812, P 〈 0.01 ) in bronchoalveolar lavage (BAL) fluid, lung injury scores (t = -6.708, P 〈 0.01), and the wet-to-dry ratio (t = - 15.595, P 〈 0.01 ) were increased in Group H; IL- 10 in BAL fluid (t = 9.093, P 〈 0.01 ) and the expression of E-cadherin (t= 10.044, P 〈 0.01) and p120-catenin (t = 13.218, P 〈 0.01) were decreased in Group H. Compared with Group H, total cell counts (t - 14.844, P 〈 0.01 ), the percentage of neutrophils (t = 18.077, P 〈 0.0 l ), IL-6 (t - 18.007, P 〈 0.01 ), and TNF-α (t =1 0.171, P 〈 0.01 ) in BAL fluid were decreased in Group H + G; IL-10 in BAL fluid (t - -7.531, P 〈 0.01 ) and the expression of E-cadherin (t = - 14.814, P 〈 0.01 ) and p 120-catenin (t = -9.114, P 〈 0.01 ) were increased in Group H + G. In vitro, compared with the nonstretching group, the levels of IL-6 (t = 21.111, P 〈 0.01 ) and TNF-α (t - 15.270, P 〈 0.01 ) were increased in the 20% cyclic stretching group; the levels of IL- 10 (t = 5.450, P 〈 0.01 ) and the expression of E-cadherin (t = 17.736, P 〈 0.01 ) and p 120-catenin (t = 16.136, P 〈 0.01 ) were decreased in the 20% cyclic stretching group. Compared with the stretching group, the levels of IL-6 (t = 11.818, P 〈 0.01) and TNF-α (t = 8.631, P 〈 0.01 ) decreased in the glutamine group; the levels of IL- 10 (t = 3.203, P 〈 0.05) and the expression of E-cadherin (t= 13.567, P 〈 0.01) and p 120-catenin (t = -10.013, P 〈 0.01) were increased in the glutamine group. Conclusions: High tidal volume mechanical ventilation and 20% cyclic stretching could cause VIM. Glutamine regulates VIM by improving cytokines and increasing the adherens junctions, protein E-cadherin and p 120-catenin, to enhance the epithelial barrier function. 展开更多
关键词 adherens Junctions GLUTAMINE Inflammatory Cytokines Ventilation-induced Lung Injury
原文传递
Loss of p120 catenin aggravates alveolar edema of ventilation induced lung injury 被引量:6
13
作者 DAI Chen-yang DAI Guo-feng SUN Yu WANG Yue-lan 《Chinese Medical Journal》 SCIE CAS CSCD 2013年第15期2918-2922,共5页
Background p120 catenin (p120ctn) is an adheren junction protein that regulates barrier function, but its role has not been explored in alveolar edema induced by ventilation. We measured stretch-induced cell gap for... Background p120 catenin (p120ctn) is an adheren junction protein that regulates barrier function, but its role has not been explored in alveolar edema induced by ventilation. We measured stretch-induced cell gap formation in MLE 12 cells due to the loss of p120. We hypothesized that alveolar permeability was increased by high tung inflation associated with alveolar epithelia cell tight junctions being destroyed, which resulted from the loss of p120. Methods Cultured MLE12 cells were subjected to being stretched or un-stretched (control) and some cells were pretreated with pp2 (c-src inhibitor). After the end of stretching for 0, 1, 2, and 4 hours, the cells were lysed, and p120 expression and c-src activation was determined by Western blotting analysis. In vivo, SD rats were taken to different tidal volumes (Vt 7 ml/kg or 40 ml/kg, PEEP=0, respiratory rate 30-40 betas/min) for 0, 1, 2, and 4 hour and some were pretreated with pp2, and alveolar edema was calculated. Rerults It was found that p120 expression was reduced and c-src activation increased in a time-dependent and strain- dependent manner due to cyclic-stretch of the alveolar epithelial cells. These changes could be reversed by inhibition of c-src. We obtained similar changes in rats when they were subjected to large tidal volumes and the alveolar edema increased more than in rats in the low Vt group. Pretreated the rats with inhibition of c-src had less pulmonary edema induced by the high tidal volume ventilation. Conclusions Cyclic stretch MLE 12 cells induced the loss of p120 and may be the same reason by high tidal volume ventilation in rats can aggravate alveolar edema. Maintenance of p120 expression may be a novel therapeutic strategy for the prevention and treatment of ventilation induced lung injury (VILI). 展开更多
关键词 mechanical ventilation adherens junction lung injury alveolar edema
原文传递
miR-888 in MCF-7 Side Population Sphere Cells Directly Targets E-cadherin 被引量:3
14
作者 Shengjian Huang Ming Cai +3 位作者 Yinghui Zheng Longhai Zhou Qiang Wang Liangbiao Chen 《Journal of Genetics and Genomics》 SCIE CAS CSCD 2014年第1期35-42,共8页
Side population (SP) cells are a small subset of cells isolated from a cultured cancer cell line that exhibit characteristics similar to those of cancer stem cells (CSCs), such as high metastatic and tumorigenic p... Side population (SP) cells are a small subset of cells isolated from a cultured cancer cell line that exhibit characteristics similar to those of cancer stem cells (CSCs), such as high metastatic and tumorigenic potential. The molecular mechanisms that give rise to the malignant properties of SP cells are not clear. We isolated SP cells from the MCF-7 breast cancer cell line and profiled microRNA (miRNA) expression patterns between SP cell-derived spheroids and non-SP cells. SP spheroids were found to possess 42 up-regulated miRNAs and 27 down-regulated ones (above 5-fold changes). One of the up-regulated miRNAs, miR-888 computationally predicted to participate in the adherens junction (AJ) pathway, was investigated. Over-expression of miR-888 in MCF-7 cells reduced the mRNA levels of all four AJ pathway genes (E-cadherin, ACTG1, PTPRTand CDC42) that were selected for testing, whereas knocking down miR-888 reversed the trends. Western blot and flow cytometric quantitation of the membrane E-cadherin levels showed the same trend of change under these treatments. Luciferase reporter assay showed E-cadherin is a direct target of miR-888. As a potential role in intercellular adhesiveness and maintenance of malignant tissue architecture, the results indicate that miR-888 is a repressor of the AJ pathway in MCF-7 cells and that up-regulation of miR-888 contributes to aggressiveness in MCF-7 SP cells. 展开更多
关键词 Side population Cancer stem cell MICRORNA adherens junction Cancer metastasis
原文传递
The septin complex links the catenin complex to the actin cytoskeleton for establishing epithelial cell polarity 被引量:2
15
作者 Xueying Wang Wenwen Wang +8 位作者 Xiwei Wang Ming Wang Lijuan Zhu Fatima Garba Chuanhai Fu Barbara Zieger Xu Liu Xing Liu Xuebiao Yao 《Journal of Molecular Cell Biology》 SCIE CAS CSCD 2021年第6期395-408,共14页
Cell polarity is essential for spatially regulating of physiological processes in metazoans by which hormonal stimulation‒secretion coupling is precisely coupled for tissue homeostasis and organ communications.However... Cell polarity is essential for spatially regulating of physiological processes in metazoans by which hormonal stimulation‒secretion coupling is precisely coupled for tissue homeostasis and organ communications.However,the molecular mechanisms underlying epithelial cell polarity establishment remain elusive.Here,we show that septin cytoskeleton interacts with catenin complex to organize a functional domain to separate apical from basal membranes in polarized epithelial cells.Using polarized epithelial cell monolayer as a model system with transepithelial electrical resistance as functional readout,our studies show that septins are essential for epithelial cell polarization.Our proteomic analyses discovered a novel septin‒catenin complex during epithelial cell polarization.The functional relevance of septin‒catenin complex was then examined in three-dimensional(3D)culture in which suppression of septins resulted in deformation of apical lumen in cysts,a hallmark seen in polarity-deficient 3D cultures and animals.Mechanistically,septin cytoskeleton stabilizes the association of adherens catenin complex with actin cytoskeleton,and depletion or disruption of septin cytoskeleton liberates adherens junction and polarity complexes into the cytoplasm.Together,these findings reveal a previously unrecognized role for septin cytoskeleton in the polarization of the apical‒basal axis and lumen formation in polarized epithelial cells. 展开更多
关键词 SEPTIN CYTOSKELETON cell polarity adherens junction epithelial cells
原文传递
Cell surface clustering of Cadherin adhesion complex induced by antibody coated beads
16
作者 Wenjun Zhang Zhongxiang Lin Ying Hu 《Chinese Science Bulletin》 SCIE EI CAS 2000年第16期1504-1509,共6页
Cadherin receptors mediate cell-cell adhesion, signal transduction and assembly of cytoskeletons. How a single transmembrane molecule Cadherin can be involved in multiple functions through modulating its binding activ... Cadherin receptors mediate cell-cell adhesion, signal transduction and assembly of cytoskeletons. How a single transmembrane molecule Cadherin can be involved in multiple functions through modulating its binding activities with many membrane adhesion molecules and cytoskeletal components is an unanswered question which can be elucidated by clues from bead experiments. Human lung cells expressing N-Cadherin were examined. After co-incubation with anti-N-Cadherin monoclonal antibody coated beads, cell surface clustering of N-Cadherin was induced. Immunofluorescent detection demonstrated that in addition to Cadherin, β-Catenin, α-Catenin, a-Actinin and Actin fluorescence also aggregated respectively at the membrane site of bead attachment. Myosin heavy chain (MHC), another major component of Actin cytoskeleton, did not aggregate at the membrane site of bead attachment. Adhesion unrelated protein Con A and polylysine conjugated beads did not induce the clustering of adhesion molecules. It is indicated 展开更多
关键词 LATEX BEAD N-CADHERIN adherens junction adhesion molecular complex.
原文传递
上一页 1 下一页 到第
使用帮助 返回顶部