NIH 3T3 cells, a mouse fibroblast cell line used as routine target cells for transfection experiments, undergo spontaneous transformation in our experiments after they form a confluent sheet in medium containing fetal...NIH 3T3 cells, a mouse fibroblast cell line used as routine target cells for transfection experiments, undergo spontaneous transformation in our experiments after they form a confluent sheet in medium containing fetal bovina serum (FBS) or lower coneentrafcion of calf serum (CS). The transformation takes the form of foci of multiplying cells among the surrounding cells which have stopped cell division. However, no focus of transformed cells could be seen in medium containing high concentration (10%) of OS. Further experiments indicated that the frequency of transformation is highly dependent on the concentration of serum and the transformation in OS is changeable when the cells are passaged in FBS. 8H-thymidine autoradiography has been proved to be a sensitive measurement indicator for foous formation. Our results suggest that the high frequency of transformation and its dependence on confmenoy as well as on medium composition are characteristics of cell differentiation rather than mutation. The role of the NIH 3T3 cell line as a cancer-initiated cell population and its accelerated transformation by rat oncogene might be considered as a form of tumor promotion is discussed.展开更多
NF-IL6 is a member of c/EBP family and has multiple functions in regulation of cellular gene expression. We have constructed NF-IL6 expression plasmids and trans fected the NIH3T3 cells with them. The sense NF-IL6 tra...NF-IL6 is a member of c/EBP family and has multiple functions in regulation of cellular gene expression. We have constructed NF-IL6 expression plasmids and trans fected the NIH3T3 cells with them. The sense NF-IL6 transfectants showed significantly increased tumorigenicity, and the stable integration of NF-IL6 cDNA into cellular DNA and its expression were demonstrated. Our results suggest that NF-IL6 may be related to tumorigenesis.展开更多
In previous studies we have reported that a high levelof expression of mot-2 protein results in malignant transformation of NIH 3T3 cells as analyzed by anchorage indeopendent growth and nude mice assays [Kaul et al....In previous studies we have reported that a high levelof expression of mot-2 protein results in malignant transformation of NIH 3T3 cells as analyzed by anchorage indeopendent growth and nude mice assays [Kaul et al., Oncogene, 17, 907-11, 1998]. Mot-2 was found to interact withtumor suppressor protein p53. The transient overexpression of mot-2 was inhibitory to transcriptional activationfunction of p53 [Wadhwa et al., J. Biol. Chem., 273, 2958691, 1998]. We demonstrate here that mot-2 transfectedstable clonse of NIH 3T3 that showed malignant propertiesindeed show inactivation of p53 function as assayed byexogenous p53 dependent reporter. The expression levelof p53 in response to UV-irradiation was lower in NIH3T3/mot-2 as compared to NIH 3T3 cells and also exhibited delay in reaching peak. furthermore, upon serumstarvation p53 was seen to translocate to the 11ucleus inNIH 3T3, but not in its mot-2 derivative. The data suggests that mot-2 mediated cytoplasmic sequestration andinactivation of p53 may operate, at least in part, for malignant phenotype of NIH 3T3/mot-2 cells.NIH 3T3/mot-2 cells show inactivation of p53 protein展开更多
For electronic microscopic observation, we found SSV-transformed NIH 3T3 cells were different from non-transformed cells. In SSV-transformed NIH 3T3 cells nuclei cytoplasma ratio was increased and in cytoplasma the ri...For electronic microscopic observation, we found SSV-transformed NIH 3T3 cells were different from non-transformed cells. In SSV-transformed NIH 3T3 cells nuclei cytoplasma ratio was increased and in cytoplasma the ribosomes (polyribosomes were attached to the swollen rough endoplasmic reticulum. It was likely that ribosomes were lined together functionally and structionally to produce specific protein (PDGF-like protein).展开更多
Objective:To investigate the effect of luteolin on the Epithelial-mesenchymal transition(EMT)of osteosarcoma cell line U2OS and its molecular mechanism by regulating phosphoinositide 3-kinase/protein kinase B/nuclear ...Objective:To investigate the effect of luteolin on the Epithelial-mesenchymal transition(EMT)of osteosarcoma cell line U2OS and its molecular mechanism by regulating phosphoinositide 3-kinase/protein kinase B/nuclear factor-kappa B(PI3K/AKT/NF-κB)signaling pathway.Methods:U2OS cells were treated in different concentrations(10,20 and 40μmol/L)of luteolin.MTT was used to detect the effect of luteolin on the proliferation of osteosarcoma U2OS cells.Transwell chamber assay was used to detect the influence of luteolin on migration of U2OS cells.qPCR was used to detect the influence of luteolin on the mRNA expression of Bax,Bcl-2 and Caspase-2 in U2OS cells.Western blot was used to observe the change of p-PI3K,p-AKT,p-IKK and NF-κB proteins.Immunofluorescence was used to detect the influence of luteolin on the protein expression of E-cadherin and vimentim.Results:Luteolin inhibited significantly the proliferation of U2OS cells(P<0.05)in a time-concentration-dependent manner.Luteolin inhibited significantly the migration of U2OS cells(P<0.05).After treatment with luteolin,the mRNA expression of Bax and Caspase-2 was increased significantly(P<0.05),but Bcl-2 was reduced significantly(P<0.05)in U2OS cells.The protein expression of p-PI3K,p-AKT,p-IKK,NF-κB,E-cadherin and vimentin was decreased significantly(P<0.05).Conclusions:Luteolin inhibits the proliferation,migration and EMT transformation of osteosarcoma U2OS cells,which may be related to the inhibition of PI3K/AKT/NF-κB signaling pathway.展开更多
Wireless Sensor Network(WSNs)consists of a group of nodes that analyze the information from surrounding regions.The sensor nodes are responsible for accumulating and exchanging information.Generally,node local-ization...Wireless Sensor Network(WSNs)consists of a group of nodes that analyze the information from surrounding regions.The sensor nodes are responsible for accumulating and exchanging information.Generally,node local-ization is the process of identifying the target node’s location.In this research work,a Received Signal Strength Indicator(RSSI)-based optimal node localization approach is proposed to solve the complexities in the conventional node localization models.Initially,the RSSI value is identified using the Deep Neural Network(DNN).The RSSI is conceded as the range-based method and it does not require special hardware for the node localization process,also it consumes a very minimal amount of cost for localizing the nodes in 3D WSN.The position of the anchor nodes is fixed for detecting the location of the target.Further,the optimal position of the target node is identified using Hybrid T cell Immune with Lotus Effect Optimization algorithm(HTCI-LEO).During the node localization process,the average localization error is minimized,which is the objective of the optimal node localization.In the regular and irregular surfaces,this hybrid algorithm effectively performs the localization process.The suggested hybrid algorithm converges very fast in the three-dimensional(3D)environment.The accuracy of the proposed node localization process is 94.25%.展开更多
AIM: The existence and properties of alpha-fetoprotein (AFP) receptor on the surface of NIH 3T3 cells and the effects of AFP on cellular signal transduction pathway were investigated. METHODS: The effect of AFP on the...AIM: The existence and properties of alpha-fetoprotein (AFP) receptor on the surface of NIH 3T3 cells and the effects of AFP on cellular signal transduction pathway were investigated. METHODS: The effect of AFP on the proliferation of NIH 3T3 cells was measured by incorporation of 3H-TdR. Receptor-binding assay of 125I-AFP was performed to detect the properties of AFP receptor in NIH 3T3 cells. The influences of AFP on the [cAMP]i and the activities of protein kinase A (PKA) were determined. Western blot was used to detect the change of K-ras P21 protein expression. RESULTS: The proliferation of NIH 3T3 cells treated with 0-80 mg/L of AFP was significantly enhanced. The Scatchard analysis indicated that there were two classes of binding sites with KD of 2.722 x 10(-9)M (Bmax=12810 sites per cell) and 8.931 x 10(-8)M (Bmax=119700 sites per cell) respectively. In the presence of AFP (20 mg/L), the content of cAMP and activities of PKA were significantly elevated . The level of K-ras P21 protein was upregulated by AFP at the concentration of 20 mg/L. The monoclonal antibody against AFP could reverse the effects of AFP on the cAMP content, PKA activity and the expression of K-ras p21 gene. CONCLUSION: The effect of AFP on the cell proliferation was achieved by binding its receptor to trigger the signal transduction pathway of cAMP-PKA and alter the expression of K- ras p21 gene.展开更多
BACKGROUND: Pancreatic stellate cells (PSCs) play a major role in promoting pancreatic fibrosis. Transforming growth factor beta 1 (TGF-beta 1) is a critical mediator of this process. This study aimed to determine the...BACKGROUND: Pancreatic stellate cells (PSCs) play a major role in promoting pancreatic fibrosis. Transforming growth factor beta 1 (TGF-beta 1) is a critical mediator of this process. This study aimed to determine the expression of the Smad3 and Smad7 genes in the process of PSC activation, and explore the mechanisms of chronic pancreatitis. METHODS: The expressions of Smad3 and Smad7 in PSCs before and after TGF-beta 1 treatment were detected by reverse transcription-polymerase chain reaction and Western blotting analysis. Smad3 expression was detected in PSCs after treatment with 5 ng/ml of TGF-beta 1 for 24 hours. RESULTS: Smad7 expression was decreased in TGF-beta 1 -activated PSCs (P<0.05) in a dose-dependent manner. When TGF-beta 1 concentration reached 10 ng/ml, the expression of p-Smad3, Smad3, and Smad7 was inhibited (P<0.05). CONCLUSIONS: TGF-beta 1 promotes the expression of Smad3 and inhibits the expression of Smad7 during the activation of PSCs. In contrast, high-dose TGF-beta 1 downregulates the expression of Smad3 in completely activated PSCs.展开更多
The periodontal ligament-derived mesenchymal stem cell is regarded as a source of adult stem cells due to its multipotency.However, the proof of chondrogenic potential of the cells is scarce.Therefore,we investigated ...The periodontal ligament-derived mesenchymal stem cell is regarded as a source of adult stem cells due to its multipotency.However, the proof of chondrogenic potential of the cells is scarce.Therefore,we investigated the chondrogenic differentiation capacity of periodontal ligament derived mesenchymal stem cells induced by transforming growth factor(TGF)-p3 and bone morphogenetic protein(BMP)-6.After isolation of periodontal ligament stem cells(PDLSCs) from human periodontal ligament,the cells were cultured in Dulbecco’s modified Eagle’s medium(DMEM) with 20%fetal bovine serum(FBS).A mechanical force initiated chondrogenic differentiation of the cells.For chondrogenic differentiation,10μg·LTGF-β3 or 100μg·LBMP-6 and the combination treating group for synergistic effect of the growth factors.We analyzed the PDLSCs by fluorescence-activated cell sorting and chondrogenesis were evaluated by glycosaminoglycans assay,histology,immunohistochemistry and genetic analysis.PDLSCs showed mesenchymal stem cell properties proved by FACS analysis.Glycosaminoglycans contents were increased 217%by TGF-β3 and 220%by BMP-6. The synergetic effect of TGF-β3 and BMP-6 were shown up to 281%compared to control.The combination treatment increased Sox9, aggrecan and collagen II expression compared with not only controls,but also TGF-P3 or BMP-6 single treatment dramatically.The histological analysis also indicated the chondrogenic differentiation of PDLSCs in our conditions.The results of the present study demonstrate the potential of the dental stem cell as a valuable cell source for chondrogenesis,which may be applicable for regeneration of cartilage and bone fracture in the field of cell therapy.展开更多
AIM： To study the effect of discoidin I-like domaincontaining protein 3（EDIL3） depletion on the proliferation and epithelial-mesenchymal transition（EMT） in human lens epithelial cells（LECs）. METHODS： RNA inter...AIM： To study the effect of discoidin I-like domaincontaining protein 3（EDIL3） depletion on the proliferation and epithelial-mesenchymal transition（EMT） in human lens epithelial cells（LECs）. METHODS： RNA interference was used to inhibit the expression of EDIL3 in human LECs in vitro. The morphology of cells was observed using an inverted microscope. Cell proliferation was assessed using Ed U kit. Cell migration was investigated using Transwell chamber and EMT of LECs was assessed using confocal microscope and Western blotting. The transforming growth factor β（TGFβ） pathway was investigated using Western blotting. RESULTS： The data showed that silencing EDIL3 expression changed LECs morphology and suppressed LECs proliferation（P〈0.05） and migration（P〈0.01）. Furthermore, the result of Western blotting showed that EDIL3 depletion reduced the expression of α-smooth muscle actin（α-SMA）（P〈0.001） and vimentin（P〈0.01）, while increased the expression of E-cadherin（P〈0.001）. EDIL3 depletion could suppress the phosphorylation of Smad2（P〈0.01） and Smad3（P〈0.01） and the activation of exracellular signal regulated kinase（ERK）（P〈0.05）. CONCLUSION： The findings indicate that EDIL3 might participate in the proliferation and EMT in LECs via TGFβ pathway and may be a potential therapeutic target for the treatment of posterior capsule opacification.展开更多
Objective To investigate the feasibility of applying NIH3T3 cells transfected by VEGF gene to the treatment of ischemic random skin flaps.Methods Plasmid PcDNA3.1（-）/VEGF165 containing VEGF gene was transduced into ...Objective To investigate the feasibility of applying NIH3T3 cells transfected by VEGF gene to the treatment of ischemic random skin flaps.Methods Plasmid PcDNA3.1（-）/VEGF165 containing VEGF gene was transduced into the mouse NIH3T3 cells by liposome.Immunohistochemistry was used to detect the expression of VEGF protein of mouse NIH/3T3 cells in vitro.The NIH3T3 cell were stained with CM-DiI before the transplantation.展开更多
文摘NIH 3T3 cells, a mouse fibroblast cell line used as routine target cells for transfection experiments, undergo spontaneous transformation in our experiments after they form a confluent sheet in medium containing fetal bovina serum (FBS) or lower coneentrafcion of calf serum (CS). The transformation takes the form of foci of multiplying cells among the surrounding cells which have stopped cell division. However, no focus of transformed cells could be seen in medium containing high concentration (10%) of OS. Further experiments indicated that the frequency of transformation is highly dependent on the concentration of serum and the transformation in OS is changeable when the cells are passaged in FBS. 8H-thymidine autoradiography has been proved to be a sensitive measurement indicator for foous formation. Our results suggest that the high frequency of transformation and its dependence on confmenoy as well as on medium composition are characteristics of cell differentiation rather than mutation. The role of the NIH 3T3 cell line as a cancer-initiated cell population and its accelerated transformation by rat oncogene might be considered as a form of tumor promotion is discussed.
文摘NF-IL6 is a member of c/EBP family and has multiple functions in regulation of cellular gene expression. We have constructed NF-IL6 expression plasmids and trans fected the NIH3T3 cells with them. The sense NF-IL6 transfectants showed significantly increased tumorigenicity, and the stable integration of NF-IL6 cDNA into cellular DNA and its expression were demonstrated. Our results suggest that NF-IL6 may be related to tumorigenesis.
文摘In previous studies we have reported that a high levelof expression of mot-2 protein results in malignant transformation of NIH 3T3 cells as analyzed by anchorage indeopendent growth and nude mice assays [Kaul et al., Oncogene, 17, 907-11, 1998]. Mot-2 was found to interact withtumor suppressor protein p53. The transient overexpression of mot-2 was inhibitory to transcriptional activationfunction of p53 [Wadhwa et al., J. Biol. Chem., 273, 2958691, 1998]. We demonstrate here that mot-2 transfectedstable clonse of NIH 3T3 that showed malignant propertiesindeed show inactivation of p53 function as assayed byexogenous p53 dependent reporter. The expression levelof p53 in response to UV-irradiation was lower in NIH3T3/mot-2 as compared to NIH 3T3 cells and also exhibited delay in reaching peak. furthermore, upon serumstarvation p53 was seen to translocate to the 11ucleus inNIH 3T3, but not in its mot-2 derivative. The data suggests that mot-2 mediated cytoplasmic sequestration andinactivation of p53 may operate, at least in part, for malignant phenotype of NIH 3T3/mot-2 cells.NIH 3T3/mot-2 cells show inactivation of p53 protein
文摘For electronic microscopic observation, we found SSV-transformed NIH 3T3 cells were different from non-transformed cells. In SSV-transformed NIH 3T3 cells nuclei cytoplasma ratio was increased and in cytoplasma the ribosomes (polyribosomes were attached to the swollen rough endoplasmic reticulum. It was likely that ribosomes were lined together functionally and structionally to produce specific protein (PDGF-like protein).
基金Natural Science Foundation in Hainan Province(No.814357).
文摘Objective:To investigate the effect of luteolin on the Epithelial-mesenchymal transition(EMT)of osteosarcoma cell line U2OS and its molecular mechanism by regulating phosphoinositide 3-kinase/protein kinase B/nuclear factor-kappa B(PI3K/AKT/NF-κB)signaling pathway.Methods:U2OS cells were treated in different concentrations(10,20 and 40μmol/L)of luteolin.MTT was used to detect the effect of luteolin on the proliferation of osteosarcoma U2OS cells.Transwell chamber assay was used to detect the influence of luteolin on migration of U2OS cells.qPCR was used to detect the influence of luteolin on the mRNA expression of Bax,Bcl-2 and Caspase-2 in U2OS cells.Western blot was used to observe the change of p-PI3K,p-AKT,p-IKK and NF-κB proteins.Immunofluorescence was used to detect the influence of luteolin on the protein expression of E-cadherin and vimentim.Results:Luteolin inhibited significantly the proliferation of U2OS cells(P<0.05)in a time-concentration-dependent manner.Luteolin inhibited significantly the migration of U2OS cells(P<0.05).After treatment with luteolin,the mRNA expression of Bax and Caspase-2 was increased significantly(P<0.05),but Bcl-2 was reduced significantly(P<0.05)in U2OS cells.The protein expression of p-PI3K,p-AKT,p-IKK,NF-κB,E-cadherin and vimentin was decreased significantly(P<0.05).Conclusions:Luteolin inhibits the proliferation,migration and EMT transformation of osteosarcoma U2OS cells,which may be related to the inhibition of PI3K/AKT/NF-κB signaling pathway.
基金appreciation to King Saud University for funding this research through the Researchers Supporting Program number(RSPD2024R918),King Saud University,Riyadh,Saudi Arabia.
文摘Wireless Sensor Network(WSNs)consists of a group of nodes that analyze the information from surrounding regions.The sensor nodes are responsible for accumulating and exchanging information.Generally,node local-ization is the process of identifying the target node’s location.In this research work,a Received Signal Strength Indicator(RSSI)-based optimal node localization approach is proposed to solve the complexities in the conventional node localization models.Initially,the RSSI value is identified using the Deep Neural Network(DNN).The RSSI is conceded as the range-based method and it does not require special hardware for the node localization process,also it consumes a very minimal amount of cost for localizing the nodes in 3D WSN.The position of the anchor nodes is fixed for detecting the location of the target.Further,the optimal position of the target node is identified using Hybrid T cell Immune with Lotus Effect Optimization algorithm(HTCI-LEO).During the node localization process,the average localization error is minimized,which is the objective of the optimal node localization.In the regular and irregular surfaces,this hybrid algorithm effectively performs the localization process.The suggested hybrid algorithm converges very fast in the three-dimensional(3D)environment.The accuracy of the proposed node localization process is 94.25%.
基金This work was supported by National NaturalScience Fundation of China(No.39760077).
文摘AIM: The existence and properties of alpha-fetoprotein (AFP) receptor on the surface of NIH 3T3 cells and the effects of AFP on cellular signal transduction pathway were investigated. METHODS: The effect of AFP on the proliferation of NIH 3T3 cells was measured by incorporation of 3H-TdR. Receptor-binding assay of 125I-AFP was performed to detect the properties of AFP receptor in NIH 3T3 cells. The influences of AFP on the [cAMP]i and the activities of protein kinase A (PKA) were determined. Western blot was used to detect the change of K-ras P21 protein expression. RESULTS: The proliferation of NIH 3T3 cells treated with 0-80 mg/L of AFP was significantly enhanced. The Scatchard analysis indicated that there were two classes of binding sites with KD of 2.722 x 10(-9)M (Bmax=12810 sites per cell) and 8.931 x 10(-8)M (Bmax=119700 sites per cell) respectively. In the presence of AFP (20 mg/L), the content of cAMP and activities of PKA were significantly elevated . The level of K-ras P21 protein was upregulated by AFP at the concentration of 20 mg/L. The monoclonal antibody against AFP could reverse the effects of AFP on the cAMP content, PKA activity and the expression of K-ras p21 gene. CONCLUSION: The effect of AFP on the cell proliferation was achieved by binding its receptor to trigger the signal transduction pathway of cAMP-PKA and alter the expression of K- ras p21 gene.
基金supported by grants from the Natural Science Foundation of Jiangsu Province,China (No. BK2006241)the Foundation for Talents in Six Fields of Jiangsu Province (No. 07-B-038)
文摘BACKGROUND: Pancreatic stellate cells (PSCs) play a major role in promoting pancreatic fibrosis. Transforming growth factor beta 1 (TGF-beta 1) is a critical mediator of this process. This study aimed to determine the expression of the Smad3 and Smad7 genes in the process of PSC activation, and explore the mechanisms of chronic pancreatitis. METHODS: The expressions of Smad3 and Smad7 in PSCs before and after TGF-beta 1 treatment were detected by reverse transcription-polymerase chain reaction and Western blotting analysis. Smad3 expression was detected in PSCs after treatment with 5 ng/ml of TGF-beta 1 for 24 hours. RESULTS: Smad7 expression was decreased in TGF-beta 1 -activated PSCs (P<0.05) in a dose-dependent manner. When TGF-beta 1 concentration reached 10 ng/ml, the expression of p-Smad3, Smad3, and Smad7 was inhibited (P<0.05). CONCLUSIONS: TGF-beta 1 promotes the expression of Smad3 and inhibits the expression of Smad7 during the activation of PSCs. In contrast, high-dose TGF-beta 1 downregulates the expression of Smad3 in completely activated PSCs.
基金supported by the Bio & Medical Technology Development Program of the National Research Foundation(NRF) funded by the Korean government(MEST)(No.860-20110087)
文摘The periodontal ligament-derived mesenchymal stem cell is regarded as a source of adult stem cells due to its multipotency.However, the proof of chondrogenic potential of the cells is scarce.Therefore,we investigated the chondrogenic differentiation capacity of periodontal ligament derived mesenchymal stem cells induced by transforming growth factor(TGF)-p3 and bone morphogenetic protein(BMP)-6.After isolation of periodontal ligament stem cells(PDLSCs) from human periodontal ligament,the cells were cultured in Dulbecco’s modified Eagle’s medium(DMEM) with 20%fetal bovine serum(FBS).A mechanical force initiated chondrogenic differentiation of the cells.For chondrogenic differentiation,10μg·LTGF-β3 or 100μg·LBMP-6 and the combination treating group for synergistic effect of the growth factors.We analyzed the PDLSCs by fluorescence-activated cell sorting and chondrogenesis were evaluated by glycosaminoglycans assay,histology,immunohistochemistry and genetic analysis.PDLSCs showed mesenchymal stem cell properties proved by FACS analysis.Glycosaminoglycans contents were increased 217%by TGF-β3 and 220%by BMP-6. The synergetic effect of TGF-β3 and BMP-6 were shown up to 281%compared to control.The combination treatment increased Sox9, aggrecan and collagen II expression compared with not only controls,but also TGF-P3 or BMP-6 single treatment dramatically.The histological analysis also indicated the chondrogenic differentiation of PDLSCs in our conditions.The results of the present study demonstrate the potential of the dental stem cell as a valuable cell source for chondrogenesis,which may be applicable for regeneration of cartilage and bone fracture in the field of cell therapy.
基金Supported by the National Natural Science Foundation of China (No.81700839)Military logistics scientific research project (No.BWS12J030)+2 种基金Natural Science Foundation of Shanghai (No.15ZR1413200)Research Foundation for Youth of Second Military Medical University (No.2016QN13)Research Foundation for Youth of Changhai Hospital (No.CH201712)
文摘AIM： To study the effect of discoidin I-like domaincontaining protein 3（EDIL3） depletion on the proliferation and epithelial-mesenchymal transition（EMT） in human lens epithelial cells（LECs）. METHODS： RNA interference was used to inhibit the expression of EDIL3 in human LECs in vitro. The morphology of cells was observed using an inverted microscope. Cell proliferation was assessed using Ed U kit. Cell migration was investigated using Transwell chamber and EMT of LECs was assessed using confocal microscope and Western blotting. The transforming growth factor β（TGFβ） pathway was investigated using Western blotting. RESULTS： The data showed that silencing EDIL3 expression changed LECs morphology and suppressed LECs proliferation（P〈0.05） and migration（P〈0.01）. Furthermore, the result of Western blotting showed that EDIL3 depletion reduced the expression of α-smooth muscle actin（α-SMA）（P〈0.001） and vimentin（P〈0.01）, while increased the expression of E-cadherin（P〈0.001）. EDIL3 depletion could suppress the phosphorylation of Smad2（P〈0.01） and Smad3（P〈0.01） and the activation of exracellular signal regulated kinase（ERK）（P〈0.05）. CONCLUSION： The findings indicate that EDIL3 might participate in the proliferation and EMT in LECs via TGFβ pathway and may be a potential therapeutic target for the treatment of posterior capsule opacification.
文摘Objective To investigate the feasibility of applying NIH3T3 cells transfected by VEGF gene to the treatment of ischemic random skin flaps.Methods Plasmid PcDNA3.1（-）/VEGF165 containing VEGF gene was transduced into the mouse NIH3T3 cells by liposome.Immunohistochemistry was used to detect the expression of VEGF protein of mouse NIH/3T3 cells in vitro.The NIH3T3 cell were stained with CM-DiI before the transplantation.
