The aim of this study was to investigate the role of p38 mitogen-activated protein kinase(MAPK)in cell migration induced by platelet-derived growth factor(PDGF).Western blot was performed to detect the phosphorylation...The aim of this study was to investigate the role of p38 mitogen-activated protein kinase(MAPK)in cell migration induced by platelet-derived growth factor(PDGF).Western blot was performed to detect the phosphorylation of p38 in NIH3T3 cells treated with PDGF.A Transwell cell migration system was used to determine the effects of PDGF treatment on the migration of NIH3T3 cells and the influence of p38 deficiency on this process in a p38 gene knockout(p38^(−/−))mouse embryonic fibroblast cell line.On the stimulation of PDGF,the migration of NIH3T3 cells was significantly increased(P<0.001)compared to the control and p38 MAP kinase was simultaneously phosphorylated.Furthermore,the PDGF-induced cell migration was significantly blocked in p38 gene knockout(p38^(−/−))mouse embryonic fibroblasts(MEFs)(P<0.001)as compared with the wild type cells(p38+/+).p38 MAPK plays an important role in the regulation of cell migration induced by PDGF.展开更多
基金This work was supported by the National Basic Research Program of China(973 Program)(No.2002CB513005)the National Natural Science Foundation of China(Grant No.30572151)+1 种基金Guangdong Provincial Science and Technology Program(No.A1090202)the Medical Science and Technology Foundation of Guangdong Province(No.A2005367).
文摘The aim of this study was to investigate the role of p38 mitogen-activated protein kinase(MAPK)in cell migration induced by platelet-derived growth factor(PDGF).Western blot was performed to detect the phosphorylation of p38 in NIH3T3 cells treated with PDGF.A Transwell cell migration system was used to determine the effects of PDGF treatment on the migration of NIH3T3 cells and the influence of p38 deficiency on this process in a p38 gene knockout(p38^(−/−))mouse embryonic fibroblast cell line.On the stimulation of PDGF,the migration of NIH3T3 cells was significantly increased(P<0.001)compared to the control and p38 MAP kinase was simultaneously phosphorylated.Furthermore,the PDGF-induced cell migration was significantly blocked in p38 gene knockout(p38^(−/−))mouse embryonic fibroblasts(MEFs)(P<0.001)as compared with the wild type cells(p38+/+).p38 MAPK plays an important role in the regulation of cell migration induced by PDGF.
