| Background:Renal fibrosis is the main pathologic mechanism of end stage renal failure resulted from the chronic kidney disease(CKD).There is still no effective method to block the development of renal fibrosis. Research indicated that extra cellular matrix(ECM) may play a very important role in renal fibrosis. Renal fibroblasts were found to be the principle cells producing ECM. Therefore, whether renal fibrosis is able to be prevented mainly lies in whether the over proliferation and over secretion of renal fibroblasts can be blocked.Phosphatase and tensin homolog deleted on chromosome 10(PTEN) is a newly found tumor suppressor gene. PTEN protein, a dual-specificity protein and lipid phosphatase, can inhibit phosphatidylinositol-3-kinase(PI3K) signal pathway and negatively regulate mitigen-activated protein kinase(MAPK) signal pathway. Research indicated that PI3K and MAPK signal pathways were associated with biological behaviors such as cell migration, inflammation, cell proliferation and cell cycle regulation. The two signal pathways play an important role in the occurrence and progress of renal fibrosis. Therefore, PTEN probably has essential regulation effect on renal fibrosis.This study was aimed to investigate the role of PTEN protein on the progress of renal fibrosis via observing the expression of PTEN protein in cultured rat renal fibroblasts after the stimulation of TGFβ1 and the effect of PTEN protein on proliferation and secretion of collagenⅣand fibronectin in rat renal fibroblasts induced by TGFβ1.Methods:1. Rat renal fibroblasts were dissociated, purified, cultured and then identified by means of light microscope, electron microscope and immunocytochemistry.2. The cultured rat renal fibroblasts were transfected with the adenovirus containing... |
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