Abstract\nOver time, peritoneal dialysis results in functional and structural alterations of the peritoneal membrane, but the cardinal mechanisms and whether these changes ar rechargeable be not completely understood. Here, we analyze the effects of senior gamey school levels of glucose, which are establish in the dialysate, on human peritoneal mesothelial cells (HPMCs). We found that high concentrations of glucose induced epithelial-to-mesenchymal handing over (EMT) of HPMC, suggested by reduced feel of E-cadherin and increased expression of alpha-smooth brawniness actin, fibronectin, and type I collagen and by increased cell migration. standardization of glucose concentration on solar day 2 reversed the phenotypical transformation, but the changes were irreversible later 7 d of stimulant with high glucose. In addition, picture show of HPMC to high glucose resulted in a decreased expression of the antifibrotic cytokines, hepatocyte exploitation factor (HGF) and bone morphogenic protein 7 (BMP-7). Exogenous treatment with HGF resulted in a dosage-dependent prevention of high glucose-induced EMT. Both BMP-7 peptide and gene transfection with an adenoviral sender of BMP-7 also protected HPMCs from EMT. Furthermore, adenoviral BMP-7 transfection decreased peritoneal EMT and ameliorated peritoneal thicken in an animal lesson of peritoneal dialysis. In summary, high concentrations of glucose induce a reversible EMT of HPMCs, associated with decreased production of HGF and BMP-7. intervention of HPMCs with HGF or BMP-7 blocks high glucose-induced EMT, and BMP-7 ameliorates peritonealfibrosis in an animal model of peritoneal dialysis.If you want to get a full essay, order it on our website:
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