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Blocking TGF-β1 protects the peritoneal membrane from dialysate-induced damage. | LitMetric

AI Article Synopsis

  • During peritoneal dialysis (PD), mesothelial cells transition to a different cell type (MMT), causing issues with the function of the peritoneal membrane, which can lead to complications. * The study explored the use of TGF-β1-blocking peptides in mice to see if they could reduce peritoneal damage caused by PD, finding that these peptides improved tissue health and reduced harmful cell types. * Overexpression of TGF-β1 worsened peritoneal condition by increasing fibroblast levels, showing that TGF-β1 plays a significant role in the adverse effects associated with dialysis fluid on the peritoneum.

Article Abstract

During peritoneal dialysis (PD), mesothelial cells undergo mesothelial-to-mesenchymal transition (MMT), a process associated with peritoneal-membrane dysfunction. Because TGF-β1 can induce MMT, we evaluated the efficacy of TGF-β1-blocking peptides in modulating MMT and ameliorating peritoneal damage in a mouse model of PD. Exposure of the peritoneum to PD fluid induced fibrosis, angiogenesis, functional impairment, and the accumulation of fibroblasts. In addition to expressing fibroblast-specific protein-1 (FSP-1), some fibroblasts co-expressed cytokeratin, indicating their mesothelial origin. These intermediate-phenotype (Cyto(+)/FSP-1(+)) fibroblasts had features of myofibroblasts with fibrogenic capacity. PD fluid treatment triggered the appearance of CD31(+)/FSP-1(+) and CD45(+)/FSP-1(+) cells, suggesting that fibroblasts also originate from endothelial cells and from cells recruited from bone marrow. Administration of blocking peptides significantly ameliorated fibrosis and angiogenesis, improved peritoneal function, and reduced the number of FSP-1(+) cells, especially in the Cyto(+)/FSP-1(+) subpopulation. Conversely, overexpression of TGF-β1 in the peritoneum by adenovirus-mediated gene transfer led to a marked accumulation of fibroblasts, most of which derived from the mesothelium. Taken together, these results demonstrate that TGF-β1 drives the peritoneal deterioration induced by dialysis fluid and highlights a role of TGF-β1-mediated MMT in the pathophysiology of peritoneal-membrane dysfunction.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3171939PMC
http://dx.doi.org/10.1681/ASN.2010111197DOI Listing

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