Endothelial to mesenchymal transition contributes to arsenic-trioxide-induced cardiac fibrosis.

ABSTRACT: Emerging evidence has suggested the critical role of endothelial to mesenchymal transition (EndMT) in fibrotic diseases. The present study was designed to examine whether EndMT is involved in arsenic trioxide (As₂O₃)-induced cardiac fibrosis and to explore the underlying mechanisms. Cardiac dysfunction was observed in rats after exposure to As₂O₃ for 15 days using echocardiography, and the deposition of collagen was detected by Masson's trichrome staining and electron microscope. EndMT was indicated by the loss of endothelial cell markers (VE-cadherin and CD31) and the acquisition of mesenchymal cell markers (α-SMA and FSP1) determined by RT-PCR at the mRNA level and Western blot and immunofluorescence analysis at the protein level. In the in-vit

SUBMITTER: Zhang Y 

PROVIDER: S-EPMC5037371 | biostudies-literature | 2016 Sep

REPOSITORIES: biostudies-literature