![]() ![]() BMP7 treatment abolishes EMT-derived fibroblasts, suggesting that the therapeutic effect of BMP7 was at least partially due to the inhibition of EMT. Furthermore, we demonstrate that bone morphogenic protein-7 (BMP7), a member of the TGFβ superfamily, which is known to antagonize TGFβ signaling, significantly inhibits progression of liver fibrosis in these mice. R26Rstop lacZ double transgenic mice to demonstrate that hepatocytes which undergo EMT contribute substantially to the population of FSP1-positive fibroblasts in CCL 4-induced liver fibrosis. We perform lineage-tracing experiments using AlbCre. Here, we provide evidence that the pro-fibrotic growth factor, TGF-β1, induces adult mouse hepatocytes to undergo phenotypic and functional changes typical of epithelial to mesenchymal transition (EMT). ![]() The role of adult hepatocytes as contributors to the accumulation of fibroblasts in the fibrotic liver is yet undetermined. The origin of such fibroblasts is still debated, although several studies point to stellate cells as the principal source. ![]() 4 Funded by National Institutes of Health Grant DK055001-07S1.Īctivated fibroblasts are key contributors to the fibrotic extracellular matrix accumulation during liver fibrosis. 3 Funded by a postdoctoral fellowship derived from the Espinosa Fibrosis Fund and BIDMC Liver Center. 2 Funded by Grant 5K08DK074558-01 from the National Institutes of Health and the ASN Carl W. 1 Both authors contributed equally to this report. ![]() Section 1734 solely to indicate this fact. This article must therefore be hereby marked “ advertisement” in accordance with 18 U.S.C. The costs of publication of this article were defrayed in part by the payment of page charges. The first evidence for EMT involving adult primary hepatocytes was first reported by our laboratory at the 2003 Digestive Disease Week (DDW) meeting in Orlando, Florida. K.) from the National Institutes of Health, and a research fund from the Beth Israel Deaconess Medical Center for the Division of Matrix Biology. * This study was funded in part by the Espinosa Fibrosis Fund, a research grant from the Johnson & Johnson Companies, Research Grants DK62987, DK55001, DK61688, and AI53194 (to R. Glycobiology and Extracellular Matrices. ![]()
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