Hepatic stellate cell specific endoglin deletion modulates TGF-β signaling and aggravates liver fibrosis in two experimental models of murine liver injury — Muhammad Alsamman (2014) | RDL Network
Hepatic stellate cell specific endoglin deletion modulates TGF-β signaling and aggravates liver fibrosis in two experimental models of murine liver injury
Article 2014 en
Authors
MA
Muhammad Alsamman
VS
Viktor Sterzer
SM
Steffen K. Meurer
Abstract
1 min read
Background: Hepatic stellate cells (HSC) are the major source for extracellular matrix (ECM) production in liver fibrosis. Endoglin (ENG) is a type III auxiliary receptor for TGF-β that is expressed on HSCs. Due to different splicing there are two ENG isoforms, L- and S-Endoglin, which modulate TGF-β signaling differentially. TGF-β is the a profibrotic cytokine expressed in response to liver injury. This study analyzes the role of ENG and TGF-β signaling in two models of experimental liver fibrosis by cell line specific endoglin deletion in HSCs.
Muhammad Alsamman, Viktor Sterzer, Steffen K. Meurer, Hacer Sahin, Ute Schaeper, Deniz Kuscuoglu, Pavel Strnad, Ralf Weiskirchen, Christian Trautwein, David Scholten
Steffen K. Meurer, Muhammad Alsamman, Hacer Sahin, Hermann E. Wasmuth, Tatiana Kisseleva, David A. Brenner, Christian Trautwein, Ralf Weiskirchen, David Scholten
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