Lipopolysaccharide Reverses Hepatic Stellate Cell Activation In Vitro and In Vivo via Modulation of c‐Myb and SMAD7
Abstract
During liver injury, the perisinusoidal quiescent hepatic stellate cells (HSCs) become activated and transdifferentiate into highly proliferative myofibroblastic phenotype (aHSCs) that expresses α‐smooth muscle actin (αSMA) and platelet‐derived growth factor β receptor (PDGFβR). aHSCs are the major fibrogenic cell type regardless of etiology of chronic liver disease. Their interactions with gut‐derived bacterial lipopolysaccharide (LPS), a potent inflammatory mediator, are implicated in hepatic fibrogenesis. However, evidence also indicates that LPS can attenuate fibrogenic characteristics of aHSCs. We examined molecular mechanisms of anti‐fibrogenic effects of LPS on aHSCs in vitro and in vivo.
Document Details
- Document Type
- Pub Defense Publication
- Publication Date
- Apr 01, 2019
- Source ID
- 10.1096/fasebj.2019.33.1_supplement.126.8
Entities
People
- Akanksha Sharma
Organizations
- Cincinnati Children's Hospital Medical Center
- United States Department of Defense
- United States Department of Veterans Affairs