Abstract
Activation of quiescent hepatic stellate cells (HSCs) into myofibroblast-like cells is a key event of liver fibrosis, and adipogenic transcription factors, PPAR-γ and C/EBP-α, reverse HSC activation. As albumin was reported to maintain the quiescent phenotype of stellate cells, we examined whether it plays a role in PPAR-γ and C/EBP-α-mediated effects. Pancreatic stellate cells (PSCs) were isolated from rat pancreas and used in their culture-activated phenotype. Forced expression of PPAR-γ or C/EBP-α in PSCs increased albumin mRNA and protein levels by >2.5-fold, which is accompanied with increased C/EBP-β binding to albumin promoter. PPAR-γ and C/EBP-α also induced a phenotypic switch from activated to quiescent cells and, interestingly, suppression of albumin using short-hairpin RNA (shRNA) blocked their effects. Therefore, our findings suggest that albumin may be a downstream effector of PPAR-γ and C/EBP-α in PSCs and that it can be an attractive molecular target for anti-fibrotic therapies.
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