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.
Original language | English |
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Pages (from-to) | 640-644 |
Number of pages | 5 |
Journal | Biochemical and biophysical research communications |
Volume | 391 |
Issue number | 1 |
DOIs | |
Publication status | Published - 2010 Jan 1 |
Bibliographical note
Funding Information:We thank Ho Kim and Kyunghee Noh for technical assistance. This work was supported by the Korea Science and Engineering Foundation (KOSEF) grant funded by the Korea government (MOST) (No. 2009-0076453 ).
Keywords
- Albumin
- Fibrosis
- Lipid droplet formation
- PPAR-γ
- Pancreatic stellate cells
ASJC Scopus subject areas
- Biophysics
- Biochemistry
- Molecular Biology
- Cell Biology