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Cited 16 time in webofscience Cited 16 time in scopus
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Albumin mediates PPAR-gamma or C/EBP-alpha-induced phenotypic changes in pancreatic stellate cells

Authors
Kim, NayoungChoi, SoyoungLim, ChaeseungLee, HongsikOh, Junseo
Issue Date
1-Jan-2010
Publisher
ACADEMIC PRESS INC ELSEVIER SCIENCE
Keywords
Albumin; Pancreatic stellate cells; Lipid droplet formation; Fibrosis; PPAR-gamma
Citation
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS, v.391, no.1, pp.640 - 644
Indexed
SCIE
SCOPUS
Journal Title
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS
Volume
391
Number
1
Start Page
640
End Page
644
URI
https://scholarworks.korea.ac.kr/kumedicine/handle/2020.sw.kumedicine/15209
DOI
10.1016/j.bbrc.2009.11.112
ISSN
0006-291X
Abstract
Activation of quiescent hepatic stellate cells (HSCs) into myofibroblast-like cells is a key event of liver fibrosis. and adipogenic transcription factors, PPAR-gamma and C/EBP-alpha, reverse HSC activation. As albumin was reported to maintain the quiescent phenotype of stellate cells, we examined whether it plays a role in PPAR-gamma and C/EBP-alpha-mediated effects. Pancreatic stellate cells (PSCs) were isolated from rat pancreas and used in their culture-activated phenotype. Forced expression of PPAR-gamma or C/EBP-alpha in PSCs increased albumin mRNA and protein levels by >2 5-fold, which is accompanied with increased C/EBP-beta binding to albumin promoter. PPAR-gamma and C/EBP-alpha 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-gamma and C/EBP-alpha in PSCs and that it can be an attractive molecular target for anti-fibrotic therapies. (C) 2009 Elsevier Inc All rights reserved.
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