Albumin mediates PPAR-gamma or C/EBP-alpha-induced phenotypic changes in pancreatic stellate cells

Biochemical and Biophysical Research Communications
N KimJunseo Oh

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.

References

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Citations

Jul 7, 2011·Antioxidants & Redox Signaling·Minoti ApteJeremy Wilson
Jun 16, 2012·Cellular and Molecular Life Sciences : CMLS·Feng ZhangShizhong Zheng
Jan 14, 2011·Lung Cancer : Journal of the International Association for the Study of Lung Cancer·Jun ZhongMichael Roth
Jan 1, 2010·Cancers·Hansjörg HabischMax G Bachem
Jun 13, 2018·Frontiers in Immunology·Heng LiGuo-Jun Zhao
Feb 18, 2017·World Journal of Gastroenterology : WJG·Ratnakar R BynigeriRupjyoti Talukdar
Jan 24, 2012·Biochemical and Biophysical Research Communications·Soyoung ChoiJunseo Oh

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