Albumin mediates PPAR-γ or C/EBP-α-induced phenotypic changes in pancreatic stellate cells

Nayoung Kim, Soyoung Choi, Chaeseung Lim, Hongsik Lee, Junseo Oh

Research output: Contribution to journalArticlepeer-review

19 Citations (Scopus)


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 languageEnglish
Pages (from-to)640-644
Number of pages5
JournalBiochemical and biophysical research communications
Issue number1
Publication statusPublished - 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 ).


  • Albumin
  • Fibrosis
  • Lipid droplet formation
  • PPAR-γ
  • Pancreatic stellate cells

ASJC Scopus subject areas

  • Biophysics
  • Biochemistry
  • Molecular Biology
  • Cell Biology


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