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

Nayoung Kim; Soyoung Choi; Chaeseung Lim; Hongsik Lee; Jun Seo Oh

doi:10.1016/j.bbrc.2009.11.112

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

Nayoung Kim
, Soyoung Choi
, Chaeseung Lim
, Hongsik Lee
, Jun Seo Oh^*

^*Corresponding author for this work

Research output: Contribution to journal › Article › peer-review

23 Citations (Scopus)

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
Pages (from-to)	640-644
Number of pages	5
Journal	Biochemical and biophysical research communications
Volume	391
Issue number	1
DOIs	https://doi.org/10.1016/j.bbrc.2009.11.112
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

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10.1016/j.bbrc.2009.11.112

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

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.",

keywords = "Albumin, Fibrosis, Lipid droplet formation, PPAR-γ, Pancreatic stellate cells",

author = "Nayoung Kim and Soyoung Choi and Chaeseung Lim and Hongsik Lee and Oh, \{Jun Seo\}",

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 ).",

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T1 - Albumin mediates PPAR-γ or C/EBP-α-induced phenotypic changes in pancreatic stellate cells

AU - Kim, Nayoung

AU - Choi, Soyoung

AU - Lim, Chaeseung

AU - Lee, Hongsik

AU - Oh, Jun Seo

N1 - 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 ).

PY - 2010/1/1

Y1 - 2010/1/1

N2 - 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.

AB - 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.

KW - Albumin

KW - Fibrosis

KW - Lipid droplet formation

KW - PPAR-γ

KW - Pancreatic stellate cells

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

Abstract

Bibliographical note

Keywords

ASJC Scopus subject areas

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