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A peroxisome-proliferator activated receptor-γ ligand could regulate the expression of leptin receptor on human hepatic stellate cells

Authors
 Jung Il Lee  ;  Yong-Han Paik  ;  Min Ah Kim  ;  Yong Woon Shin  ;  Hyung Gil Kim  ;  Dong Haeng Lee  ;  Kye Sook Kwon  ;  Seok Jeong  ;  Yong Soo Kim  ;  Jin Woo Lee  ;  Kwan Sik Lee 
Citation
 HISTOCHEMISTRY AND CELL BIOLOGY, Vol.127(5) : 495-502, 2007 
Journal Title
 HISTOCHEMISTRY AND CELL BIOLOGY 
ISSN
 0948-6143 
Issue Date
2007
MeSH
Actins/metabolism ; Blotting, Western ; Cell Differentiation/drug effects ; Cell Proliferation/drug effects ; Cells, Cultured ; Extracellular Signal-Regulated MAP Kinases/metabolism ; Gene Expression Regulation/drug effects ; Humans ; Hypoglycemic Agents/pharmacology ; Leptin/pharmacology ; Ligands ; Liver/cytology ; Liver/drug effects ; Liver/metabolism* ; Models, Biological ; PPAR gamma/agonists ; PPAR gamma/metabolism* ; Phosphorylation/drug effects ; Platelet-Derived Growth Factor/pharmacology ; RNA, Messenger/genetics ; RNA, Messenger/metabolism ; Receptors, Cell Surface/genetics* ; Receptors, Leptin ; Sterol Regulatory Element Binding Protein 1/genetics ; Thiazolidinediones/pharmacology
Abstract
Leptin is a peptide known to play a profibrogenic role in hepatic stellate cells (HSCs). Peroxisome-proliferator activated receptor (PPAR)-γ ligands are suggested to have an anti-fibrogenic effect on HSCs. Since the association of these two factors in HSC activation has not been demonstrated, we hypothesized that PPAR-γ ligands would suppress leptin-induced HSC activation and regulate leptin receptor expression. Immortalized human HSCs were activated by either leptin or platelet-derived growth factor (PDGF) in one group. In another group, ciglitazone, a PPAR-γ ligand, was treated before the leptin or PDGF stimulation. Proliferation of human HSCs was achieved by both PDGF and leptin, and this could be suppressed by ciglitazone. PPAR-γ mRNA expression was diminished in activated HSCs either by PDGF or leptin, and this was reversed by ciglitazone in both cases. Leptin receptor (OB-R) mRNA expression increased in activated HSCs either by PDGF or leptin, and the expression was inhibited by ciglitazone. Another adipogenic transcription factor, sterol regulatory element-binding protein-1c (SREBP-1c) mRNA expression was decreased either by PDGF or leptin. However, this effect was not reversed by ciglitazone pre-treatment. The inhibitory effect of ciglitazone on leptin-induced HSC proliferation was associated with the reversion of extracellular factor-regulated kinases (ERKs) activation. HSCs were OB-R expressing cells, and ciglitazone could regulate the expression of OB-R mRNA.
Full Text
http://link.springer.com/article/10.1007%2Fs00418-007-0282-x
DOI
10.1007/s00418-007-0282-x
Appears in Collections:
1. College of Medicine (의과대학) > Dept. of Internal Medicine (내과학교실) > 1. Journal Papers
Yonsei Authors
Paik, Yong Han(백용한)
Lee, Kwan Sik(이관식) ORCID logo https://orcid.org/0000-0002-3672-1198
URI
https://ir.ymlib.yonsei.ac.kr/handle/22282913/96094
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