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

DC FieldValueLanguage
dc.contributor.author백용한-
dc.contributor.author이관식-
dc.date.accessioned2014-12-21T16:39:12Z-
dc.date.available2014-12-21T16:39:12Z-
dc.date.issued2007-
dc.identifier.issn0948-6143-
dc.identifier.urihttps://ir.ymlib.yonsei.ac.kr/handle/22282913/96094-
dc.description.abstractLeptin 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.-
dc.description.statementOfResponsibilityopen-
dc.format.extent495~502-
dc.relation.isPartOfHISTOCHEMISTRY AND CELL BIOLOGY-
dc.rightsCC BY-NC-ND 2.0 KR-
dc.rights.urihttps://creativecommons.org/licenses/by-nc-nd/2.0/kr/-
dc.subject.MESHActins/metabolism-
dc.subject.MESHBlotting, Western-
dc.subject.MESHCell Differentiation/drug effects-
dc.subject.MESHCell Proliferation/drug effects-
dc.subject.MESHCells, Cultured-
dc.subject.MESHExtracellular Signal-Regulated MAP Kinases/metabolism-
dc.subject.MESHGene Expression Regulation/drug effects-
dc.subject.MESHHumans-
dc.subject.MESHHypoglycemic Agents/pharmacology-
dc.subject.MESHLeptin/pharmacology-
dc.subject.MESHLigands-
dc.subject.MESHLiver/cytology-
dc.subject.MESHLiver/drug effects-
dc.subject.MESHLiver/metabolism*-
dc.subject.MESHModels, Biological-
dc.subject.MESHPPAR gamma/agonists-
dc.subject.MESHPPAR gamma/metabolism*-
dc.subject.MESHPhosphorylation/drug effects-
dc.subject.MESHPlatelet-Derived Growth Factor/pharmacology-
dc.subject.MESHRNA, Messenger/genetics-
dc.subject.MESHRNA, Messenger/metabolism-
dc.subject.MESHReceptors, Cell Surface/genetics*-
dc.subject.MESHReceptors, Leptin-
dc.subject.MESHSterol Regulatory Element Binding Protein 1/genetics-
dc.subject.MESHThiazolidinediones/pharmacology-
dc.titleA peroxisome-proliferator activated receptor-γ ligand could regulate the expression of leptin receptor on human hepatic stellate cells-
dc.typeArticle-
dc.contributor.collegeCollege of Medicine (의과대학)-
dc.contributor.departmentDept. of Internal Medicine (내과학)-
dc.contributor.googleauthorJung Il Lee-
dc.contributor.googleauthorYong-Han Paik-
dc.contributor.googleauthorMin Ah Kim-
dc.contributor.googleauthorYong Woon Shin-
dc.contributor.googleauthorHyung Gil Kim-
dc.contributor.googleauthorDong Haeng Lee-
dc.contributor.googleauthorKye Sook Kwon-
dc.contributor.googleauthorSeok Jeong-
dc.contributor.googleauthorYong Soo Kim-
dc.contributor.googleauthorJin Woo Lee-
dc.contributor.googleauthorKwan Sik Lee-
dc.identifier.doi10.1007/s00418-007-0282-x-
dc.admin.authorfalse-
dc.admin.mappingfalse-
dc.contributor.localIdA01829-
dc.contributor.localIdA02666-
dc.relation.journalcodeJ00992-
dc.identifier.eissn1432-119X-
dc.identifier.pmid17393179-
dc.identifier.urlhttp://link.springer.com/article/10.1007%2Fs00418-007-0282-x-
dc.contributor.alternativeNamePaik, Yong Han-
dc.contributor.alternativeNameLee, Kwan Sik-
dc.contributor.affiliatedAuthorPaik, Yong Han-
dc.contributor.affiliatedAuthorLee, Kwan Sik-
dc.rights.accessRightsnot free-
dc.citation.volume127-
dc.citation.number5-
dc.citation.startPage495-
dc.citation.endPage502-
dc.identifier.bibliographicCitationHISTOCHEMISTRY AND CELL BIOLOGY, Vol.127(5) : 495-502, 2007-
Appears in Collections:
1. College of Medicine (의과대학) > Dept. of Internal Medicine (내과학교실) > 1. Journal Papers

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