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Article: The roles of leptin and adiponectin: A novel paradigm in adipocytokine regulation of liver fibrosis and stellate cell biology

TitleThe roles of leptin and adiponectin: A novel paradigm in adipocytokine regulation of liver fibrosis and stellate cell biology
Authors
Issue Date2005
PublisherAmerican Society for Investigative Pathology. The Journal's web site is located at http://www.amjpathol.org
Citation
American Journal Of Pathology, 2005, v. 166 n. 6, p. 1655-1669 How to Cite?
AbstractAlthough leptin is a key adipokine promoting liver flbrosis, adiponectin may prevent liver injury. To determine the role of these adipokines in liver fibrosis and to understand their expression in vivo, fa/fa rats and their lean littermates were subjected to bile duct ligation (BDL). Histomorphometry for collagen and α-smooth muscle actin (α-SMA) revealed that lean rats, but not fa/fa littermates, had significant fibrosis with abundant hepatic stellate cell (HSC) activation. The lean-BDL rats had significantly higher leptin concentrations in the hepatic vein than lean sham-operated, fa/fa BDL, or fa/fa sham-operated rats. Co-localization of leptin and α-SMA in activated HSCs was observed by immunohistochemistry. Real-time reverse transcriptase-polymerase chain reaction and Western blot analysis confirmed the presence of leptin and α-SMA in activated, but not quiescent, HSCs, whereas only quiescent HSCs synthesized adiponectin mRNA and protein. Adiponectin overexpression in activated HSCs reduced proliferation, augmented apoptosis, and reduced expression of α-SMA and proliferating cell nuclear antigen. Adiponectin receptors (AdipoR1 and AdipoR2) were detected in both activated and quiescent HSCs, but only activated HSCs produced significant apoptosis after treatment with either globular or full-length adiponectin. Adiponectin may act to reverse HSC activation, maintain HSC quiescence, or significantly, may have important therapeutic implications in liver fibrosis. Copyright © American Society for Investigative Pathology.
Persistent Identifierhttp://hdl.handle.net/10722/49042
ISSN
2015 Impact Factor: 4.206
2015 SCImago Journal Rankings: 2.653
PubMed Central ID
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorDing, Xen_HK
dc.contributor.authorSaxena, NKen_HK
dc.contributor.authorLin, Sen_HK
dc.contributor.authorXu, Aen_HK
dc.contributor.authorSrinivasan, Sen_HK
dc.contributor.authorAnania, FAen_HK
dc.date.accessioned2008-06-12T06:33:10Z-
dc.date.available2008-06-12T06:33:10Z-
dc.date.issued2005en_HK
dc.identifier.citationAmerican Journal Of Pathology, 2005, v. 166 n. 6, p. 1655-1669en_HK
dc.identifier.issn0002-9440en_HK
dc.identifier.urihttp://hdl.handle.net/10722/49042-
dc.description.abstractAlthough leptin is a key adipokine promoting liver flbrosis, adiponectin may prevent liver injury. To determine the role of these adipokines in liver fibrosis and to understand their expression in vivo, fa/fa rats and their lean littermates were subjected to bile duct ligation (BDL). Histomorphometry for collagen and α-smooth muscle actin (α-SMA) revealed that lean rats, but not fa/fa littermates, had significant fibrosis with abundant hepatic stellate cell (HSC) activation. The lean-BDL rats had significantly higher leptin concentrations in the hepatic vein than lean sham-operated, fa/fa BDL, or fa/fa sham-operated rats. Co-localization of leptin and α-SMA in activated HSCs was observed by immunohistochemistry. Real-time reverse transcriptase-polymerase chain reaction and Western blot analysis confirmed the presence of leptin and α-SMA in activated, but not quiescent, HSCs, whereas only quiescent HSCs synthesized adiponectin mRNA and protein. Adiponectin overexpression in activated HSCs reduced proliferation, augmented apoptosis, and reduced expression of α-SMA and proliferating cell nuclear antigen. Adiponectin receptors (AdipoR1 and AdipoR2) were detected in both activated and quiescent HSCs, but only activated HSCs produced significant apoptosis after treatment with either globular or full-length adiponectin. Adiponectin may act to reverse HSC activation, maintain HSC quiescence, or significantly, may have important therapeutic implications in liver fibrosis. Copyright © American Society for Investigative Pathology.en_HK
dc.format.extent388 bytes-
dc.format.mimetypetext/html-
dc.languageengen_HK
dc.publisherAmerican Society for Investigative Pathology. The Journal's web site is located at http://www.amjpathol.orgen_HK
dc.relation.ispartofAmerican Journal of Pathologyen_HK
dc.rightsCreative Commons: Attribution 3.0 Hong Kong License-
dc.subject.meshIntercellular Signaling Peptides and Proteins - metabolismen_HK
dc.subject.meshLeptin - metabolismen_HK
dc.subject.meshLiver Cirrhosis - metabolism - pathologyen_HK
dc.subject.meshObesity - metabolismen_HK
dc.subject.meshActins - metabolismen_HK
dc.titleThe roles of leptin and adiponectin: A novel paradigm in adipocytokine regulation of liver fibrosis and stellate cell biologyen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0002-9440&volume=166&issue=6&spage=1655&epage=1669&date=2005&atitle=The+roles+of+leptin+and+adiponectin:+a+novel+paradigm+in+adipocytokine+regulation+of+liver+fibrosis+and+stellate+cell+biologyen_HK
dc.identifier.emailXu, A:amxu@hkucc.hku.hken_HK
dc.identifier.authorityXu, A=rp00485en_HK
dc.description.naturepublished_or_final_versionen_HK
dc.identifier.pmid15920151-
dc.identifier.pmcidPMC1602420en_HK
dc.identifier.scopuseid_2-s2.0-19544378172en_HK
dc.identifier.hkuros107674-
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-19544378172&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume166en_HK
dc.identifier.issue6en_HK
dc.identifier.spage1655en_HK
dc.identifier.epage1669en_HK
dc.identifier.isiWOS:000229387100009-
dc.publisher.placeUnited Statesen_HK
dc.identifier.scopusauthoridDing, X=8505591700en_HK
dc.identifier.scopusauthoridSaxena, NK=36106505400en_HK
dc.identifier.scopusauthoridLin, S=8505591200en_HK
dc.identifier.scopusauthoridXu, A=7202655409en_HK
dc.identifier.scopusauthoridSrinivasan, S=8250066800en_HK
dc.identifier.scopusauthoridAnania, FA=6701470713en_HK

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