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Article: Leptin induces TGF-β synthesis through functional leptin receptor expressed by human peritoneal mesothelial cell

TitleLeptin induces TGF-β synthesis through functional leptin receptor expressed by human peritoneal mesothelial cell
Authors
KeywordsCAPD
JAK-STAT
Leptin
Leptin receptor
Mesothelial cell
TGF-β
Issue Date2006
PublisherNature Publishing Group. The Journal's web site is located at http://www.nature.com/ki/index.html
Citation
Kidney International, 2006, v. 69 n. 11, p. 2078-2086 How to Cite?
AbstractMarked increase in leptin concentration in spent peritoneal dialysate has been reported following continuous ambulatory peritoneal dialysis treatment. The present study was designed to determine whether functional leptin receptor is expressed by human peritoneal mesothelial cells and if so, the possible implication in dialysis. Expression of leptin receptors in cultured mesothelial cells and omental tissue was examined. The effect of leptin on the production of transforming growth factor-β (TGF-β) by mesothelial cells in the presence or absence of high glucose was determined using in vitro culture model of human peritoneal mesothelial cells and adipocytes. The signaling mechanism involved in leptin-induced TGF-β synthesis by mesothelial cells was studied. Both mRNA and protein of the full-length leptin receptor are constitutively expressed in mesothelial cells. The leptin receptor expression in mesothelial cells was upregulated by glucose but not leptin. In adipocytes, glucose increased the mRNA expression and synthesis of leptin. The Janus kinase-signal transducers and activation (JAK-STAT) signal transduction pathway in mesothelial cells was activated by either exogenous or adipocytes-derived leptin. Exogenous leptin induced the release of TGF-β by mesothelial cells. The TGF-β synthesis induced by leptin was amplified by glucose through increased leptin receptor expression. Our novel findings reveal that functional leptin receptor is present on human peritoneal mesothelial cells. The leptin-induced TGF-β synthesis in mesothelial cells is associated with the expression of leptin receptor and the activation of the JAK-STAT signal transduction pathway. © 2006 International Society of Nephrology.
Persistent Identifierhttp://hdl.handle.net/10722/162988
ISSN
2015 Impact Factor: 7.683
2015 SCImago Journal Rankings: 3.181
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorLeung, JCKen_HK
dc.contributor.authorChan, LYYen_HK
dc.contributor.authorTang, SCWen_HK
dc.contributor.authorChu, KMen_HK
dc.contributor.authorLai, KNen_HK
dc.date.accessioned2012-09-05T05:26:16Z-
dc.date.available2012-09-05T05:26:16Z-
dc.date.issued2006en_HK
dc.identifier.citationKidney International, 2006, v. 69 n. 11, p. 2078-2086en_HK
dc.identifier.issn0085-2538en_HK
dc.identifier.urihttp://hdl.handle.net/10722/162988-
dc.description.abstractMarked increase in leptin concentration in spent peritoneal dialysate has been reported following continuous ambulatory peritoneal dialysis treatment. The present study was designed to determine whether functional leptin receptor is expressed by human peritoneal mesothelial cells and if so, the possible implication in dialysis. Expression of leptin receptors in cultured mesothelial cells and omental tissue was examined. The effect of leptin on the production of transforming growth factor-β (TGF-β) by mesothelial cells in the presence or absence of high glucose was determined using in vitro culture model of human peritoneal mesothelial cells and adipocytes. The signaling mechanism involved in leptin-induced TGF-β synthesis by mesothelial cells was studied. Both mRNA and protein of the full-length leptin receptor are constitutively expressed in mesothelial cells. The leptin receptor expression in mesothelial cells was upregulated by glucose but not leptin. In adipocytes, glucose increased the mRNA expression and synthesis of leptin. The Janus kinase-signal transducers and activation (JAK-STAT) signal transduction pathway in mesothelial cells was activated by either exogenous or adipocytes-derived leptin. Exogenous leptin induced the release of TGF-β by mesothelial cells. The TGF-β synthesis induced by leptin was amplified by glucose through increased leptin receptor expression. Our novel findings reveal that functional leptin receptor is present on human peritoneal mesothelial cells. The leptin-induced TGF-β synthesis in mesothelial cells is associated with the expression of leptin receptor and the activation of the JAK-STAT signal transduction pathway. © 2006 International Society of Nephrology.en_HK
dc.languageengen_US
dc.publisherNature Publishing Group. The Journal's web site is located at http://www.nature.com/ki/index.htmlen_HK
dc.relation.ispartofKidney Internationalen_HK
dc.subjectCAPDen_HK
dc.subjectJAK-STATen_HK
dc.subjectLeptinen_HK
dc.subjectLeptin receptoren_HK
dc.subjectMesothelial cellen_HK
dc.subjectTGF-βen_HK
dc.subject.meshCells, Cultureden_US
dc.subject.meshEpithelial Cells - Physiologyen_US
dc.subject.meshHumansen_US
dc.subject.meshLeptin - Physiologyen_US
dc.subject.meshPeritoneum - Cytologyen_US
dc.subject.meshReceptors, Cell Surface - Biosynthesisen_US
dc.subject.meshReceptors, Leptinen_US
dc.subject.meshTransforming Growth Factor Beta - Biosynthesisen_US
dc.titleLeptin induces TGF-β synthesis through functional leptin receptor expressed by human peritoneal mesothelial cellen_HK
dc.typeArticleen_HK
dc.identifier.emailLeung, JCK: jckleung@hku.hken_HK
dc.identifier.emailTang, SCW: scwtang@hku.hken_HK
dc.identifier.emailChu, KM: chukm@hkucc.hku.hken_HK
dc.identifier.emailLai, KN: knlai@hku.hken_HK
dc.identifier.authorityLeung, JCK=rp00448en_HK
dc.identifier.authorityTang, SCW=rp00480en_HK
dc.identifier.authorityChu, KM=rp00435en_HK
dc.identifier.authorityLai, KN=rp00324en_HK
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1038/sj.ki.5000409en_HK
dc.identifier.pmid16641931en_HK
dc.identifier.scopuseid_2-s2.0-33745287133en_HK
dc.identifier.hkuros116388-
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-33745287133&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume69en_HK
dc.identifier.issue11en_HK
dc.identifier.spage2078en_HK
dc.identifier.epage2086en_HK
dc.identifier.isiWOS:000238112100029-
dc.publisher.placeUnited Kingdomen_HK
dc.identifier.scopusauthoridLeung, JCK=7202180349en_HK
dc.identifier.scopusauthoridChan, LYY=8108378300en_HK
dc.identifier.scopusauthoridTang, SCW=7403437082en_HK
dc.identifier.scopusauthoridChu, KM=7402453538en_HK
dc.identifier.scopusauthoridLai, KN=7402135706en_HK
dc.identifier.citeulike1674774-

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