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Article: Adiponectin Deficiency Protects Mice From Chemically Induced Colonic Inflammation

TitleAdiponectin Deficiency Protects Mice From Chemically Induced Colonic Inflammation
Authors
Issue Date2007
PublisherWB Saunders Co. The Journal's web site is located at http://www.elsevier.com/locate/gastro
Citation
Gastroenterology, 2007, v. 132 n. 2, p. 601-614 How to Cite?
AbstractBackground & Aims: Adiponectin (APN) is an adipokine that regulates insulin sensitivity and is anti-inflammatory in atherosclerosis. The goal of this study was to investigate the role of APN in intestinal inflammation. Methods: APN knockout (KO) mice and their wild-type (WT) littermates received dextran sulfate sodium (DSS) or trinitrobenzene sulfonic acid (TNBS) to induce intestinal inflammation. Clinical and histologic scores and proliferation of epithelial cells were assessed. Cytokines and APN levels were measured. Expression of APN and heparin binding epidermal growth factor (HB-EGF) was analyzed by immunohistochemistry. Expression of APN and its receptors, HB-EGF, and basic fibroblast growth factor (bFGF) messenger RNA was assessed by reverse-transcription polymerase chain reaction. Association of serum APN with HB-EGF and bFGF was studied by coimmunoprecipitation. Results: APN KO mice are protected from chemically induced colitis; administration of APN restores inflammation. APN is expressed in the colon, luminal APN associates with colonic epithelial cells. In vitro, APN increases production of proinflammatory cytokines from colonic tissue. Expression of colonic APN overlaps with that of bFGF and HB-EGF, which play a protective role in colitis. Circulating APN binds to bFGF and HB-EGF, likely inhibiting their protective activity. Inhibition of EGF receptor signaling, which is required for biologic activity of HB-EGF, restores inflammation in APN KO mice. Conclusions: APN deficiency is associated with protection from chemically induced colitis. APN exerts proinflammatory activities in the colon by inducing production of proinflammatory cytokines and inhibiting bioactivity of protective growth factors. Thus, in colitis, APN exerts an opposite role compared with atherosclerosis. © 2007 AGA Institute.
Persistent Identifierhttp://hdl.handle.net/10722/78381
ISSN
2015 Impact Factor: 18.187
2015 SCImago Journal Rankings: 7.170
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorFayad, Ren_HK
dc.contributor.authorPini, Men_HK
dc.contributor.authorSennello, JAen_HK
dc.contributor.authorCabay, RJen_HK
dc.contributor.authorChan, Len_HK
dc.contributor.authorXu, Aen_HK
dc.contributor.authorFantuzzi, Gen_HK
dc.date.accessioned2010-09-06T07:42:15Z-
dc.date.available2010-09-06T07:42:15Z-
dc.date.issued2007en_HK
dc.identifier.citationGastroenterology, 2007, v. 132 n. 2, p. 601-614en_HK
dc.identifier.issn0016-5085en_HK
dc.identifier.urihttp://hdl.handle.net/10722/78381-
dc.description.abstractBackground & Aims: Adiponectin (APN) is an adipokine that regulates insulin sensitivity and is anti-inflammatory in atherosclerosis. The goal of this study was to investigate the role of APN in intestinal inflammation. Methods: APN knockout (KO) mice and their wild-type (WT) littermates received dextran sulfate sodium (DSS) or trinitrobenzene sulfonic acid (TNBS) to induce intestinal inflammation. Clinical and histologic scores and proliferation of epithelial cells were assessed. Cytokines and APN levels were measured. Expression of APN and heparin binding epidermal growth factor (HB-EGF) was analyzed by immunohistochemistry. Expression of APN and its receptors, HB-EGF, and basic fibroblast growth factor (bFGF) messenger RNA was assessed by reverse-transcription polymerase chain reaction. Association of serum APN with HB-EGF and bFGF was studied by coimmunoprecipitation. Results: APN KO mice are protected from chemically induced colitis; administration of APN restores inflammation. APN is expressed in the colon, luminal APN associates with colonic epithelial cells. In vitro, APN increases production of proinflammatory cytokines from colonic tissue. Expression of colonic APN overlaps with that of bFGF and HB-EGF, which play a protective role in colitis. Circulating APN binds to bFGF and HB-EGF, likely inhibiting their protective activity. Inhibition of EGF receptor signaling, which is required for biologic activity of HB-EGF, restores inflammation in APN KO mice. Conclusions: APN deficiency is associated with protection from chemically induced colitis. APN exerts proinflammatory activities in the colon by inducing production of proinflammatory cytokines and inhibiting bioactivity of protective growth factors. Thus, in colitis, APN exerts an opposite role compared with atherosclerosis. © 2007 AGA Institute.en_HK
dc.languageengen_HK
dc.publisherWB Saunders Co. The Journal's web site is located at http://www.elsevier.com/locate/gastroen_HK
dc.relation.ispartofGastroenterologyen_HK
dc.subject.meshAdiponectin - deficiency - genetics - pharmacologyen_HK
dc.subject.meshAnimalsen_HK
dc.subject.meshChemokine CXCL2en_HK
dc.subject.meshChemokines - metabolismen_HK
dc.subject.meshColitis - chemically induced - metabolism - pathology - prevention & controlen_HK
dc.subject.meshColon - drug effects - metabolism - pathologyen_HK
dc.subject.meshCytokines - metabolismen_HK
dc.subject.meshDextran Sulfateen_HK
dc.subject.meshDisease Models, Animalen_HK
dc.subject.meshEpidermal Growth Factor - metabolismen_HK
dc.subject.meshFemaleen_HK
dc.subject.meshFibroblast Growth Factor 2 - metabolismen_HK
dc.subject.meshIntercellular Signaling Peptides and Proteinsen_HK
dc.subject.meshInterleukin-6 - metabolismen_HK
dc.subject.meshIntestinal Mucosa - metabolismen_HK
dc.subject.meshMiceen_HK
dc.subject.meshMice, Inbred C57BLen_HK
dc.subject.meshMice, Knockouten_HK
dc.subject.meshOrgan Culture Techniquesen_HK
dc.subject.meshReceptors, Adiponectinen_HK
dc.subject.meshReceptors, Cell Surface - metabolismen_HK
dc.subject.meshSeverity of Illness Indexen_HK
dc.subject.meshTime Factorsen_HK
dc.subject.meshTrinitrobenzenesulfonic Aciden_HK
dc.titleAdiponectin Deficiency Protects Mice From Chemically Induced Colonic Inflammationen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0016-5085&volume=132&spage=601&epage=14&date=2007&atitle=Adiponectin+deficiency+protects+mice+from+chemically+induced+colonic+inflammation.en_HK
dc.identifier.emailXu, A:amxu@hkucc.hku.hken_HK
dc.identifier.authorityXu, A=rp00485en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1053/j.gastro.2006.11.026en_HK
dc.identifier.pmid17258715-
dc.identifier.scopuseid_2-s2.0-33847065560en_HK
dc.identifier.hkuros129064en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-33847065560&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume132en_HK
dc.identifier.issue2en_HK
dc.identifier.spage601en_HK
dc.identifier.epage614en_HK
dc.identifier.isiWOS:000244604200020-
dc.publisher.placeUnited Statesen_HK
dc.identifier.scopusauthoridFayad, R=6603494213en_HK
dc.identifier.scopusauthoridPini, M=8541727600en_HK
dc.identifier.scopusauthoridSennello, JA=6505794569en_HK
dc.identifier.scopusauthoridCabay, RJ=6506937586en_HK
dc.identifier.scopusauthoridChan, L=24439401800en_HK
dc.identifier.scopusauthoridXu, A=7202655409en_HK
dc.identifier.scopusauthoridFantuzzi, G=7006088951en_HK

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