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Article: Hypoxia dysregulates the production of adiponectin and plasminogen activator inhibitor-1 independent of reactive oxygen species in adipocytes

TitleHypoxia dysregulates the production of adiponectin and plasminogen activator inhibitor-1 independent of reactive oxygen species in adipocytes
Authors
KeywordsAdipocyte
Adiponectin and adipokine
Hypoxia
Obesity
Issue Date2006
PublisherAcademic Press. The Journal's web site is located at http://www.elsevier.com/wps/find/journaldescription.cws_home/622790/description
Citation
Biochemical And Biophysical Research Communications, 2006, v. 341 n. 2, p. 549-556 How to Cite?
AbstractLow plasma levels of adiponectin (hypoadiponectinemia) and elevated circulating concentrations of plasminogen activator inhibitor (PAI)-1 are causally associated with obesity-related insulin resistance and cardiovascular disease. However, the mechanism that mediates the aberrant production of these two adipokines in obesity remains poorly understood. In this study, we investigated the effects of hypoxia and reactive oxygen species (ROS) on production of adiponectin and PAI-1 in 3T3-L1 adipocytes. Quantitative PCR and immunoassays showed that ambient hypoxia markedly suppressed adiponectin mRNA expression and its protein secretion, and increased PAI-1 production in mature adipocytes. Dimethyloxallyl glycine, a stabilizer of hypoxia-inducible factor 1α (HIF-1α), mimicked the hypoxia-mediated modulations of these two adipokines. Hypoxia caused a modest elevation of ROS in adipocytes. However, ablation of intracellular ROS by antioxidants failed to alleviate hypoxia-induced aberrant production of adiponectin and PAI-1. On the other hand, the antioxidants could reverse hydrogen peroxide (H2O 2)-induced dysregulation of adiponectin and PAI-1 production. H 2O2 treatment decreased the expression levels of peroxisome proliferator-activated receptor gamma (PPARγ) and CCAAT/enhancer binding protein (C/EBPα), but had no effect on HIF-1α, whereas hypoxia stabilized HIF-1α and decreased expression of C/EBPα, but not PPARγ. Taken together, these data suggest that hypoxia and ROS decrease adiponectin production and augment PAI-1 expression in adipocytes via distinct signaling pathways. These effects may contribute to hypoadiponectinemia and elevated PAI-1 levels in obesity, type 2 diabetes, and cardiovascular diseases. © 2006 Elsevier Inc. All rights reserved.
Persistent Identifierhttp://hdl.handle.net/10722/76240
ISSN
2015 Impact Factor: 2.371
2015 SCImago Journal Rankings: 1.152
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorChen, Ben_HK
dc.contributor.authorLam, KSLen_HK
dc.contributor.authorWang, Yen_HK
dc.contributor.authorWu, Den_HK
dc.contributor.authorLam, MCen_HK
dc.contributor.authorShen, Jen_HK
dc.contributor.authorWong, Len_HK
dc.contributor.authorHoo, RLCen_HK
dc.contributor.authorZhang, Jen_HK
dc.contributor.authorXu, Aen_HK
dc.date.accessioned2010-09-06T07:19:07Z-
dc.date.available2010-09-06T07:19:07Z-
dc.date.issued2006en_HK
dc.identifier.citationBiochemical And Biophysical Research Communications, 2006, v. 341 n. 2, p. 549-556en_HK
dc.identifier.issn0006-291Xen_HK
dc.identifier.urihttp://hdl.handle.net/10722/76240-
dc.description.abstractLow plasma levels of adiponectin (hypoadiponectinemia) and elevated circulating concentrations of plasminogen activator inhibitor (PAI)-1 are causally associated with obesity-related insulin resistance and cardiovascular disease. However, the mechanism that mediates the aberrant production of these two adipokines in obesity remains poorly understood. In this study, we investigated the effects of hypoxia and reactive oxygen species (ROS) on production of adiponectin and PAI-1 in 3T3-L1 adipocytes. Quantitative PCR and immunoassays showed that ambient hypoxia markedly suppressed adiponectin mRNA expression and its protein secretion, and increased PAI-1 production in mature adipocytes. Dimethyloxallyl glycine, a stabilizer of hypoxia-inducible factor 1α (HIF-1α), mimicked the hypoxia-mediated modulations of these two adipokines. Hypoxia caused a modest elevation of ROS in adipocytes. However, ablation of intracellular ROS by antioxidants failed to alleviate hypoxia-induced aberrant production of adiponectin and PAI-1. On the other hand, the antioxidants could reverse hydrogen peroxide (H2O 2)-induced dysregulation of adiponectin and PAI-1 production. H 2O2 treatment decreased the expression levels of peroxisome proliferator-activated receptor gamma (PPARγ) and CCAAT/enhancer binding protein (C/EBPα), but had no effect on HIF-1α, whereas hypoxia stabilized HIF-1α and decreased expression of C/EBPα, but not PPARγ. Taken together, these data suggest that hypoxia and ROS decrease adiponectin production and augment PAI-1 expression in adipocytes via distinct signaling pathways. These effects may contribute to hypoadiponectinemia and elevated PAI-1 levels in obesity, type 2 diabetes, and cardiovascular diseases. © 2006 Elsevier Inc. All rights reserved.en_HK
dc.languageengen_HK
dc.publisherAcademic Press. The Journal's web site is located at http://www.elsevier.com/wps/find/journaldescription.cws_home/622790/descriptionen_HK
dc.relation.ispartofBiochemical and Biophysical Research Communicationsen_HK
dc.subjectAdipocyteen_HK
dc.subjectAdiponectin and adipokineen_HK
dc.subjectHypoxiaen_HK
dc.subjectObesityen_HK
dc.subject.meshAdipocytes - metabolism-
dc.subject.meshAdiponectin - biosynthesis - metabolism-
dc.subject.meshAnoxia - metabolism-
dc.subject.meshPlasminogen Activator Inhibitor 1 - biosynthesis-
dc.subject.meshReactive Oxygen Species - metabolism-
dc.titleHypoxia dysregulates the production of adiponectin and plasminogen activator inhibitor-1 independent of reactive oxygen species in adipocytesen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0006-291X&volume=341&issue=2&spage=549&epage=556&date=2006&atitle=Hypoxia+dysregulates+the+production+of+adiponectin+and+plasminogen+activator+inhibitor-1+independent+of+reactive+oxygen+species+in+adipocytesen_HK
dc.identifier.emailLam, KSL: ksllam@hku.hken_HK
dc.identifier.emailWang, Y: yuwanghk@hku.hken_HK
dc.identifier.emailShen, J: shenjg@hku.hken_HK
dc.identifier.emailHoo, RLC: rubyhoo@hkucc.hku.hken_HK
dc.identifier.emailXu, A: amxu@hkucc.hku.hken_HK
dc.identifier.authorityLam, KSL=rp00343en_HK
dc.identifier.authorityWang, Y=rp00239en_HK
dc.identifier.authorityShen, J=rp00487en_HK
dc.identifier.authorityHoo, RLC=rp01334en_HK
dc.identifier.authorityXu, A=rp00485en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1016/j.bbrc.2006.01.004en_HK
dc.identifier.pmid16427606-
dc.identifier.scopuseid_2-s2.0-31444447850en_HK
dc.identifier.hkuros131671en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-31444447850&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume341en_HK
dc.identifier.issue2en_HK
dc.identifier.spage549en_HK
dc.identifier.epage556en_HK
dc.identifier.isiWOS:000235414400039-
dc.publisher.placeUnited Statesen_HK
dc.identifier.scopusauthoridChen, B=8836680100en_HK
dc.identifier.scopusauthoridLam, KSL=8082870600en_HK
dc.identifier.scopusauthoridWang, Y=34973733700en_HK
dc.identifier.scopusauthoridWu, D=7404297751en_HK
dc.identifier.scopusauthoridLam, MC=36879143100en_HK
dc.identifier.scopusauthoridShen, J=7404929947en_HK
dc.identifier.scopusauthoridWong, L=25123484000en_HK
dc.identifier.scopusauthoridHoo, RLC=6602369766en_HK
dc.identifier.scopusauthoridZhang, J=35504391800en_HK
dc.identifier.scopusauthoridXu, A=7202655409en_HK

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