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Article: Upregulation of UCP2 by adiponectin: The involvement of mitochondrial superoxide and hnRNP K

TitleUpregulation of UCP2 by adiponectin: The involvement of mitochondrial superoxide and hnRNP K
Authors
KeywordsAdiponectin
Cycloheximide
Animal cell
Biological monitoring
Cell fractionation
Issue Date2012
PublisherPublic Library of Science. The Journal's web site is located at http://www.plosone.org/home.action
Citation
Plos One, 2012, v. 7 n. 2 How to Cite?
AbstractBackground: The adipocyte-derived hormone adiponectin elicits protective functions against fatty liver diseases and hepatic injuries at least in part by stimulating the expression of a mitochondrial inner membrane transporter, uncoupling protein 2 (UCP2). The present study was designed to investigate the cellular and molecular mechanisms underlying adiponectin-induced UCP2 expression. Methodology/Principal Findnigs: Mice were treated with adiponectin and/or different drug inhibitors. Parenchymal (PCs) and nonparenchymal (NPCs) cells were fractionated from the liver tissues for mitochondria isolation, Western blotting and quantitative PCR analysis. Mitochondrial superoxide production was monitored by MitoSOX staining and flow cytometry analysis. Compared to control mice, the expression of UCP2 was significantly lower in NPCs, but not PCs of adiponectin knockout mice (AKO). Both chronic and acute treatment with adiponectin selectively increased the mRNA and protein abundance of UCP2 in NPCs, especially in the enriched endothelial cell fractions. The transcription inhibitor actinomycin D could not block adiponectin-induced UCP2 expression, whereas the protein synthesis inhibitor cycloheximide inhibited the elevation of UCP2 protein but not its mRNA levels. Mitochondrial content of heterogeneous nuclear ribonucleoprotein K (hnRNP K), a nucleic acid binding protein involved in regulating mRNA transportation and stabilization, was significantly enhanced by adiponectin, which also evoked a transient elevation of mitochondrial superoxide. Rotenone, an inhibitor of mitochondrial respiratory complex I, abolished adiponectin-induced superoxide production, hnRNP K recruitment and UCP2 expression. Conclusions/Significance: Mitochondrial superoxide production stimulated by adiponectin serves as a trigger to initiate the translocation of hnRNP K, which in turn promotes UCP2 expressions in liver. © 2012 Zhou et al.
Persistent Identifierhttp://hdl.handle.net/10722/146886
ISSN
2014 Impact Factor: 3.234
2014 SCImago Journal Rankings: 1.300
PubMed Central ID
ISI Accession Number ID
Funding AgencyGrant Number
Research Grants Council of Hong KongHKU777908M
National Basic Research Program of China2010CB945500
US National Institutes of HealthHL-51586
Funding Information:

This work is supported by Research Grants Council of Hong Kong (Project no. HKU777908M), the National Basic Research Program of China (2010CB945500). Adiponectin knockout mice were kindly provided by Dr. Lawrence Chan at Baylor College of Medicine, who generated these mice with the support of the US National Institutes of Health grant HL-51586. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.

References

 

DC FieldValueLanguage
dc.contributor.authorZhou, Men_HK
dc.contributor.authorXu, Aen_HK
dc.contributor.authorTam, PKHen_HK
dc.contributor.authorLam, KSLen_HK
dc.contributor.authorHuang, Ben_HK
dc.contributor.authorLiang, Yen_HK
dc.contributor.authorLee, IKen_HK
dc.contributor.authorWu, Den_HK
dc.contributor.authorWang, Yen_HK
dc.date.accessioned2012-05-23T05:48:30Z-
dc.date.available2012-05-23T05:48:30Z-
dc.date.issued2012en_HK
dc.identifier.citationPlos One, 2012, v. 7 n. 2en_HK
dc.identifier.issn1932-6203en_HK
dc.identifier.urihttp://hdl.handle.net/10722/146886-
dc.description.abstractBackground: The adipocyte-derived hormone adiponectin elicits protective functions against fatty liver diseases and hepatic injuries at least in part by stimulating the expression of a mitochondrial inner membrane transporter, uncoupling protein 2 (UCP2). The present study was designed to investigate the cellular and molecular mechanisms underlying adiponectin-induced UCP2 expression. Methodology/Principal Findnigs: Mice were treated with adiponectin and/or different drug inhibitors. Parenchymal (PCs) and nonparenchymal (NPCs) cells were fractionated from the liver tissues for mitochondria isolation, Western blotting and quantitative PCR analysis. Mitochondrial superoxide production was monitored by MitoSOX staining and flow cytometry analysis. Compared to control mice, the expression of UCP2 was significantly lower in NPCs, but not PCs of adiponectin knockout mice (AKO). Both chronic and acute treatment with adiponectin selectively increased the mRNA and protein abundance of UCP2 in NPCs, especially in the enriched endothelial cell fractions. The transcription inhibitor actinomycin D could not block adiponectin-induced UCP2 expression, whereas the protein synthesis inhibitor cycloheximide inhibited the elevation of UCP2 protein but not its mRNA levels. Mitochondrial content of heterogeneous nuclear ribonucleoprotein K (hnRNP K), a nucleic acid binding protein involved in regulating mRNA transportation and stabilization, was significantly enhanced by adiponectin, which also evoked a transient elevation of mitochondrial superoxide. Rotenone, an inhibitor of mitochondrial respiratory complex I, abolished adiponectin-induced superoxide production, hnRNP K recruitment and UCP2 expression. Conclusions/Significance: Mitochondrial superoxide production stimulated by adiponectin serves as a trigger to initiate the translocation of hnRNP K, which in turn promotes UCP2 expressions in liver. © 2012 Zhou et al.en_HK
dc.languageengen_US
dc.publisherPublic Library of Science. The Journal's web site is located at http://www.plosone.org/home.actionen_HK
dc.relation.ispartofPLoS ONEen_HK
dc.rightsCreative Commons: Attribution 3.0 Hong Kong License-
dc.subjectAdiponectin-
dc.subjectCycloheximide-
dc.subjectAnimal cell-
dc.subjectBiological monitoring-
dc.subjectCell fractionation-
dc.titleUpregulation of UCP2 by adiponectin: The involvement of mitochondrial superoxide and hnRNP Ken_HK
dc.typeArticleen_HK
dc.identifier.emailXu, A: amxu@hkucc.hku.hken_HK
dc.identifier.emailWang, Y: yuwanghk@hku.hken_HK
dc.identifier.authorityXu, A=rp00485en_HK
dc.identifier.authorityWang, Y=rp00239en_HK
dc.description.naturepublished_or_final_version-
dc.identifier.doi10.1371/journal.pone.0032349en_HK
dc.identifier.pmid22359684-
dc.identifier.pmcidPMC3281141-
dc.identifier.scopuseid_2-s2.0-84863121852en_HK
dc.identifier.hkuros199690en_US
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-84863121852&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume7en_HK
dc.identifier.issue2en_HK
dc.identifier.isiWOS:000302796200153-
dc.publisher.placeUnited Statesen_HK
dc.identifier.scopusauthoridZhou, M=14629760500en_HK
dc.identifier.scopusauthoridXu, A=7202655409en_HK
dc.identifier.scopusauthoridTam, PKH=55273108100en_HK
dc.identifier.scopusauthoridLam, KSL=55192819200en_HK
dc.identifier.scopusauthoridHuang, B=27169619500en_HK
dc.identifier.scopusauthoridLiang, Y=55273172800en_HK
dc.identifier.scopusauthoridLee, IK=36071537600en_HK
dc.identifier.scopusauthoridWu, D=7404297751en_HK
dc.identifier.scopusauthoridWang, Y=34973733700en_HK

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