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Article: Upregulation of UCP2 by adiponectin: The involvement of mitochondrial superoxide and hnRNP K
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TitleUpregulation of UCP2 by adiponectin: The involvement of mitochondrial superoxide and hnRNP K
 
AuthorsZhou, M1
Xu, A1
Tam, PKH1
Lam, KSL1
Huang, B1
Liang, Y1
Lee, IK2
Wu, D3
Wang, Y1
 
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
 
CitationPlos One, 2012, v. 7 n. 2 [How to Cite?]
DOI: http://dx.doi.org/10.1371/journal.pone.0032349
 
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.
 
ISSN1932-6203
2013 Impact Factor: 3.534
2013 SCImago Journal Rankings: 1.724
 
DOIhttp://dx.doi.org/10.1371/journal.pone.0032349
 
PubMed Central IDPMC3281141
 
ISI Accession Number IDWOS:000302796200153
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.

 
ReferencesReferences in Scopus
 
DC FieldValue
dc.contributor.authorZhou, M
 
dc.contributor.authorXu, A
 
dc.contributor.authorTam, PKH
 
dc.contributor.authorLam, KSL
 
dc.contributor.authorHuang, B
 
dc.contributor.authorLiang, Y
 
dc.contributor.authorLee, IK
 
dc.contributor.authorWu, D
 
dc.contributor.authorWang, Y
 
dc.date.accessioned2012-05-23T05:48:30Z
 
dc.date.available2012-05-23T05:48:30Z
 
dc.date.issued2012
 
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.
 
dc.description.naturepublished_or_final_version
 
dc.identifier.citationPlos One, 2012, v. 7 n. 2 [How to Cite?]
DOI: http://dx.doi.org/10.1371/journal.pone.0032349
 
dc.identifier.doihttp://dx.doi.org/10.1371/journal.pone.0032349
 
dc.identifier.hkuros199690
 
dc.identifier.isiWOS:000302796200153
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.

 
dc.identifier.issn1932-6203
2013 Impact Factor: 3.534
2013 SCImago Journal Rankings: 1.724
 
dc.identifier.issue2
 
dc.identifier.pmcidPMC3281141
 
dc.identifier.pmid22359684
 
dc.identifier.scopuseid_2-s2.0-84863121852
 
dc.identifier.urihttp://hdl.handle.net/10722/146886
 
dc.identifier.volume7
 
dc.languageeng
 
dc.publisherPublic Library of Science. The Journal's web site is located at http://www.plosone.org/home.action
 
dc.publisher.placeUnited States
 
dc.relation.ispartofPLoS ONE
 
dc.relation.referencesReferences in Scopus
 
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 K
 
dc.typeArticle
 
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<contributor.author>Lam, KSL</contributor.author>
<contributor.author>Huang, B</contributor.author>
<contributor.author>Liang, Y</contributor.author>
<contributor.author>Lee, IK</contributor.author>
<contributor.author>Wu, D</contributor.author>
<contributor.author>Wang, Y</contributor.author>
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Author Affiliations
  1. The University of Hong Kong
  2. Kyungpook National University
  3. Chinese Academy of Sciences