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Article: Improved functional recovery to I/R injury in hearts from lipocalin-2 deficiency mice: restoration of mitochondrial function and phospholipids remodeling

TitleImproved functional recovery to I/R injury in hearts from lipocalin-2 deficiency mice: restoration of mitochondrial function and phospholipids remodeling
Authors
KeywordsLipocalin
Animal experiment
Biogenesis
Cell density
Heart
Issue Date2012
PublisherE-Century Publishing Corporation. The Journal's web site is located at http://www.ajtr.org
Citation
American Journal of Translational Research, 2012, v. 4 n. 1, p. 60-71 How to Cite?
Abstract
AIMS: Recent clinical and experimental evidences demonstrate an association between augmented circulating lipocalin-2 [a pro-inflammatory adipokine] and cardiac dysfunction. However, little is known about the pathophysi-ological role of lipocalin-2 in heart. The present study was designed to compare the heart functions of mice with normal (WT) or deficient lipocalin-2 (Lcn2-KO) expression. METHODS AND RESULTS: Echocardiographic analysis revealed that the myocardial contractile function was significantly improved in hearts of Lcn2-KO mice, under both standard chow and high fat diet conditions. The heart function before and after I/R injury (20-min of global ischemia followed by 60-min of reperfusion) was assessed using the Langendorff perfusion system. Compared to WT littermates, hearts from Lcn2-KO mice showed improved functional recovery and reduced infarct size following I/R. Under baseline condition, the mitochondrial function of Lcn2-KO hearts was significantly enhanced, as demonstrated by biochemical analysis of respiratory chain activity and markers of biogenesis, as well as electron microscopic investigation of the mitochondrial ultrastructure. Acute or chronic administration of lipocalin-2 impaired cardiac functional recovery to I/R and dampened the mitochondrial function in hearts of Lcn2-KO mice. These effects were associated with an extensive modification of the fatty acyl chain compositions of intracellular phospholipids. For example, lipocalin-2 facilitated the redistribution of linoleic acid (C18:2) among different types of phospholipids, including cardiolipin, a structurally unique phospholipid located mainly on the inner membrane of mitochondria. CONCLUSIONS: Lack of lipocalin-2 improved the functional recovery of isolated mice hearts subjected to I/R, which is associated with restoration of mitochondrial function and phospholipids remodeling.
Persistent Identifierhttp://hdl.handle.net/10722/159686
ISSN
2013 Impact Factor: 3.226
2013 SCImago Journal Rankings: 1.788
PubMed Central ID
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorYang, Ben_HK
dc.contributor.authorFan, Pen_HK
dc.contributor.authorXu, Aen_HK
dc.contributor.authorLam, KSLen_HK
dc.contributor.authorBerger, Ten_HK
dc.contributor.authorMak, TWen_HK
dc.contributor.authorTse, HFen_HK
dc.contributor.authorYue, JWSen_HK
dc.contributor.authorSong, Een_HK
dc.contributor.authorVanhoutte, PMen_HK
dc.contributor.authorSweeney, Gen_HK
dc.contributor.authorWang, Yen_HK
dc.date.accessioned2012-08-16T05:54:01Z-
dc.date.available2012-08-16T05:54:01Z-
dc.date.issued2012en_HK
dc.identifier.citationAmerican Journal of Translational Research, 2012, v. 4 n. 1, p. 60-71en_HK
dc.identifier.issn1943-8141en_HK
dc.identifier.urihttp://hdl.handle.net/10722/159686-
dc.description.abstractAIMS: Recent clinical and experimental evidences demonstrate an association between augmented circulating lipocalin-2 [a pro-inflammatory adipokine] and cardiac dysfunction. However, little is known about the pathophysi-ological role of lipocalin-2 in heart. The present study was designed to compare the heart functions of mice with normal (WT) or deficient lipocalin-2 (Lcn2-KO) expression. METHODS AND RESULTS: Echocardiographic analysis revealed that the myocardial contractile function was significantly improved in hearts of Lcn2-KO mice, under both standard chow and high fat diet conditions. The heart function before and after I/R injury (20-min of global ischemia followed by 60-min of reperfusion) was assessed using the Langendorff perfusion system. Compared to WT littermates, hearts from Lcn2-KO mice showed improved functional recovery and reduced infarct size following I/R. Under baseline condition, the mitochondrial function of Lcn2-KO hearts was significantly enhanced, as demonstrated by biochemical analysis of respiratory chain activity and markers of biogenesis, as well as electron microscopic investigation of the mitochondrial ultrastructure. Acute or chronic administration of lipocalin-2 impaired cardiac functional recovery to I/R and dampened the mitochondrial function in hearts of Lcn2-KO mice. These effects were associated with an extensive modification of the fatty acyl chain compositions of intracellular phospholipids. For example, lipocalin-2 facilitated the redistribution of linoleic acid (C18:2) among different types of phospholipids, including cardiolipin, a structurally unique phospholipid located mainly on the inner membrane of mitochondria. CONCLUSIONS: Lack of lipocalin-2 improved the functional recovery of isolated mice hearts subjected to I/R, which is associated with restoration of mitochondrial function and phospholipids remodeling.en_HK
dc.languageengen_US
dc.publisherE-Century Publishing Corporation. The Journal's web site is located at http://www.ajtr.orgen_HK
dc.relation.ispartofAmerican Journal of Translational Researchen_HK
dc.rightsCreative Commons: Attribution 3.0 Hong Kong License-
dc.subjectLipocalinen_HK
dc.subjectAnimal experimenten_HK
dc.subjectBiogenesisen_HK
dc.subjectCell densityen_HK
dc.subjectHearten_HK
dc.titleImproved functional recovery to I/R injury in hearts from lipocalin-2 deficiency mice: restoration of mitochondrial function and phospholipids remodelingen_HK
dc.typeArticleen_HK
dc.identifier.emailXu, A: amxu@hkucc.hku.hken_HK
dc.identifier.emailLam, KSL: ksllam@hku.hken_HK
dc.identifier.emailTse, HF: hftse@hkucc.hku.hken_HK
dc.identifier.emailVanhoutte, PM: vanhoutt@hku.hk-
dc.identifier.emailWang, Y: yuwanghk@hku.hk-
dc.identifier.authorityTse, HF=rp00428en_HK
dc.identifier.authorityVanhoutte, PM=rp00238en_HK
dc.identifier.authorityTse, HF=rp00428en_HK
dc.description.naturepublished_or_final_version-
dc.identifier.pmid22355443-
dc.identifier.pmcidPMC3280429-
dc.identifier.scopuseid_2-s2.0-84863031506en_HK
dc.identifier.hkuros204773en_US
dc.identifier.hkuros213331-
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-84863031506&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume4en_HK
dc.identifier.issue1en_HK
dc.identifier.spage60en_HK
dc.identifier.epage71en_HK
dc.identifier.isiWOS:000318277600006-
dc.publisher.placeUnited Statesen_HK
dc.identifier.scopusauthoridWang, Y=34973733700en_HK
dc.identifier.scopusauthoridSweeney, G=7102852659en_HK
dc.identifier.scopusauthoridVanhoutte, PM=7202304247en_HK
dc.identifier.scopusauthoridSong, E=54785178800en_HK
dc.identifier.scopusauthoridYue, JWS=55266953300en_HK
dc.identifier.scopusauthoridTse, HF=7006070805en_HK
dc.identifier.scopusauthoridMak, TW=55203443000en_HK
dc.identifier.scopusauthoridBerger, T=12242304800en_HK
dc.identifier.scopusauthoridLam, KSL=55192819200en_HK
dc.identifier.scopusauthoridXu, A=55212499600en_HK
dc.identifier.scopusauthoridFan, P=55266967800en_HK
dc.identifier.scopusauthoridYang, B=55267956100en_HK

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