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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
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TitleImproved functional recovery to I/R injury in hearts from lipocalin-2 deficiency mice: restoration of mitochondrial function and phospholipids remodeling
 
AuthorsYang, B2
Fan, P2
Xu, A2
Lam, KSL2
Berger, T3
Mak, TW3
Tse, HF2
Yue, JWS2
Song, E2
Vanhoutte, PM2
Sweeney, G1
Wang, Y2
 
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
 
CitationAmerican Journal of Translational Research, 2012, v. 4 n. 1, p. 60-71 [How to Cite?]
 
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.
 
ISSN1943-8141
 
PubMed Central IDPMC3280429
 
ReferencesReferences in Scopus
 
DC FieldValue
dc.contributor.authorYang, B
 
dc.contributor.authorFan, P
 
dc.contributor.authorXu, A
 
dc.contributor.authorLam, KSL
 
dc.contributor.authorBerger, T
 
dc.contributor.authorMak, TW
 
dc.contributor.authorTse, HF
 
dc.contributor.authorYue, JWS
 
dc.contributor.authorSong, E
 
dc.contributor.authorVanhoutte, PM
 
dc.contributor.authorSweeney, G
 
dc.contributor.authorWang, Y
 
dc.date.accessioned2012-08-16T05:54:01Z
 
dc.date.available2012-08-16T05:54:01Z
 
dc.date.issued2012
 
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.
 
dc.description.naturepublished_or_final_version
 
dc.identifier.citationAmerican Journal of Translational Research, 2012, v. 4 n. 1, p. 60-71 [How to Cite?]
 
dc.identifier.epage71
 
dc.identifier.hkuros204773
 
dc.identifier.hkuros213331
 
dc.identifier.issn1943-8141
 
dc.identifier.issue1
 
dc.identifier.pmcidPMC3280429
 
dc.identifier.pmid22355443
 
dc.identifier.scopuseid_2-s2.0-84863031506
 
dc.identifier.spage60
 
dc.identifier.urihttp://hdl.handle.net/10722/159686
 
dc.identifier.volume4
 
dc.languageeng
 
dc.publisherE-Century Publishing Corporation. The Journal's web site is located at http://www.ajtr.org
 
dc.publisher.placeUnited States
 
dc.relation.ispartofAmerican Journal of Translational Research
 
dc.relation.referencesReferences in Scopus
 
dc.rightsCreative Commons: Attribution 3.0 Hong Kong License
 
dc.subjectLipocalin
 
dc.subjectAnimal experiment
 
dc.subjectBiogenesis
 
dc.subjectCell density
 
dc.subjectHeart
 
dc.titleImproved functional recovery to I/R injury in hearts from lipocalin-2 deficiency mice: restoration of mitochondrial function and phospholipids remodeling
 
dc.typeArticle
 
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<contributor.author>Berger, T</contributor.author>
<contributor.author>Mak, TW</contributor.author>
<contributor.author>Tse, HF</contributor.author>
<contributor.author>Yue, JWS</contributor.author>
<contributor.author>Song, E</contributor.author>
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Author Affiliations
  1. York University
  2. The University of Hong Kong
  3. Princess Margaret Hospital University of Toronto