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Article: N-acetylcysteine attenuates PKCβ2 overexpression and myocardial hypertrophy in streptozotocin-induced diabetic rats

TitleN-acetylcysteine attenuates PKCβ2 overexpression and myocardial hypertrophy in streptozotocin-induced diabetic rats
Authors
Issue Date2007
PublisherOxford University Press. The Journal's web site is located at http://cardiovascres.oxfordjournals.org
Citation
Cardiovascular Research, 2007, v. 73 n. 4, p. 770-782 How to Cite?
AbstractObjective: Oxidative stress-mediated activation of protein kinase C (PKC) β2 in the myocardium has been implicated in the development of cardiomyopathy. Overexpression of PKCβ2 is associated with increased expression of connective tissue growth factor (CTGF) in myocardium, resulting in myocardial hypertrophy. We hypothesized that chronic treatment with the antioxidant N-acetylcysteine (NAC) would normalize oxidative stress-mediated overexpression of myocardial PKCβ2 and CTGF and attenuate the development of myocardial hypertrophy. Methods: Control and streptozotocin-induced diabetic rats were treated with NAC in drinking water for 8 weeks. At termination rats were surgically prepared for hemodynamic measurement, subsequent to which their hearts were removed to evaluate cardiac performance and histological and biochemical changes. Further, the role of PKCβ2 in hyperglycemia-induced cardiomyocyte hypertrophy was tested in cultured neonatal cardiomyocytes. Results: Myocardial hypertrophy, characterized by an increased ratio of ventricle weight to body weight and cardiomyocyte cross-sectional area was found to be higher in untreated diabetic rats. Further, in myocardium, increased levels of 15-F2t-isoprostane were accompanied by an increased expression of membrane-bound PKCβ2 and CTGF. N-acetylcysteine treatment not only attenuated these changes but also prevented hyperglycemia-induced hypertrophy in cultured neonatal rat cardiomyocytes. Conclusions: The results suggest that PKCβ2 overexpression represents a mechanism causing hyperglycemia-mediated myocardial hypertrophy, which can be prevented by the antioxidant N-acetylcysteine. © 2006 European Society of Cardiology.
Persistent Identifierhttp://hdl.handle.net/10722/147240
ISSN
2015 Impact Factor: 5.465
2015 SCImago Journal Rankings: 2.897
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorXia, Zen_US
dc.contributor.authorKuo, KHen_US
dc.contributor.authorNagareddy, PRen_US
dc.contributor.authorWang, Fen_US
dc.contributor.authorGuo, Zen_US
dc.contributor.authorGuo, Ten_US
dc.contributor.authorJiang, Jen_US
dc.contributor.authorMcneill, JHen_US
dc.date.accessioned2012-05-29T06:00:58Z-
dc.date.available2012-05-29T06:00:58Z-
dc.date.issued2007en_US
dc.identifier.citationCardiovascular Research, 2007, v. 73 n. 4, p. 770-782en_US
dc.identifier.issn0008-6363en_US
dc.identifier.urihttp://hdl.handle.net/10722/147240-
dc.description.abstractObjective: Oxidative stress-mediated activation of protein kinase C (PKC) β2 in the myocardium has been implicated in the development of cardiomyopathy. Overexpression of PKCβ2 is associated with increased expression of connective tissue growth factor (CTGF) in myocardium, resulting in myocardial hypertrophy. We hypothesized that chronic treatment with the antioxidant N-acetylcysteine (NAC) would normalize oxidative stress-mediated overexpression of myocardial PKCβ2 and CTGF and attenuate the development of myocardial hypertrophy. Methods: Control and streptozotocin-induced diabetic rats were treated with NAC in drinking water for 8 weeks. At termination rats were surgically prepared for hemodynamic measurement, subsequent to which their hearts were removed to evaluate cardiac performance and histological and biochemical changes. Further, the role of PKCβ2 in hyperglycemia-induced cardiomyocyte hypertrophy was tested in cultured neonatal cardiomyocytes. Results: Myocardial hypertrophy, characterized by an increased ratio of ventricle weight to body weight and cardiomyocyte cross-sectional area was found to be higher in untreated diabetic rats. Further, in myocardium, increased levels of 15-F2t-isoprostane were accompanied by an increased expression of membrane-bound PKCβ2 and CTGF. N-acetylcysteine treatment not only attenuated these changes but also prevented hyperglycemia-induced hypertrophy in cultured neonatal rat cardiomyocytes. Conclusions: The results suggest that PKCβ2 overexpression represents a mechanism causing hyperglycemia-mediated myocardial hypertrophy, which can be prevented by the antioxidant N-acetylcysteine. © 2006 European Society of Cardiology.en_US
dc.languageengen_US
dc.publisherOxford University Press. The Journal's web site is located at http://cardiovascres.oxfordjournals.orgen_US
dc.relation.ispartofCardiovascular Researchen_US
dc.subject.meshAcetylcysteine - Therapeutic Useen_US
dc.subject.meshAnimalsen_US
dc.subject.meshAntioxidants - Therapeutic Useen_US
dc.subject.meshCardiomegaly - Enzymology - Pathology - Prevention & Controlen_US
dc.subject.meshCell Size - Drug Effectsen_US
dc.subject.meshCells, Cultureden_US
dc.subject.meshCollagen Type I - Analysisen_US
dc.subject.meshCollagen Type Ii - Analysisen_US
dc.subject.meshConnective Tissue Growth Factoren_US
dc.subject.meshDiabetes Mellitus, Experimental - Enzymology - Pathologyen_US
dc.subject.meshDinoprost - Analogs & Derivatives - Analysis - Blooden_US
dc.subject.meshGlucose - Pharmacologyen_US
dc.subject.meshImmediate-Early Proteins - Metabolismen_US
dc.subject.meshImmunohistochemistryen_US
dc.subject.meshIntercellular Signaling Peptides And Proteins - Metabolismen_US
dc.subject.meshMaleen_US
dc.subject.meshMyocardium - Chemistry - Enzymologyen_US
dc.subject.meshMyocytes, Cardiac - Drug Effects - Pathologyen_US
dc.subject.meshOxidative Stressen_US
dc.subject.meshProtein Kinase C - Metabolismen_US
dc.subject.meshRatsen_US
dc.subject.meshRats, Wistaren_US
dc.subject.meshSuperoxides - Analysisen_US
dc.titleN-acetylcysteine attenuates PKCβ2 overexpression and myocardial hypertrophy in streptozotocin-induced diabetic ratsen_US
dc.typeArticleen_US
dc.identifier.emailXia, Z:zyxia@hkucc.hku.hken_US
dc.identifier.authorityXia, Z=rp00532en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1016/j.cardiores.2006.11.033en_US
dc.identifier.pmid17250813-
dc.identifier.scopuseid_2-s2.0-33846880290en_US
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-33846880290&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume73en_US
dc.identifier.issue4en_US
dc.identifier.spage770en_US
dc.identifier.epage782en_US
dc.identifier.isiWOS:000245301800019-
dc.publisher.placeUnited Kingdomen_US
dc.identifier.citeulike1622124-

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