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Nox4-derived reactive oxygen species mediate cardiomyocyte injury in early type 1 diabetes

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dc.contributor.author Maalouf R.M.
dc.contributor.author Eid A.A.
dc.contributor.author Gorin Y.C.
dc.contributor.author Block K.
dc.contributor.author Escobar G.P.
dc.contributor.author Bailey S.
dc.contributor.author Abboud H.E.
dc.contributor.editor
dc.date Feb-2012
dc.date.accessioned 2017-09-07T06:59:56Z
dc.date.available 2017-09-07T06:59:56Z
dc.date.issued 2012
dc.identifier 10.1152/ajpcell.00331.2011
dc.identifier.isbn
dc.identifier.issn 03636143
dc.identifier.uri http://hdl.handle.net/10938/11217
dc.description.abstract Oxidative stress contributes to diabetic cardiomyopathy. This study explored the role of the NADPH oxidase Nox4 as a source of reactive oxygen species (ROS) involved in the development of diabetic cardiomyopathy. Phosphorothioated antisense (AS) or sense (S) oligonucleotides for Nox4 were administered for 2 wk to rats made diabetic by streptozotocin. NADPH oxidase activity, ROS generation, and the expression of Nox4, but Nox1 or Nox2, were increased in left ventricular tissue of the diabetic rats. Expression of molecular markers of hypertrophy and myofibrosis including fibronectin, collagen, α-smooth muscle actin, and β-myosin heavy chain were also increased. These parameters were attenuated by the administration of AS but not S Nox4. Moreover, the impairment of contractility observed in diabetic rats was prevented in AS-but not S-treated animals. Exposure of cultured cardiac myocytes to 25 mM glucose [high glucose (HG)] increased NADPH oxidase activity, the expression of Nox4, and molecular markers of cardiac injury. These effects of HG were prevented in cells infected with adenoviral vector containing a dominant negative form of Nox4. This study provides strong evidence that Nox4 is an important source of ROS in the left ventricle and that Nox4-derived ROS contribute to cardiomyopathy at early stages of type 1 diabetes. © 2012 by the American Physiological Society.
dc.format.extent
dc.language English
dc.publisher BETHESDA
dc.relation.ispartof Publication Name: American Journal of Physiology - Cell Physiology; Publication Year: 2012; Volume: 302; no. 3;
dc.relation.ispartofseries
dc.relation.uri
dc.source Scopus
dc.subject.other
dc.title Nox4-derived reactive oxygen species mediate cardiomyocyte injury in early type 1 diabetes
dc.type Article
dc.contributor.affiliation Maalouf, R.M., Department of Medicine, University of Texas Health Science Center, San Antonio, TX, United States, Faculty of Natural and Applied Sciences, Notre Dame University, Louaize, Lebanon
dc.contributor.affiliation Eid, A.A., Department of Medicine, University of Texas Health Science Center, San Antonio, TX, United States, Department of Anatomy, Cell Biology and Physiology, Faculty of Medicine, American University of Beirut, Beirut, Lebanon
dc.contributor.affiliation Gorin, Y.C., Department of Medicine, University of Texas Health Science Center, San Antonio, TX, United States
dc.contributor.affiliation Block, K., Department of Medicine, University of Texas Health Science Center, San Antonio, TX, United States, South Texas Veterans Healthcare System, San Antonio, TX, United States
dc.contributor.affiliation Escobar, G.P., Department of Medicine, University of Texas Health Science Center, San Antonio, TX, United States
dc.contributor.affiliation Bailey, S., Department of Medicine, University of Texas Health Science Center, San Antonio, TX, United States
dc.contributor.affiliation Abboud, H.E., Department of Medicine, University of Texas Health Science Center, San Antonio, TX, United States, South Texas Veterans Healthcare System, San Antonio, TX, United States
dc.contributor.authorAddress Maalouf, R. M.; Department of Medicine, University of Texas Health Science Center, 7703 Floyd Curl Dr, San Antonio, TX 78229-3900, United States; email: rita.maalouf@ndu.edu.lb
dc.contributor.authorCorporate University: American University of Beirut Medical Center; Faculty: Faculty of Medicine; Department: Anatomy, Cell Biology and Physiological Sciences;
dc.contributor.authorDepartment Anatomy, Cell Biology and Physiological Sciences
dc.contributor.authorDivision
dc.contributor.authorEmail rita.maalouf@ndu.edu.lb
dc.contributor.authorFaculty Faculty of Medicine
dc.contributor.authorInitials Maalouf, RM
dc.contributor.authorInitials Eid, AA
dc.contributor.authorInitials Gorin, YC
dc.contributor.authorInitials Block, K
dc.contributor.authorInitials Escobar, GP
dc.contributor.authorInitials Bailey, S
dc.contributor.authorInitials Abboud, HE
dc.contributor.authorOrcidID
dc.contributor.authorReprintAddress Maalouf, RM (reprint author), Univ Texas Hlth Sci Ctr San Antonio, Dept Med, Div Cardiol, M1501,7703 Floyd Curl Dr, San Antonio, TX 78229 USA.
dc.contributor.authorResearcherID
dc.contributor.authorUniversity American University of Beirut Medical Center
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dc.description.citedCount 29
dc.description.citedTotWOSCount 32
dc.description.citedWOSCount 32
dc.format.extentCount
dc.identifier.articleNo
dc.identifier.coden AJPCD
dc.identifier.pubmedID 22031600
dc.identifier.scopusID 84856248012
dc.identifier.url
dc.publisher.address 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
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dc.relation.ispartofConferenceCode
dc.relation.ispartofConferenceDate
dc.relation.ispartofConferenceHosting
dc.relation.ispartofConferenceLoc
dc.relation.ispartofConferenceSponsor
dc.relation.ispartofConferenceTitle
dc.relation.ispartofFundingAgency
dc.relation.ispartOfISOAbbr Am. J. Physiol.-Cell Physiol.
dc.relation.ispartOfIssue 3
dc.relation.ispartOfPart
dc.relation.ispartofPubTitle American Journal of Physiology - Cell Physiology
dc.relation.ispartofPubTitleAbbr Am. J. Physiol. Cell Physiol.
dc.relation.ispartOfSpecialIssue
dc.relation.ispartOfSuppl
dc.relation.ispartOfVolume 302
dc.source.ID WOS:000299787300012
dc.type.publication Journal
dc.subject.otherAuthKeyword Cardiac injury
dc.subject.otherAuthKeyword NADPH oxidases
dc.subject.otherAuthKeyword Oxidative stress
dc.subject.otherChemCAS collagen, 9007-34-5
dc.subject.otherChemCAS fibronectin, 86088-83-7
dc.subject.otherChemCAS Actins
dc.subject.otherChemCAS Collagen, 9007-34-5
dc.subject.otherChemCAS Cybb protein, rat, 1.6.-
dc.subject.otherChemCAS Fibronectins
dc.subject.otherChemCAS Glucose, 50-99-7
dc.subject.otherChemCAS Membrane Glycoproteins
dc.subject.otherChemCAS NADH, NADPH Oxidoreductases, 1.6.-
dc.subject.otherChemCAS NADPH Oxidase, 1.6.3.1
dc.subject.otherChemCAS NADPH oxidase 1, 1.6.99.-
dc.subject.otherChemCAS Nox4 protein, rat, 1.6.-
dc.subject.otherChemCAS Oligonucleotides, Antisense
dc.subject.otherChemCAS Reactive Oxygen Species
dc.subject.otherChemCAS Ventricular Myosins, 3.6.1.-
dc.subject.otherIndex adenovirus vector
dc.subject.otherIndex alpha smooth muscle actin
dc.subject.otherIndex antisense oligonucleotide
dc.subject.otherIndex collagen
dc.subject.otherIndex fibronectin
dc.subject.otherIndex myosin heavy chain beta
dc.subject.otherIndex reactive oxygen metabolite
dc.subject.otherIndex reduced nicotinamide adenine dinucleotide phosphate oxidase 1
dc.subject.otherIndex reduced nicotinamide adenine dinucleotide phosphate oxidase 2
dc.subject.otherIndex reduced nicotinamide adenine dinucleotide phosphate oxidase 4
dc.subject.otherIndex animal experiment
dc.subject.otherIndex animal model
dc.subject.otherIndex article
dc.subject.otherIndex controlled study
dc.subject.otherIndex diabetic cardiomyopathy
dc.subject.otherIndex heart function
dc.subject.otherIndex heart left ventricle
dc.subject.otherIndex heart muscle fibrosis
dc.subject.otherIndex heart muscle injury
dc.subject.otherIndex heart ventricle hypertrophy
dc.subject.otherIndex in vitro study
dc.subject.otherIndex in vivo study
dc.subject.otherIndex insulin dependent diabetes mellitus
dc.subject.otherIndex male
dc.subject.otherIndex nonhuman
dc.subject.otherIndex oxidative stress
dc.subject.otherIndex priority journal
dc.subject.otherIndex protein expression
dc.subject.otherIndex rat
dc.subject.otherIndex upregulation
dc.subject.otherIndex Actins
dc.subject.otherIndex Animals
dc.subject.otherIndex Cells, Cultured
dc.subject.otherIndex Collagen
dc.subject.otherIndex Diabetes Mellitus, Experimental
dc.subject.otherIndex Diabetes Mellitus, Type 1
dc.subject.otherIndex Diabetic Cardiomyopathies
dc.subject.otherIndex Fibronectins
dc.subject.otherIndex Glucose
dc.subject.otherIndex Heart Ventricles
dc.subject.otherIndex Humans
dc.subject.otherIndex Male
dc.subject.otherIndex Membrane Glycoproteins
dc.subject.otherIndex Myocytes, Cardiac
dc.subject.otherIndex NADH, NADPH Oxidoreductases
dc.subject.otherIndex NADPH Oxidase
dc.subject.otherIndex Oligonucleotides, Antisense
dc.subject.otherIndex Oxidative Stress
dc.subject.otherIndex Rats
dc.subject.otherIndex Rats, Sprague-Dawley
dc.subject.otherIndex Reactive Oxygen Species
dc.subject.otherIndex Ventricular Myosins
dc.subject.otherIndex Animalia
dc.subject.otherIndex Rattus
dc.subject.otherKeywordPlus NADPH OXIDASE 4
dc.subject.otherKeywordPlus NAD(P)H OXIDASE
dc.subject.otherKeywordPlus MESANGIAL CELLS
dc.subject.otherKeywordPlus FAILING HEART
dc.subject.otherKeywordPlus NOX FAMILY
dc.subject.otherKeywordPlus EXPRESSION
dc.subject.otherKeywordPlus ACTIVATION
dc.subject.otherKeywordPlus APOPTOSIS
dc.subject.otherKeywordPlus REVEALS
dc.subject.otherKeywordPlus MYOFIBROBLASTS
dc.subject.otherWOS Cell Biology
dc.subject.otherWOS Physiology


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