NADPH oxidase hyperactivity induces plantaris atrophy in heart failure rats

Página do item simplificado
dc.contributorSistema FMUSP-HC: Faculdade de Medicina da Universidade de São Paulo (FMUSP) e Hospital das Clínicas da FMUSP
dc.contributor.authorBECHARA, Luiz R. G.
dc.contributor.authorMOREIRA, Jose B. N.
dc.contributor.authorJANNIG, Paulo R.
dc.contributor.authorVOLTARELLI, Vanessa A.
dc.contributor.authorDOURADO, Paulo M.
dc.contributor.authorVASCONCELOS, Andrea R.
dc.contributor.authorSCAVONE, Cristoforo
dc.contributor.authorRAMIRES, Paulo R.
dc.contributor.authorBRUM, Patricia C.
dc.date.accessioned2015-02-06T19:51:49Z
dc.date.available2015-02-06T19:51:49Z
dc.date.issued2014
dc.description.abstractBackground: Skeletal muscle wasting is associated with poor prognosis and increased mortality in heart failure (HF) patients. Glycolytic muscles are more susceptible to catabolic wasting than oxidative ones. This is particularly important in HF since glycolytic muscle wasting is associated with increased levels of reactive oxygen species (ROS). However, the main ROS sources involved in muscle redox imbalance in HF have not been characterized. Therefore, we hypothesized that NADPH oxidases would be hyperactivated in the plantaris muscle of infarcted rats, contributing to oxidative stress and hyperactivation of the ubiquitin-proteasome system(UPS), ultimately leading to atrophy. Methods: Rats were submitted to myocardial infarction (MI) or Sham surgery. Four weeks after surgery, MI and Sham groups underwent eight weeks of treatment with apocynin, a NADPH oxidase inhibitor, or placebo. NADPH oxidase activity, oxidative stress markers, NF-kappa B activity, p38 MAPK phosphorylation, mRNA and sarcolemmal protein levels of NADPH oxidase components, UPS activation and fiber cross-sectional area were assessed in the plantaris muscle. Results: The plantaris of MI rats displayed atrophy associated with increased Nox2 mRNA and sarcolemmal protein levels, NADPH oxidase activity, ROS production, lipid hydroperoxides levels, NF-kappa B activity, p38 MAPK phosphorylation and UPS activation. NADPH oxidase inhibition by apocynin prevented MI-induced skeletal muscle atrophy by reducing ROS production, NF-kappa B hyperactivation, p38 MAPK phosphorylation and proteasomal hyperactivity. Conclusion: Our data provide evidence for NADPH oxidase hyperactivation as an important source of ROS production leading to plantaris atrophy in heart failure rats, suggesting that this enzyme complex plays key role in skeletal muscle wasting in HF.
dc.description.indexMEDLINE
dc.description.sponsorshipFundacao de Amparo a Pesquisa do Estado de Sao Paulo, Brazil (FAPESP) [2008/57252-3]
dc.description.sponsorshipFAPESP [2010/50048-1]
dc.description.sponsorshipConselho Nacional de Pesquisa e Desenvolvimento (CNPq) [302201/2011-44]
dc.identifier.citationINTERNATIONAL JOURNAL OF CARDIOLOGY, v.175, n.3, p.499-507, 2014
dc.identifier.doi10.1016/j.ijcard.2014.06.046
dc.identifier.eissn1874-1754
dc.identifier.issn0167-5273
dc.identifier.urihttps://observatorio.fm.usp.br/handle/OPI/8730
dc.language.isoeng
dc.publisherELSEVIER IRELAND LTD
dc.relation.ispartofInternational Journal of Cardiology
dc.rightsrestrictedAccess
dc.rights.holderCopyright ELSEVIER IRELAND LTD
dc.subjectHeart failure
dc.subjectSkeletal muscle
dc.subjectOxidative stress
dc.subjectNADPH oxidase
dc.subjectAtrophy
dc.subject.otherkappa-b activation
dc.subject.otherskeletal-muscle
dc.subject.othernitric-oxide
dc.subject.othersympathetic hyperactivity
dc.subject.otheroxidative stress
dc.subject.otherexpression
dc.subject.otherapocynin
dc.subject.otherdysfunction
dc.subject.otherinhibitors
dc.subject.otherantioxidant
dc.subject.wosCardiac & Cardiovascular Systems
dc.titleNADPH oxidase hyperactivity induces plantaris atrophy in heart failure rats
dc.typearticle
dc.type.categoryoriginal article
dc.type.versionpublishedVersion
dspace.entity.typePublication
hcfmusp.affiliation.countryNoruega
hcfmusp.affiliation.countryisono
hcfmusp.author.externalBECHARA, Luiz R. G.:Univ Sao Paulo, Escola Educ Fis & Esporte, BR-05508900 Sao Paulo, Brazil
hcfmusp.author.externalMOREIRA, Jose B. N.:Univ Sao Paulo, Escola Educ Fis & Esporte, BR-05508900 Sao Paulo, Brazil; Norwegian Univ Sci & Technol NTNU, KG Jebsen Ctr Exercise Med, Trondheim, Norway
hcfmusp.author.externalJANNIG, Paulo R.:Univ Sao Paulo, Escola Educ Fis & Esporte, BR-05508900 Sao Paulo, Brazil
hcfmusp.author.externalVOLTARELLI, Vanessa A.:Univ Sao Paulo, Escola Educ Fis & Esporte, BR-05508900 Sao Paulo, Brazil
hcfmusp.author.externalVASCONCELOS, Andrea R.:Univ Sao Paulo, Inst Biomed Sci, Dept Pharmacol, BR-05508900 Sao Paulo, Brazil
hcfmusp.author.externalSCAVONE, Cristoforo:Univ Sao Paulo, Inst Biomed Sci, Dept Pharmacol, BR-05508900 Sao Paulo, Brazil
hcfmusp.author.externalRAMIRES, Paulo R.:Univ Sao Paulo, Escola Educ Fis & Esporte, BR-05508900 Sao Paulo, Brazil
hcfmusp.author.externalBRUM, Patricia C.:Univ Sao Paulo, Escola Educ Fis & Esporte, BR-05508900 Sao Paulo, Brazil
hcfmusp.citation.scopus54
hcfmusp.contributor.author-fmusphcPAULO MAGNO MARTINS DOURADO
hcfmusp.description.beginpage499
hcfmusp.description.endpage507
hcfmusp.description.issue3
hcfmusp.description.volume175
hcfmusp.origemWOS
hcfmusp.origem.scopus2-s2.0-84905081157
hcfmusp.origem.wosWOS:000340251600021
hcfmusp.publisher.cityCLARE
hcfmusp.publisher.countryIRELAND
hcfmusp.relation.referenceAl Ghouleh I, 2011, FREE RADICAL BIO MED, V51, P1271, DOI 10.1016/j.freeradbiomed.2011.06.011
hcfmusp.relation.referenceAltenhofer S, 2014, ANTIOXID RE IN PRESS
hcfmusp.relation.referenceBacurau AVN, 2009, J APPL PHYSIOL, V106, P1631, DOI 10.1152/japplphysiol.91067.2008
hcfmusp.relation.referenceBarbieri SS, 2004, FREE RADICAL BIO MED, V37, P156, DOI 10.1016/j.freeradbiomed.2004.04.020
hcfmusp.relation.referenceBaumer AT, 2007, CLIN EXP HYPERTENS, V29, P287, DOI 10.1080/10641960701500398
hcfmusp.relation.referenceBedard K, 2007, PHYSIOL REV, V87, P245, DOI 10.1152/physrev.00044.2005
hcfmusp.relation.referenceBrown DI, 2009, FREE RADICAL BIO MED, V47, P1239, DOI 10.1016/j.freeradbiomed.2009.07.023
hcfmusp.relation.referenceBrum PC, 2014, EXP PHYSIOL, V99, P616, DOI 10.1113/expphysiol.2013.076844
hcfmusp.relation.referenceBrum PC, 2011, BRAZ J MED BIOL RES, V44, P827, DOI 10.1590/S0100-879X2011000900002
hcfmusp.relation.referenceCampos JC, 2012, PLOS ONE, V7, DOI 10.1371/journal.pone.0052764
hcfmusp.relation.referenceChen YR, 2014, CIRC RES, V114, P524, DOI 10.1161/CIRCRESAHA.114.300559
hcfmusp.relation.referenceCheng GJ, 2001, GENE, V269, P131, DOI 10.1016/S0378-1119(01)00449-8
hcfmusp.relation.referenceCoirault C, 2007, AM J PHYSIOL-HEART C, V292, pH1009, DOI 10.1152/ajpheart.00438.2006
hcfmusp.relation.referenceCunha TF, 2012, PLOS ONE, V7, DOI 10.1371/journal.pone.0041701
hcfmusp.relation.referenceDahlman JM, 2012, METHODS MOL BIOL, V798, P505, DOI 10.1007/978-1-61779-343-1_30
hcfmusp.relation.referenceFulster S, 2013, EUR HEART J, V34, P512, DOI 10.1093/eurheartj/ehs381
hcfmusp.relation.referenceGeng TY, 2011, AM J PATHOL, V178, P1738, DOI 10.1016/j.ajpath.2011.01.005
hcfmusp.relation.referenceGielen S, 2012, CIRCULATION, V125, P2716, DOI 10.1161/CIRCULATIONAHA.111.047381
hcfmusp.relation.referenceGielen S, 2003, J AM COLL CARDIOL, V42, P861, DOI 10.1016/S0735-1097(03)00848-9
hcfmusp.relation.referenceHayashi T, 2005, DIABETES OBES METAB, V7, P334, DOI 10.1111/j.1463-1326.2004.00393.x
hcfmusp.relation.referenceHERMESLIMA M, 1995, FREE RADICAL BIO MED, V19, P271, DOI 10.1016/0891-5849(95)00020-X
hcfmusp.relation.referenceHeumuller S, 2008, HYPERTENSION, V51, P211, DOI 10.1161/HYPERTENSIONAHA.107.100214
hcfmusp.relation.referenceJannig PR, 2014, PLOS ONE, V9, DOI 10.1371/journal.pone.0085820
hcfmusp.relation.referenceJaquet V, 2009, ANTIOXID REDOX SIGN, V11, P2535, DOI 10.1089/ARS.2009.2585
hcfmusp.relation.referenceKriegenburg F, 2011, ANTIOXID REDOX SIGN, V15, P2265, DOI 10.1089/ars.2010.3590
hcfmusp.relation.referenceLaurindo FRM, 2002, METHOD ENZYMOL, V352, P432
hcfmusp.relation.referenceLi P, 2007, AM J PATHOL, V170, P599, DOI 10.2353/ajpath.2007.060505
hcfmusp.relation.referenceLi YP, 2003, AM J PHYSIOL-CELL PH, V285, pC806, DOI 10.1152/ajpcell.00129.2003
hcfmusp.relation.referenceLi YP, 1998, FASEB J, V12, P871
hcfmusp.relation.referenceLiberman M, 2008, ARTERIOSCL THROM VAS, V28, P463, DOI 10.1161/ATVBAHA.107.156745
hcfmusp.relation.referenceLinke A, 2005, CIRCULATION, V111, P1763, DOI 10.1161/01.CIR.0000165503.08661.E5
hcfmusp.relation.referenceLiu Y, 2010, MOL CELL BIOCHEM, V343, P143, DOI 10.1007/s11010-010-0508-4
hcfmusp.relation.referenceMarin-Garcia J, 2001, CARDIOVASC RES, V52, P103, DOI 10.1016/S0008-6363(01)00368-6
hcfmusp.relation.referenceMatsushima S, 2009, AM J PHYSIOL-HEART C, V297, pH409, DOI 10.1152/ajpheart.01332.2008
hcfmusp.relation.referenceMoreira JBN, 2013, J APPL PHYSIOL, V114, P1029, DOI 10.1152/japplphysiol.00760.2012
hcfmusp.relation.referenceOelze M, 2011, J VASC RES, V48, P275, DOI 10.1159/000320627
hcfmusp.relation.referenceOhta Y, 2011, AM J PHYSIOL-HEART C, V300, pH1637, DOI 10.1152/ajpheart.01185.2009
hcfmusp.relation.referencePechanova O, 2009, PHARMACOL REP, V61, P116
hcfmusp.relation.referencePowers SK, 2010, EXP PHYSIOL, V95, P1, DOI 10.1113/expphysiol.2009.050526
hcfmusp.relation.referenceSchulze PC, 2003, BASIC RES CARDIOL, V98, P267, DOI 10.1007/s00395-003-0411-1
hcfmusp.relation.referenceSemprun-Prieto LC, 2011, BIOCHEM BIOPH RES CO, V409, P217, DOI 10.1016/j.bbrc.2011.04.122
hcfmusp.relation.referenceSimonyi Agnes, 2012, Front Biosci (Elite Ed), V4, P2183
hcfmusp.relation.referenceSolomon V, 1996, J BIOL CHEM, V271, P26690
hcfmusp.relation.referenceTEICHHOLZ LE, 1976, AM J CARDIOL, V37, P7, DOI 10.1016/0002-9149(76)90491-4
hcfmusp.relation.referenceTrueblood NA, 2005, AM J PHYSIOL-HEART C, V288, pH244, DOI 10.1152/ajpheart.00042.2004
hcfmusp.relation.referenceWhitehead NP, 2010, PLOS ONE, V5, DOI 10.1371/journal.pone.0015354
hcfmusp.relation.referenceWilliams HC, 2007, J CARDIOVASC PHARM, V50, P9, DOI 10.1097/FJC.0b013e318063e820
hcfmusp.relation.referenceWyke SM, 2004, BRIT J CANCER, V91, P1742, DOI 10.1038/sj.bjc.6602165
hcfmusp.relation.referenceYu Z, 2008, PLOS ONE, V3, DOI 10.1371/journal.pone.0002086
hcfmusp.scopus.lastupdate2024-05-10
relation.isAuthorOfPublicationf228a0bc-d589-45c3-a297-3f75f333599c
relation.isAuthorOfPublication.latestForDiscoveryf228a0bc-d589-45c3-a297-3f75f333599c
Arquivos
Pacote Original
Agora exibindo 1 - 1 de 1
Nenhuma Miniatura disponível
Nome:
art_BECHARA_NADPH_oxidase_hyperactivity_induces_plantaris_atrophy_in_heart_2014.PDF
Tamanho:
1.12 MB
Formato:
Adobe Portable Document Format
Descrição:
publishedVersion (English)
Baixar
Coleções
Artigos e Materiais de Revistas Científicas - HC/InCor