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dc.contributor.CRUESPUniversidade Estadual de Campinaspt_BR
dc.typeArtigo de periódicopt_BR
dc.titleA role for focal adhesion kinase in cardiac mitochondrial biogenesis induced by mechanical stresspt_BR
dc.contributor.authorTornatore, TFpt_BR
dc.contributor.authorCosta, APpt_BR
dc.contributor.authorClemente, CFMZpt_BR
dc.contributor.authorJudice, Cpt_BR
dc.contributor.authorRocco, SApt_BR
dc.contributor.authorCalegari, VCpt_BR
dc.contributor.authorCardoso, Lpt_BR
dc.contributor.authorCardoso, ACpt_BR
dc.contributor.authorGoncalves, Apt_BR
dc.contributor.authorFranchini, KGpt_BR
unicamp.author.emailfranchin@unicamp.brpt_BR
unicamp.authorTornatore, Thais F. Dalla Costa, Ana Paula Clemente, Carolina F. M. Z. Judice, Carla Rocco, Silvana A. Calegari, Vivian C. Cardoso, Leandro Cardoso, Alisson C. Goncalves, Anderson, Jr. Franchini, Kleber G. Univ Estadual Campinas, Sch Med, Dept Internal Med, Sao Paulo, Brazilpt_BR
dc.subjectmechanical stresspt_BR
dc.subjectheartpt_BR
dc.subjectsignal transductionpt_BR
dc.subjectmitochondriapt_BR
dc.subjecthypertrophypt_BR
dc.subject.wosTranscriptional Coactivator Pgc-1-alphapt_BR
dc.subject.wosPressure-overloadpt_BR
dc.subject.wosOxidative Stresspt_BR
dc.subject.wosEarly Activationpt_BR
dc.subject.wosHeart-failurept_BR
dc.subject.wosRat-heartpt_BR
dc.subject.wosHypertrophypt_BR
dc.subject.wosMusclept_BR
dc.subject.wosMicept_BR
dc.subject.wosCardiomyopathypt_BR
dc.description.abstractTornatore TF, Dalla Costa AP, Clemente CF, Judice C, Rocco SA, Calegari VC, Cardoso L, Cardoso AC, Gon alves Jr A, Franchini KG. A role for focal adhesion kinase in cardiac mitochondrial biogenesis induced by mechanical stress. Am J Physiol Heart Circ Physiol 300: H902-H912, 2011. First published December 10, 2010; doi:10.1152/ajpheart.00319.2010.-We studied the implication of focal adhesion kinase (FAK) in cardiac mitochondrial biogenesis induced by mechanical stress. Prolonged stretching (2-12 h) of neonatal rat ventricular myocytes (NRVM) upregulated the main components of mitochondrial transcription cascade [peroxisome proliferator-activated receptor coactivator-1 (PGC-1 alpha), nuclear respiratory factor (NRF-1), and mitochondrial transcription factor A]. Concomitantly, prolonged stretching enhanced mitochondrial biogenesis [copy number of mitochondrial DNA (mtDNA), content of the subunit IV of cytochrome oxidase, and mitochondrial staining-green fluorescence intensity of Mitotracker green] and induced the hypertrophic growth (cell size and atrial natriuretic peptide transcripts) of NRVM. Furthermore, the stretching of NRVM enhanced phosphorylation, nuclear localization, and association of FAK with PGC-1 alpha. Recombinant FAK COOH-terminal, but not the NH(2)-terminal or kinase domain, precipitated PGC-1 alpha from nuclear extracts of NRVM. Depletion of FAK by RNA interference suppressed the upregulation of PGC-1 alpha and NRF-1 and markedly attenuated the enhanced mitochondrial biogenesis and hypertrophic growth of stretched NRVM. In the context of energy metabolism, FAK depletion became manifest by a reduction of ATP levels in stretched NRVM. Complementary studies in adult mice left ventricle demonstrated that pressure overload upregulated PGC-1 alpha, NRF-1, and mtDNA. In vivo FAK silencing transiently attenuated the upregulation of PGC-1 alpha, NRF-1, and mtDNA, as well as the left ventricular hypertrophy induced by pressure overload. In conclusion, activation of FAK signaling seems to be important for conferring enhanced mitochondrial biogenesis coupled to the hypertrophic growth of cardiomyocytes in response to mechanical stress, via control of mitochondrial transcription cascade.pt
dc.description.noteo TEXTO COMPLETO DESTE ARTIGO, ESTARÁ DISPONÍVEL À PARTIR DE AGOSTO DE 2015.pt
dc.relation.ispartofAmerican Journal Of Physiology-heart And Circulatory Physiologypt_BR
dc.relation.ispartofabbreviationAm. J. Physiol.-Heart Circul. Physiol.pt_BR
dc.publisher.cityBethesdapt_BR
dc.publisher.countryEUApt_BR
dc.publisherAmer Physiological Socpt_BR
dc.date.issued2011pt_BR
dc.date.monthofcirculationMARpt_BR
dc.identifier.citationAmerican Journal Of Physiology-heart And Circulatory Physiology. Amer Physiological Soc, v. 300, n. 3, n. H902, n. H912, 2011.pt_BR
dc.language.isoenpt_BR
dc.description.volume300pt_BR
dc.description.issuenumber3pt_BR
dc.description.firstpageH902pt_BR
dc.description.lastpageH912pt_BR
dc.rightsembargopt_BR
dc.sourceWeb of Sciencept_BR
dc.identifier.issn0363-6135pt_BR
dc.identifier.wosidWOS:000287914900023pt_BR
dc.identifier.doi10.1152/ajpheart.00319.2010pt_BR
dc.date.available2014-07-30T13:42:46Z
dc.date.available2015-11-26T17:28:29Z-
dc.date.accessioned2014-07-30T13:42:46Z
dc.date.accessioned2015-11-26T17:28:29Z-
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dc.identifier.urihttp://www.repositorio.unicamp.br/jspui/handle/REPOSIP/53712
dc.identifier.urihttp://repositorio.unicamp.br/jspui/handle/REPOSIP/53712-
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