Smoking is associated with remodeling of gap junction in the rat heart: Smoker's paradox explanation?

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dc.contributor.authorNovo, Rosangela
dc.contributor.authorFreire, Cristiana M.
dc.contributor.authorFelisbino, Sergio
dc.contributor.authorMinicucci, Marcos F.
dc.contributor.authorAzevedo, Paula S.
dc.contributor.authorZornoff, Leonardo A. M.
dc.contributor.authorPaiva, Sergio A. R.
dc.contributor.institutionUniversidade Estadual Paulista (Unesp)
dc.date.accessioned2014-05-27T11:28:37Z
dc.date.available2014-05-27T11:28:37Z
dc.date.issued2013-03-01
dc.description.abstractBackground: In a previous study utilizing the rat model, exposure to tobacco smoke for 5 weeks increased survival after AMI, despite similar age and infarct size between the smokers and nonsmokers, and absence of reperfusion. Objective: Thus, this study aimed to analyze the effects of exposure to tobacco smoke on intensity, distribution or phosphorylation of connexin 43 in the rat heart. Methods: Wistar rats weighing 100 g were randomly allocated into 2 groups: 1) Control (n = 25); 2) Exposed to tobacco smoke (ETS), n = 23. After 5 weeks, left ventricular morphometric analysis, immunohisthochemistry and western blotting for connexin 43 (Cx43) were performed. Results: Collagen volume fraction, cross-sectional areas, and ventricular weight were not statistically different between control and ETS. ETS showed lower stain intensity of Cx43 at intercalated disks (Control: 2.32 ± 0.19; ETS: 1.73 ± 0.18; p = 0.04). The distribution of CX43 at intercalated disks did not differ between the groups (Control: 3.73 ± 0.12; ETS: 3.20 ± 0.17; p = 0.18). ETS rats showed higher levels of dephosphorylated form of Cx43 (Control: 0.45 ± 0.11; ETS: 0.90 ± 0.11; p = 0.03). On the other hand, total Cx43 did not differ between control and ETS groups (Control: 0.75 ± 0.19; ETS: 0.93 ± 0.27; p = 0.58). Conclusion: Exposure to tobacco smoke resulted in cardiac gap junction remodeling, characterized by alterations in the quantity and phosphorylation of the Cx43, in rats hearts. This finding could explain the smoker's paradox observed in some studies.en
dc.description.affiliationInstituto de Biociências de Botucatu, Botucatu, SP
dc.format.extent274-280
dc.identifierhttp://dx.doi.org/10.5935/abc.20130065
dc.identifier.citationArquivos Brasileiros de Cardiologia, v. 100, n. 3, p. 274-280, 2013.
dc.identifier.doi10.5935/abc.20130065
dc.identifier.file2-s2.0-84876559654.pdf
dc.identifier.issn0066-782X
dc.identifier.issn1678-4170
dc.identifier.scopus2-s2.0-84876559654
dc.identifier.urihttp://hdl.handle.net/11449/74774
dc.language.isoeng
dc.relation.ispartofArquivos Brasileiros de Cardiologia
dc.relation.ispartofjcr1.318
dc.rights.accessRightsAcesso aberto
dc.sourceScopus
dc.subjectArrhythmias,cardiac
dc.subjectRats
dc.subjectSmoke inhalation injury/mortality
dc.subjectSmoking/physiopathology
dc.subjectcarbon monoxide
dc.subjectcarboxyhemoglobin
dc.subjectcollagen
dc.subjectconnexin 43
dc.subjectnicotine
dc.subjecttar
dc.subjecttobacco smoke
dc.subjectanimal experiment
dc.subjectanimal model
dc.subjectanimal tissue
dc.subjectcontrolled study
dc.subjectenvironmental exposure
dc.subjectimmunohistochemistry
dc.subjectmale
dc.subjectmorphometrics
dc.subjectnonhuman
dc.subjectprotein dephosphorylation
dc.subjectprotein phosphorylation
dc.subjectrat
dc.subjectsmoking
dc.subjectvideodensitometry
dc.subjectWestern blotting
dc.titleSmoking is associated with remodeling of gap junction in the rat heart: Smoker's paradox explanation?en
dc.typeArtigo
dcterms.licensehttp://www.scielo.br/revistas/abc/iaboutj.htm
unesp.campusUniversidade Estadual Paulista (Unesp), Instituto de Biociências, Botucatupt

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