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dc.contributor.authorYang, Dongyan
dc.contributor.authorZhang, Lei
dc.contributor.authorZhang, Zhisheng
dc.contributor.authorHu, Sulei
dc.contributor.authorFu, Yanbo
dc.contributor.authorLaukkanen, Jari
dc.contributor.authorLi, Gang
dc.date.accessioned2019-02-22T13:02:24Z
dc.date.available2019-08-29T21:35:41Z
dc.date.issued2019
dc.identifier.citationYang, D., Zhang, L., Zhang, Z., Hu, S., Fu, Y., Laukkanen, J., & Li, G. (2019). Silencing of C3G increases cardiomyocyte survival inhibition and apoptosis via regulation of p-ERK1/2 and Bax. <i>Clinical and Experimental Pharmacology and Physiology</i>, <i>46</i>(3), 237-245. <a href="https://doi.org/10.1111/1440-1681.13027" target="_blank">https://doi.org/10.1111/1440-1681.13027</a>
dc.identifier.otherCONVID_28234335
dc.identifier.otherTUTKAID_78658
dc.identifier.urihttps://jyx.jyu.fi/handle/123456789/62936
dc.description.abstractExperimental studies have shown that overexpression of Rap guanine nucleotide exchange factor 1 (C3G) plays pro‐survival and anti‐apoptotic roles through molecule phosphorylated extracellular signal‐regulated kinase1/2 (p‐ERK1/2) in cardiomyocytes. However, it is still unclear if silencing of C3G may increase cell survival inhibition and apoptosis in cardiomyocytes, and whether C3G silence induced injuries are reduced by the overexpression of C3G through regulation of p‐ERK1/2 and pro‐apoptotic molecule Bax. In this study, the rat‐derived H9C2 cardiomyocytes were infected with C3G small hairpin RNA interference recombinant lentiviruses, which silenced the endogenous C3G expression in the cardiomyocytes. Then, contrary experiments were conducted using C3G overexpression. The cell proliferation and apoptosis were analyzed in the cardiomyocytes which were treated with or without hypoxia/reoxygenation (H/R). Silencing of C3G leaded to significant increase in cell survival inhibition and apoptosis, combined with aggravated the injuries induced by H/R. Overexpression of C3G reduced the injuries induced by the silencing of C3G in the cardiomyocytes via regulation of p‐ERK1/2 and Bax. In conclusion, our results provide new experimental evidence that silencing of C3G can increase cell survival inhibition and apoptosis in cardiomyocytes via regulation of p‐ERK1/2 and Bax.fi
dc.format.mimetypeapplication/pdf
dc.language.isoeng
dc.publisherWiley-Blackwell
dc.relation.ispartofseriesClinical and Experimental Pharmacology and Physiology
dc.rightsIn Copyright
dc.subject.otherBax
dc.subject.otherH9C2 cell line
dc.subject.otherRap guanine nucleotide exchange factor 1
dc.subject.otherapoptosis
dc.subject.othercardiac myocyte
dc.subject.otherp-ERK1/2
dc.titleSilencing of C3G increases cardiomyocyte survival inhibition and apoptosis via regulation of p-ERK1/2 and Bax
dc.typearticle
dc.identifier.urnURN:NBN:fi:jyu-201902211616
dc.contributor.laitosLiikuntatieteellinen tiedekuntafi
dc.contributor.laitosFaculty of Sport and Health Sciencesen
dc.type.urihttp://purl.org/eprint/type/JournalArticle
dc.date.updated2019-02-21T13:15:08Z
dc.type.coarhttp://purl.org/coar/resource_type/c_2df8fbb1
dc.description.reviewstatuspeerReviewed
dc.format.pagerange237-245
dc.relation.issn0305-1870
dc.relation.numberinseries3
dc.relation.volume46
dc.type.versionacceptedVersion
dc.rights.copyright© 2018 John Wiley & Sons Australia, Ltd
dc.rights.accesslevelopenAccessfi
dc.subject.ysoohjelmoitunut solukuolema
dc.subject.ysoproteiinit
dc.subject.ysosydän
dc.subject.ysolihassolut
dc.subject.ysohenkiinjääminen
dc.format.contentfulltext
jyx.subject.urihttp://www.yso.fi/onto/yso/p6280
jyx.subject.urihttp://www.yso.fi/onto/yso/p4332
jyx.subject.urihttp://www.yso.fi/onto/yso/p16731
jyx.subject.urihttp://www.yso.fi/onto/yso/p25540
jyx.subject.urihttp://www.yso.fi/onto/yso/p14692
dc.rights.urlhttp://rightsstatements.org/page/InC/1.0/?language=en
dc.relation.doi10.1111/1440-1681.13027
dc.type.okmA1


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