Periostin alters transcriptional profile in a rat model of isoproterenol-induced cardiotoxicity

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dc.contributor.authorSozmen, M.
dc.contributor.authorDevrim, A. K.
dc.contributor.authorKabak, Y. B.
dc.contributor.authorDevrim, T.
dc.date.accessioned2020-06-25T18:34:21Z
dc.date.available2020-06-25T18:34:21Z
dc.date.issued2019
dc.departmentKırıkkale Üniversitesi
dc.descriptionSozmen, Mahmut/0000-0001-7976-4051
dc.description.abstractPeriostin is an extracellular matrix protein from the fasciclin family that guides cellular trafficking and extracellular matrix organization. Periostin stimulates mature cardiomyocytes to reenter the cell cycle. The molecular mechanism behind such stimulation remains to be explored. A DNA microarray technology constituting 30,429 gene-level probe sets was utilized to investigate effects of recombinant murine periostin peptide on the gene expression pattern in a rat model of isoproterenol (ISO)-induced myocardial injury. The experiment was performed on 84 adult male Sprague-Dawley rats in four groups (n = 21): (1) control group, (2) only periostin applied group, (3) ISO cardiotoxicity group, and (4) ISO + periostin group. The experiment was continued for 28 days, and rats were killed on days 1, 7, and 28 (n = 7). Microarray analyses revealed that periostin significantly altered the expression of at least +/- 2-fold of 2474 genes in the ISO + periostin group compared to the ISO cardiotoxicity group of which 521 genes altered out of 30,429 gene-level probe sets. Ingenuity pathway analysis indicated that multiple pathway networks were affected by periostin, with predominant changes occurring in the expression of genes involved in oxidative phosphorylation, oxidative stress, fatty acid metabolism, and TNF-alpha NF-kappa B signaling pathways. These findings indicate that periostin alters gene expression profile in the ISO-induced myocardial injury and modulates local myocardial inflammation, possibly mitigating inflammation through TNF-alpha NF-kappa B signaling pathway along with a decreased Casp7 activity and apoptotic cell death.en_US
dc.description.sponsorshipOndokuz Mayis University Scientific Research and Development Support Program, Samsun [PYO.VET.1901.13]; Turkish Scientific Research Council (TUBITAK-TOVAG), Ankara, Turkey [114O734]en_US
dc.description.sponsorshipThe author(s) disclosed receipt of the following financial support for the research, authorship, and/or publication of this article: This project was financially supported by Ondokuz Mayis University Scientific Research and Development Support Program (Project No.: PYO.VET.1901.13), Samsun, and Turkish Scientific Research Council (TUBITAK-TOVAG; Project No.: 114O734), Ankara, Turkey.en_US
dc.identifier.citationSözmen M, Devrim A, Kabak Y, Devrim T. Periostin alters transcriptional profile in a rat model of isoproterenol-induced cardiotoxicity. Human & Experimental Toxicology. 2019;38(2):255-266.en_US
dc.identifier.doi10.1177/0960327118802617
dc.identifier.endpage266en_US
dc.identifier.issn0960-3271
dc.identifier.issn1477-0903
dc.identifier.issue2en_US
dc.identifier.pmid30303030
dc.identifier.scopus2-s2.0-85060145821
dc.identifier.scopusqualityQ2
dc.identifier.startpage255en_US
dc.identifier.urihttps://doi.org/10.1177/0960327118802617
dc.identifier.urihttps://hdl.handle.net/20.500.12587/7877
dc.identifier.volume38en_US
dc.identifier.wosWOS:000456381600010
dc.identifier.wosqualityQ4
dc.indekslendigikaynakWeb of Science
dc.indekslendigikaynakScopus
dc.indekslendigikaynakPubMed
dc.language.isoen
dc.publisherSage Publications Ltden_US
dc.relation.ispartofHuman & Experimental Toxicology
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanıen_US
dc.rightsinfo:eu-repo/semantics/openAccessen_US
dc.subjectCardiotoxicityen_US
dc.subjectgene expressionen_US
dc.subjectisoproterenolen_US
dc.subjectmicroarrayen_US
dc.subjectperiostinen_US
dc.subjectraten_US
dc.titlePeriostin alters transcriptional profile in a rat model of isoproterenol-induced cardiotoxicityen_US
dc.typeArticle

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