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Aging-associated changes in oxidative stress, cell proliferation, and apoptosis are prevented in the prostate of transgenic rats overexpressing regucalcin

dc.contributor.authorVaz, Cátia
dc.contributor.authorMarques, Ricardo
dc.contributor.authorBaptista, Cláudio
dc.contributor.authorSocorro, Sílvia
dc.date.accessioned2019-12-04T17:28:24Z
dc.date.available2019-12-04T17:28:24Z
dc.date.issued2015-12
dc.description.abstractRegucalcin (RGN) is a calcium (Ca(2+))-binding protein that displays a characteristic downregulated expression with aging in several tissues. Besides its role in regulating intracellular Ca(2+) homeostasis, RGN has been associated with the control of oxidative stress, cell proliferation, and apoptosis. Thus, the diminished expression of RGN with aging may contribute to the age-associated deterioration of cell function. In the present study, we hypothesized that the maintenance of high expression levels of RGN may prevent age-related alterations in the processes mentioned previously. First, we confirmed that RGN expression is significantly diminished in the prostate of 8-, 9-, 12-, and 24-months wild-type rats. Then, the effect of aging on lipid peroxidation, antioxidant defenses, cell proliferation, and apoptosis in the prostate of wild-type controls and transgenic rats overexpressing RGN (Tg-RGN) was investigated. The activity of glutathione and the antioxidant capacity were increased in Tg-RGN rats in response to the age-associated increase in thiobarbituric acid reactive substances levels, an effect not seen in wild type. Overexpression of RGN also counteracted the effect of aging increasing prostate cell proliferation. In contrast to wild-type animals, the prostate weight of Tg-RGN did not change with aging and was underpinned by the diminished expression of stem cell factor and c-kit, and increased expression of p53. In addition, aged Tg-RGN animals displayed increased expression (activity) of apoptosis regulators, therefore not showing the age-induced resistance to apoptosis observed in wild type. Altogether, these findings indicate the protective role of RGN against the development of age-related pathologies, such as, for example, prostate cancer.pt_PT
dc.description.versioninfo:eu-repo/semantics/publishedVersionpt_PT
dc.identifier.doi10.1016/j.trsl.2015.08.009pt_PT
dc.identifier.urihttp://hdl.handle.net/10400.6/7667
dc.language.isoengpt_PT
dc.peerreviewedyespt_PT
dc.relationROLE OF REGUCALCIN IN BREAST CELLS PROLIFERATION AND TUMOR DEVELOPMENT
dc.subjectAgingpt_PT
dc.subjectProstate cancerpt_PT
dc.subjectRegucalcinpt_PT
dc.titleAging-associated changes in oxidative stress, cell proliferation, and apoptosis are prevented in the prostate of transgenic rats overexpressing regucalcinpt_PT
dc.typejournal article
dspace.entity.typePublication
oaire.awardTitleROLE OF REGUCALCIN IN BREAST CELLS PROLIFERATION AND TUMOR DEVELOPMENT
oaire.awardURIinfo:eu-repo/grantAgreement/FCT/5876/PEst-OE%2FSAU%2FUI0709%2F2014/PT
oaire.awardURIinfo:eu-repo/grantAgreement/FCT//SFRH%2FBD%2F70316%2F2010/PT
oaire.awardURIinfo:eu-repo/grantAgreement/FCT/SFRH/SFRH%2FBD%2F66875%2F2009/PT
oaire.citation.endPage705pt_PT
oaire.citation.issue6pt_PT
oaire.citation.startPage693pt_PT
oaire.citation.titleTranslational Research, The Journal of Laboratory and Clinical Medicinept_PT
oaire.citation.volume166pt_PT
oaire.fundingStream5876
oaire.fundingStreamSFRH
person.familyNameVaz
person.familyNameMaia Baptista
person.familyNameSocorro
person.givenNameCátia
person.givenNameCláudio Jorge
person.givenNameSílvia Cristina da Cruz Marques
person.identifierhttps://scholar.google.pt/citations?user=hFKOd_QAAAAJ&hl=pt-PT&oi=ao
person.identifierhttps://scholar.google.pt/citations?user=PA3L_h8AAAAJ&hl=pt-PT
person.identifier.ciencia-id1C1D-F91F-D937
person.identifier.ciencia-id5115-FCBD-A31F
person.identifier.ciencia-idAB17-5C25-1F2C
person.identifier.orcid0000-0002-7720-4234
person.identifier.orcid0000-0002-5658-5445
person.identifier.orcid0000-0001-8181-488X
person.identifier.scopus-author-id23097426600
person.identifier.scopus-author-id23097994600
project.funder.identifierhttp://doi.org/10.13039/501100001871
project.funder.identifierhttp://doi.org/10.13039/501100001871
project.funder.identifierhttp://doi.org/10.13039/501100001871
project.funder.nameFundação para a Ciência e a Tecnologia
project.funder.nameFundação para a Ciência e a Tecnologia
project.funder.nameFundação para a Ciência e a Tecnologia
rcaap.embargofctCopyright cedido à editora no momento da publicação.pt_PT
rcaap.rightsclosedAccesspt_PT
rcaap.typearticlept_PT
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