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dc.contributor.authorRoginska Dorota
dc.contributor.authorKawa Milosz P
dc.contributor.authorPius-Sadowska Ewa
dc.contributor.authorLejkowska Renata
dc.contributor.authorLuczkowska Karolina
dc.contributor.authorWiszniewska Barbara
dc.contributor.authorKaarniranta Kai
dc.contributor.authorPaterno Jussi J
dc.contributor.authorSchmidt Christian A
dc.contributor.authorMachalinski Boguslaw
dc.contributor.authorMachalinska Anna
dc.date.accessioned2017-12-18T12:56:53Z
dc.date.available2017-12-18T12:56:53Z
dc.date.issued2017
dc.identifier.urihttps://erepo.uef.fi/handle/123456789/5098
dc.description.abstractThe aim of the study was to investigate the influence of complement component C3 global depletion on the biological structure and function of the aged retina. In vivo morphology (OCT), electrophysiological function (ERG), and the expression of selected oxidative stress-, apoptosis-, and autophagy-related proteins were assessed in retinas of 12-month-old C3-deficient and WT mice. Moreover, global gene expression in retinas was analyzed by RNA arrays. We found that the absence of active C3 was associated with (1) alleviation of the age-dependent decrease in retinal thickness and gradual deterioration of retinal bioelectrical function, (2) significantly higher levels of antioxidant enzymes (catalase and glutathione reductase) and the antiapoptotic survivin and Mcl-1/Bak dimer, (3) lower expression of the cellular oxidative stress marker—4HNE—and decreased activity of proapoptotic caspase-3, (4) ameliorated retinal autophagic activity with localization of ubiquitinated protein conjugates commonly along the retinal pigment epithelium (RPE) layer, and (5) significantly increased expression of several gene sets associated with maintenance of the physiological functions of the neural retina. Our findings shed light on mechanisms of age-related retinal alterations by identifying C3 as a potential therapeutic target for retinal aging.en
dc.language.isoENen
dc.publisherHindawi Limiteden
dc.relation.ispartofseriesOxidative Medicine and Cellular Longevityen
dc.relation.urihttp://dx.doi.org/10.1155/2017/5306790en
dc.rightsCC BY http://creativecommons.org/licenses/by/4.0/en
dc.titleDepletion of the Third Complement Component Ameliorates Age-Dependent Oxidative Stress and Positively Modulates Autophagic Activity in Aged Retinas in a Mouse Modelen
dc.description.versionpublished versionen
dc.contributor.departmentSchool of Medicine / Clinical Medicineen
uef.solecris.id49139791en
dc.type.publicationinfo:eu-repo/semantics/articleen
dc.rights.accessrights© Authorsen
dc.relation.doi10.1155/2017/5306790en
dc.description.reviewstatuspeerRevieweden
dc.relation.articlenumber5306790en
dc.relation.issn1942-0900en
dc.relation.volume2017en
dc.rights.accesslevelopenAccessen
dc.type.okmA1en
dc.type.versioninfo:eu-repo/semantics/publishedVersionen
uef.solecris.openaccessOpen access -julkaisukanavassa ilmestynyt julkaisu


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