000046952 001__ 46952
000046952 005__ 20210121114452.0
000046952 0247_ $$2doi$$a10.14814/phy2.12626
000046952 0248_ $$2sideral$$a93349
000046952 037__ $$aART-2015-93349
000046952 041__ $$aeng
000046952 100__ $$aMartín-Pardillos, A
000046952 245__ $$aEffects of donor age and proliferative aging on the phenotype stability of rat aortic smooth muscle cells
000046952 260__ $$c2015
000046952 5060_ $$aAccess copy available to the general public$$fUnrestricted
000046952 5203_ $$aAge-related effects of the vascular wall have been associated with several hemodynamic dysfunctions, including medial vascular calcification. Vascular aging has been traditionally addressed using proliferative senescence of vascu- lar smooth muscle cells (VSMC) in vitro, which induces osteoblastic transition and favors calcification in vitro. In this work, we have analyzed the relation- ship between organismal aging and proliferative senescence by comparing the proliferative aging of VSMC obtained from young, mature, and old rats (2-, 12-, and 24-month cell lines [CL], respectively). VSMC proliferated to more than 100 cumulative population doublings (CPD) without evidence of prolif- erative senescence, most likely as a consequence of telomerase induction. The apoptosis rate increased with CPD in all three CL, but the oxidation status of the cells was not modified. The magnitude of all gene expression changes caused by CPD was higher than the magnitude of the changes caused by donor age: the expressions of VSMC markers a-actin and SM22a decreased, while the expressions of transcription factors Msx2 and Runx2 and of bone morphogenetic protein-2 increased. Treatment of the cells with 2 mmol/L Pi revealed that the intensity of the effect of CPD on calcium deposition was greater than the effect of donor age. In conclusion, the proliferative lifespan of VSMC magnifies the effect of donor age on the osteoblastic transition of VSMC, therefore suggesting that in vivo vascular aging changes can be less dramatic than what is shown by in vitro aging.
000046952 536__ $$9info:eu-repo/grantAgreement/ES/DGA/B42$$9info:eu-repo/grantAgreement/ES/MINECO/SAF2012-33898
000046952 540__ $$9info:eu-repo/semantics/openAccess$$aby$$uhttp://creativecommons.org/licenses/by/3.0/es/
000046952 592__ $$a0.826$$b2015
000046952 593__ $$aPhysiology (medical)$$c2015$$dQ2
000046952 593__ $$aPhysiology$$c2015$$dQ3
000046952 655_4 $$ainfo:eu-repo/semantics/article$$vinfo:eu-repo/semantics/publishedVersion
000046952 700__ $$0(orcid)0000-0003-3457-323X$$aSorribas Alejaldre, Victor$$uUniversidad de Zaragoza
000046952 7102_ $$11000$$2807$$aUniversidad de Zaragoza$$bDpto. Anat.Pat.Med.Leg.For.To.$$cArea Toxicología
000046952 773__ $$g3, 11 (2015), e12626$$pPhysiol. reports$$tPhysiological Reports$$x2051-817X
000046952 8564_ $$s7128029$$uhttps://zaguan.unizar.es/record/46952/files/texto_completo.pdf$$yVersión publicada
000046952 8564_ $$s86133$$uhttps://zaguan.unizar.es/record/46952/files/texto_completo.jpg?subformat=icon$$xicon$$yVersión publicada
000046952 909CO $$ooai:zaguan.unizar.es:46952$$particulos$$pdriver
000046952 951__ $$a2021-01-21-10:46:42
000046952 980__ $$aARTICLE