000070699 001__ 70699
000070699 005__ 20180522140725.0
000070699 0247_ $$2doi$$a10.1371/journal.pone.0032632
000070699 0248_ $$2sideral$$a76500
000070699 037__ $$aART-2012-76500
000070699 041__ $$aeng
000070699 100__ $$0(orcid)0000-0001-5193-7782$$aCalvo, A.C.
000070699 245__ $$aGenetic biomarkers for ALS disease in transgenic SOD1 G93A mice
000070699 260__ $$c2012
000070699 5060_ $$aAccess copy available to the general public$$fUnrestricted
000070699 5203_ $$aThe pathophysiological mechanisms of both familial and sporadic Amyotrophic Lateral Sclerosis (ALS) are unknown, although growing evidence suggests that skeletal muscle tissue is a primary target of ALS toxicity. Skeletal muscle biopsies were performed on transgenic SOD1G93A mice, a mouse model of ALS, to determine genetic biomarkers of disease longevity. Mice were anesthetized with isoflurane, and three biopsy samples were obtained per animal at the three main stages of the disease. Transcriptional expression levels of seventeen genes, Ankrd1, Calm1, Col19a1, Fbxo32, Gsr, Impa1, Mef2c, Mt2, Myf5, Myod1, Myog, Nnt, Nogo A, Pax7, Rrad, Sln and Snx10, were tested in each muscle biopsy sample. Total RNA was extracted using TRIzol Reagent according to the manufacturer's protocol, and variations in gene expression were assayed by real-time PCR for all of the samples. The Pearson correlation coefficient was used to determine the linear correlation between transcriptional expression levels throughout disease progression and longevity. Consistent with the results obtained from total skeletal muscle of transgenic SOD1G93A mice and 74-day-old denervated mice, five genes (Mef2c, Gsr, Col19a1, Calm1 and Snx10) could be considered potential genetic biomarkers of longevity in transgenic SOD1G93A mice. These results are important because they may lead to the exploration of previously unexamined tissues in the search for new disease biomarkers and even to the application of these findings in human studies.
000070699 536__ $$9info:eu-repo/grantAgreement/ES/ISCIII/EC08-00049$$9info:eu-repo/grantAgreement/ES/ISCIII/PI07-1283$$9info:eu-repo/grantAgreement/ES/ISCIII/PI10-01787
000070699 540__ $$9info:eu-repo/semantics/openAccess$$aby$$uhttp://creativecommons.org/licenses/by/3.0/es/
000070699 590__ $$a3.73$$b2012
000070699 591__ $$aMULTIDISCIPLINARY SCIENCES$$b7 / 57 = 0.123$$c2012$$dQ1$$eT1
000070699 655_4 $$ainfo:eu-repo/semantics/article$$vinfo:eu-repo/semantics/publishedVersion
000070699 700__ $$aManzano, R.
000070699 700__ $$aAtencia-Cibreiro, G.
000070699 700__ $$0(orcid)0000-0003-0156-4230$$aOliván, S.
000070699 700__ $$0(orcid)0000-0001-8301-6902$$aMuñoz, M.J.$$uUniversidad de Zaragoza
000070699 700__ $$0(orcid)0000-0001-5740-0185$$aZaragoza, P.$$uUniversidad de Zaragoza
000070699 700__ $$aCordero-Vázquez, P.
000070699 700__ $$aEsteban-Pérez, J.
000070699 700__ $$aGarcía-Redondo, A.
000070699 700__ $$0(orcid)0000-0001-5687-6704$$aOsta, R.$$uUniversidad de Zaragoza
000070699 7102_ $$11005$$2315$$aUniversidad de Zaragoza$$bDepartamento de Farmacología y Fisiología$$cFarmacología
000070699 7102_ $$11001$$2420$$aUniversidad de Zaragoza$$bDepartamento de Anatomía, Embriología y Genética Animal$$cGenética
000070699 773__ $$g7, 3 (2012), e32632 [10 pp]$$pPLoS One$$tPLoS One$$x1932-6203
000070699 8564_ $$s203599$$uhttp://zaguan.unizar.es/record/70699/files/texto_completo.pdf$$yVersión publicada
000070699 8564_ $$s127562$$uhttp://zaguan.unizar.es/record/70699/files/texto_completo.jpg?subformat=icon$$xicon$$yVersión publicada
000070699 909CO $$ooai:zaguan.unizar.es:70699$$particulos$$pdriver
000070699 951__ $$a2018-05-22-13:32:20
000070699 980__ $$aARTICLE