Ishemia-Reperfusion Enhances Gapdh Nitration In Aging Skeletal Muscle

dc.contributor.utaustinauthorHammers, David W.en
dc.contributor.utaustinauthorFarrar, Rogeren
dc.creatorBailey, C. E.en
dc.creatorHammers, D. W.en
dc.creatorDeFord, J. H.en
dc.creatorDimayuga, V. L.en
dc.creatorAmaning, J. K.en
dc.creatorFarrar, R.en
dc.creatorPapaconstantinou, J.en
dc.date.accessioned2015-04-16T13:57:22Zen
dc.date.available2015-04-16T13:57:22Zen
dc.date.issued2011-10en
dc.description.abstractAging and skeletal muscle ischemia/reperfusion (I/R) injury leads to decreased contractile force generation that increases severely with age. Our studies show that glyceraldehyde-3-phosphate dehydrogenase (GAPDH) protein expression is significantly decreased at 3 and 5 days reperfusion in the young mouse muscle and at 1, 3, 5, and 7 days in the aged muscle. Using PCR, we have shown that GAPDH mRNA levels in young and old muscle increase at 5 days reperfusion compared to control, suggesting that the protein deficit is not transcriptional. Furthermore, while total tyrosine nitration did not increase in the young muscle, GAPDH nitration increased significantly at 1 and 3 days reperfusion. In contrast, total tyrosine nitration in aged muscle increased significantly at 1, 3, and 5 days of reperfusion, with increases in GAPDH nitration at the same time points. We conclude that GAPDH protein levels decrease following I/R, that this is not transcriptionally mediated, that the aged muscle experiences greater oxidative stress, protein modification and GAPDH degradation, possibly contributing to decreased muscle function. We propose that tyrosine nitration enhances GAPDH degradation following I/R and that the persistent decrease of GAPDH in aged muscle is due to the prolonged increase in oxidative modification in this age group.en
dc.description.departmentBiochemistryen
dc.identifier.citationC. Eric Bailey, David W. Hammers, James H. DeFord, Vincent L. Dimayuga, James K. Amaning, Roger Farrar, and John Papaconstantinou. AGING, Vol. 3 No 10, pp. 1003-1017; (Oct., 2011)en
dc.identifier.doien
dc.identifier.issn1945-4589en
dc.identifier.urihttp://hdl.handle.net/2152/29295en
dc.language.isoEnglishen
dc.relation.ispartofserialAging-Usen_US
dc.rightsAdministrative deposit of works to UT Digital Repository: This works author(s) is or was a University faculty member, student or staff member; this article is already available through open access or the publisher allows a PDF version of the article to be freely posted online. The library makes the deposit as a matter of fair use (for scholarly, educational, and research purposes), and to preserve the work and further secure public access to the works of the University.en
dc.subjectskeletal muscleen
dc.subjectgapdhen
dc.subjectnitrationen
dc.subjectischemia/reperfusionen
dc.subjectagingen
dc.subjectchaperone-mediated autophagyen
dc.subjectnitric-oxide synthaseen
dc.subjectglyceraldehyde-3-phosphate dehydrogenaseen
dc.subjectoxidative stressen
dc.subjectcell-deathen
dc.subject3-nitropropionic aciden
dc.subjectischemia-reperfusionen
dc.subjecttranslation arresten
dc.subjectprotein-synthesisen
dc.subjects-nitrosylationen
dc.subjectcell biologyen
dc.titleIshemia-Reperfusion Enhances Gapdh Nitration In Aging Skeletal Muscleen
dc.typeArticleen

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