دورية أكاديمية

Middle-age abolishes cardioprotection conferred by thioredoxin-1 in mice.

التفاصيل البيبلوغرافية
العنوان: Middle-age abolishes cardioprotection conferred by thioredoxin-1 in mice.
المؤلفون: Perez, V.1 (AUTHOR), Zaobornyj, T.1,2 (AUTHOR), Vico, T.1,2 (AUTHOR), Vanasco, V.1,2 (AUTHOR), Marchini, T.1,2 (AUTHOR), Godoy, E.1 (AUTHOR), Alvarez, S.1,2 (AUTHOR), Evelson, P.1,2 (AUTHOR), Donato, M.1 (AUTHOR), Gelpi, R.J.1 (AUTHOR), D'Annunzio, V.1 (AUTHOR) vdannunzio@fmed.uba.ar
المصدر: Archives of Biochemistry & Biophysics. Mar2024, Vol. 753, pN.PAG-N.PAG. 1p.
مصطلحات موضوعية: *TRANSGENIC mice, *ISCHEMIC postconditioning, *MICE, *HYDROGEN peroxide, *MIDDLE age, *NITRATION
مستخلص: Thioredoxin-1 (Trx1) has cardioprotective effects on ischemia/reperfusion (I/R) injury, although its role in ischemic postconditioning (PostC) in middle-aged mice is not understood. This study aimed to evaluate if combining two cardioprotective strategies, such as Trx1 overexpression and PostC, could exert a synergistic effect in reducing infarct size in middle-aged mice. Young or middle-aged wild-type mice (Wt), transgenic mice overexpressing Trx1, and dominant negative (DN-Trx1) mutant of Trx1 mice were used. Mice hearts were subjected to I/R or PostC protocol. Infarct size, hydrogen peroxide (H 2 O 2) production, protein nitration, Trx1 activity, mitochondrial function, and Trx1, pAkt and pGSK3β expression were measured. PostC could not reduce infarct size even in the presence of Trx1 overexpression in middle-aged mice. This finding was accompanied by a lack of Akt and GSK3β phosphorylation, and Trx1 expression (in Wt group). Trx1 activity was diminished and H 2 O 2 production and protein nitration were increased in middle-age. The respiratory control rate dropped after I/R in Wt-Young and PostC restored this value, but not in middle-aged groups. Our results showed that Trx1 plays a key role in the PostC protection mechanism in young but not middle-aged mice, even in the presence of Trx1 overexpression. [Display omitted] • Postconditioning and Trx-1 overexpression cannot reduce infarction in middle age. • Postconditioning and Trx-1 overexpression trigger similar intracellular mechanisms. • In middle age, a redox imbalance takes place. [ABSTRACT FROM AUTHOR]
قاعدة البيانات: Academic Search Index
الوصف
تدمد:00039861
DOI:10.1016/j.abb.2023.109880