p66Shc signaling is involved in stress responses elicited by anthracycline treatment of rat cardiomyoblasts

Archives of Toxicology
Susana F SampaioPaulo J Oliveira

Abstract

The adaptor protein p66Shc modulates cellular redox status integrating oxidative stress with mitochondrial stress responses. Upon oxidative stress, p66Shc is translocated to mitochondria or mitochondria-associated membranes in a multi-step process, resulting in locally increased reactive oxygen species production. This signaling pathway is believed to be important in the context of drug-induced organ toxicity. The use of anthracyclines as anticancer agents is limited due to a dose-dependent and cumulative toxicity resulting in cardiomyopathy. Treatment with the anthracycline doxorubicin (DOX) results in a dose-dependent and cumulative cardiotoxicity which is mediated, at least in part, by increased oxidative stress. In the present study, we investigated for the first time whether p66Shc signaling is activated during DOX treatment of the rat cardiomyoblast H9c2 cell line. We further tested whether the transcriptional factor FoxO3a, which activates target genes responsible for apoptosis and cell cycle arrest, is also involved in p66Shc-dependent redox signaling pathway. Our results suggest that DOX treatment induces p66Shc protein up-regulation specifically in nuclear fractions. Increased nuclear expression of FoxO3a was also det...Continue Reading

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Citations

Feb 19, 2020·Archives of Toxicology·Jan G HengstlerJorrit J Hornberg
Jun 6, 2019·Basic Research in Cardiology·Kerstin BoenglerRainer Schulz
Aug 28, 2020·Frontiers in Pharmacology·Concetta IsideLucia Altucci
Dec 31, 2019·Oxidative Medicine and Cellular Longevity·Yan-Zhao WuChen Xiong
Mar 28, 2020·Circulation Research·Kendall B WallacePaulo J Oliveira
May 1, 2021·Journal of Fungi·Kseniia A PalkinaNadezhda M Markina
Nov 2, 2021·Journal of Biochemical and Molecular Toxicology·Huaping ZhangHui Zhou

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