Resveratrol Attenuates Copper-Induced Senescence by Improving Cellular Proteostasis

• Tipo: Artigo em Revista Científica Internacional
• Data: 2017

Autores

Matos, Liliana (Autor) FMDUP; Gouveia, Alexandra (Autor) FCNAUP; Almeida, H (Autor) Outra

Revista

Título: Oxidative Medicine and Cellular Longevity

Vol. 2 Nº 3

ISSN: 1942-0900

Editora: Hindawi

Indexação

ISI Web of Knowledge - 21 Citações

Scopus - 21 Citações

Outras Informações

ID Authenticus: P-00M-HFT

DOI: 10.1155/2017/3793817

Abstract (EN): Copper sulfate-induced premature senescence (CuSO4-SIPS) consistently mimetized molecular mechanisms of replicative senescence, particularly at the endoplasmic reticulum proteostasis level. In fact, disruption of protein homeostasis has been associated to age-related cell/ tissue dysfunction and human disorders susceptibility. Resveratrol is a polyphenolic compound with proved antiaging properties under particular conditions. In this setting, we aimed to evaluate resveratrol ability to attenuate cellular senescence induction and to unravel related molecular mechanisms. Using CuSO4-SIPS WI-38 fibroblasts, resveratrol is shown to attenuate typical senescence alterations on cell morphology, senescence-associated beta-galactosidase activity, and cell proliferation. The mechanisms implicated in this antisenescence effect seem to be independent of senescence-associated genes and proteins regulation but are reliant on cellular proteostasis improvement. In fact, resveratrol supplementation restores copperinduced increased protein content, attenuates BiP level, and reduces carbonylated and polyubiquitinated proteins by autophagy induction. Our data provide compelling evidence for the beneficial effects of resveratrol by mitigating CuSO4-SIPS stressful consequences by the modulation of protein quality control systems. These findings highlight the importance of a balanced cellular proteostasis and add further knowledge on molecular mechanisms mediating resveratrol antisenescence effects. Moreover, they contribute to identifying specific molecular targets whose modulation will prevent age-associated cell dysfunction and improve human healthspan.

Idioma: Inglês

Tipo (Avaliação Docente): Científica

Nº de páginas: 12