Please use this identifier to cite or link to this item: https://repositorio.unifesp.br/handle/11600/31083
Title: Thioredoxin-1 promotes survival in cells exposed to S-nitrosoglutathione: Correlation with reduction of intracellular levels of nitrosothiols and up-regulation of the ERK1/2 MAP Kinases
Authors: Arai, Roberto J. [UNIFESP]
Ogata, Fernando T. [UNIFESP]
Batista, Wagner L. [UNIFESP]
Masutani, Hiroshi
Yodoi, Junji
Debbas, Victor [UNIFESP]
Augusto, Ohara
Stern, Arnold
Monteiro, Hugo P. [UNIFESP]
Universidade Federal de São Paulo (UNIFESP)
Kyoto Univ
Universidade de São Paulo (USP)
NYU
Keywords: Thioredoxin
Nitrosothiol
Nitric oxide
Nitrotyrosine
p21Ras
ERK1/2 MAP kinases
Issue Date: 1-Dec-2008
Publisher: Elsevier B.V.
Citation: Toxicology and Applied Pharmacology. San Diego: Academic Press Inc Elsevier Science, v. 233, n. 2, p. 227-237, 2008.
Abstract: Accumulating evidence indicates that post-translational protein modifications by nitric oxide and its derived species are critical effectors of redox signaling in cells. These protein modifications are most likely controlled by intracellular reductants. Among them, the importance of the 12 kDa dithiol protein thioredoxin-1 (TRX-1) has been increasingly recognized. However, the effects of TRX-1 in cells exposed to exogenous nitrosothiols remain little understood. We investigated the levels of intracellular nitrosothiols and survival signaling in HeLa cells over-expressing TRX-1 and exposed to S-nitrosoglutahione (GSNO). A role for TRX-1 expression on GSNO catabolism and cell viability was demonstrated by the concentration-dependent effects of GSNO on decreasing TRX-1 expression, activation of capase-3, and increasing cell death. the over-expressaion of TRX-1 in HeLa cells partially attenuated caspase-3 activation and enhanced cell viability upon GSNO treatment. This was correlated with reduction of intracellular levels of nitrosothiols and increasing levels of nitrite and nitrotyrosine. the involvement of ERK, p38 and JNK pathways were investigated in parental cells treated with GSNO. Activation of ERK1/2 MAP kinases was shown to be critical for survival signaling. lit cells over-expressing TRX-1, basal phosphorylation levels of ERK1/2 MAP kinases were higher and further increased after GSNO treatment. These results indicate that the enhanced cell viability promoted by TRX-1 correlates with its capacity to regulate the levels of intracellular nitiosothiols and to up-regulate the survival signaling pathway mediated by the ERK1/2 MAP kinases.
URI: http://repositorio.unifesp.br/handle/11600/31083
ISSN: 0041-008X
Other Identifiers: http://dx.doi.org/10.1016/j.taap.2008.07.023
Appears in Collections:Em verificação - Geral

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