Navegando por Palavras-chave "Sodium nitroprusside"

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    Estudos dos efeitos de concentrações crescentes de óxido nitrico no processo de morte por perda de adesão ao substrato (Anoikis): o papel desempenhado no processo pela proteína Src quinase
    (Universidade Federal de São Paulo (UNIFESP), 2017-05-30) Costa, Paulo Eduardo da [UNIFESP]; Monteiro, Hugo Pequeno [UNIFESP]; http://lattes.cnpq.br/6154759166234850; http://lattes.cnpq.br/2047870426131771; Universidade Federal de São Paulo (UNIFESP)
    The study of cell death induced by loss of adhesion (anoikis) is essential to understand how metastatic tumor cells may develop resistance to this type of cell death. Among a number of factors that can influence anoikis, nitric oxide has your role little known in relation to this issue. In adhered cells, it is known that nitric oxide induces cellular proliferation at low concentrations, as well as induces cell death after the treatment with high concentrations. However, in our study, we observed that detached cells behave in a different mode when treated with increase concentrations of NO: Low concentrations of NO induces drop on cell viability in detached HeLa cells, as well as increase levels of cleaved caspase-3. Since high concentrations of NO induces anoikis protection, with increase on cell viability, decreased of caspase-3 cleavage and decrase of expression of Bim protein. Src kinase has been shown to have key role in this mechanism, being phosphorylated and nitrosylated following treatment with high concentrations of NO. Inhibition of Src, can reverse this protection induced by high concentrations of NO with respect to cell viability and expression of Bim protein.These viability results were reproduced in Nex8H metastatic melanomas, but not in non metastatic melanomas Nex10C. In HeLa cells kept in suspension, NO in high concentrations induced cell disaggregation in a Src dependent manner. NO-dependent disaggregation can be reproduced in murine melanoma cells Nex8H and Nex10C. Increasing concentrations of NO decreased the effectiveness of reattachment of HeLa cells kept in suspension. Src kinase showed no role in the process. We know that tumor cells often produce high concentrations of NO. This study shows up as a first step in understanding how these cells can migrate from a primary to a secondary source and got to readhere regarding the role of increasing concentrations of NO in the process.
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    Protein tyrosine phosphatase alpha regulates cell detachment and cell death profiles induced by nitric oxide donors in the A(431) human carcinoma cell line
    (Maney Publishing, 2011-01-01) Costa, Paulo E. da [UNIFESP]; Batista, Wagner L. [UNIFESP]; Curcio, Marli F. [UNIFESP]; Moraes, Miriam S. [UNIFESP]; Borges, Roberta Eller [UNIFESP]; Nascimento, Patricia A. [UNIFESP]; Travassos, Luiz R. [UNIFESP]; Monteiro, Hugo P. [UNIFESP]; Universidade Federal de São Paulo (UNIFESP)
    We investigated the role of protein tyrosine phosphatase-alpha (PTP alpha) expression in the cell death profile of the A431 human carcinoma cell line that was induced by cytotoxic concentrations of the nitric oxide (NO) donors sodium nitroprusside (SNP) and 3,3-bis-(aminoethyl)-1-hydroxy-2-oxo-1-triazene (NOC-18). Both NO donors promoted extensive cell detachment in A431 parental cells as compared to the detachment observed for A431 cells that ectopically expressed PTP alpha (A431 (A27B(PTP alpha)) cells). the NO-induced cell death characteristics for both cell lines were examined. After incubation for 10 hours with 2.0 mM SNP, attached or detached A431 cells underwent apoptosis. Cells were highly positive for Annexin-V, featured increased cleavage of procaspase-8, activation of downstream caspase-3, and activation of poly-ADP-ribose polymerase 1 (PARP-1). in contrast, exposure of A431 (A27B(PTP alpha)) cells to 2.0 mM SNP produced an increase in the release of lactate dehydrogenase and enhanced incorporation of propidium iodide. in addition, A431 (A27B(PTP alpha)) cells showed partial inhibition of the activities of caspase-8, caspase-3, and PARP-1 upon detachment and cell death induced by SNP treatment. Results indicate that necrotic cell damage was induced, characterized by cellular swelling and lysis. We conclude from these results that PTP alpha regulates the A431 tumor cell death profile mediated by NO donors. Expression of PTP alpha or its absence may determine the occurrence of NO-induced cell death with necrotic or apoptotic features, respectively.