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Deregulated expression of A1, Bcl-2, Bcl-xL, and Mcl-1 antiapoptotic proteins and Bid, Bad, and Bax proapoptotic genes in polycythemia vera patients

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Elainy Patricia Lino Gasparotto ; Raquel Tognon ; Aline Fernanda Ferreira ; Gislane Lelis Vilela Oliveira ; Patrícia Vianna Bonini Palma ; Maria Aparecida Zanichelli ; Elizabeth Xisto Souto ; Carlos Eduardo Engel Velano ; Belinda Pinto Simões ; Rita de Cassia Viu Carrara ; Simone Kashima ; Dimas Tadeu Covas ; Fabíola Attie de Castro ; Ana Maria de Souza
Número total de Autores: 14
Tipo de documento: Artigo Científico
Fonte: Brazilian Journal of Pharmaceutical Sciences; v. 47, n. 4, p. -, Dez. 2011.
Resumo

Apoptosis deregulation might have a role in the pathophysiology of polycythemia vera (PV). This study evaluated Bcl-2 molecule expression in CD34+ cells and leukocytes in 12 PV patients. Gene expression was investigated by real time PCR using SybrGreen Quantitect kit and protein expression was evaluated by western-blotting. JAK2 V617F mutation was detected according to Baxter et al (2005). CD34+ cells from PV patients presented higher levels of A1 and Mcl-1 expression (median: 22.6 and 5.2, respectively) in comparison with controls (0.9 and 0.5, p=0.004 and p=0.020); while Bcl-2 and Bcl-xL expression decreased in PV patients (0.18 and 1.19) compared with controls (1.39 and 2.01, p=0.006 and p=0.020). CD34+ cells in PV patients showed an elevated Bid expression (14.4) in comparison with healthy subjects (1.0; p=0.002). Patients' leukocytes showed an A1 augmentation (7.41, p=0.001) and a reduced expression of Bax (0.19; p=0.040) and Bad (0.2; p=0.030). There was no correlation between JAK2 V617F allele burden and molecular expression. PV patients showed alterations in Bcl-2 members' expression, which may interfere with control of apoptotic machinery and contribute to disease pathogenesis. (AU)

Processo FAPESP: 06/50094-8 - Expressão de gênese de proteínas pró e antiapoptóticas em doenças mieloproliferativas crônicas
Beneficiário:Fabíola Attié de Castro
Linha de fomento: Auxílio à Pesquisa - Apoio a Jovens Pesquisadores