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

• Autor(a) principal: Gasparotto, Elainy Patricia Lino
• Data de Publicação: 2011
• Outros Autores: Tognon, Raquel, Ferreira, Aline Fernanda, Oliveira, Gislane Lelis Vilela, Palma, Patrícia Vianna Bonini, Zanichelli, Maria Aparecida, Souto, Elizabeth Xisto, Velano, Carlos Eduardo Engel, Simões, Belinda Pinto, Carrara, Rita de Cassia Viu, Kashima, Simone, Covas, Dimas Tadeu, Castro, Fabíola Attie de, Souza, Ana Maria de
• Tipo de documento: Artigo
• Idioma: eng
• Título da fonte: Brazilian Journal of Pharmaceutical Sciences
• Texto Completo: https://www.revistas.usp.br/bjps/article/view/10952
• topic: Policitemia vera; Mutação gênica; Expressão gênica; Apoptose; Membros da Família Bcl-2; Polycythemia vera; Gene mutation; Gene expression; Apoptosis; Bcl-2 family members

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.