Navegando por Palavras-chave "endoplasmic reticulum"

Agora exibindo 1 - 4 de 4
  • Nenhuma Miniatura disponível
    Item
    Somente Metadadados
    Apoptotic effect of ethanol is potentiated by caffeine-induced calcium release in rat astrocytes
    (Elsevier B.V., 2006-01-30) Hirata, H.; Machado, L. S.; Okuno, C. S.; Brasolin, A.; Lopes, G. S.; Smaili, Soraya Soubhi [UNIFESP]; Universidade Federal de São Paulo (UNIFESP)
    In this study, we investigated agents that increased intracellular calcium levels and their correlation with apoptotic cell death induction. We used rat astrocytes to investigate the increase in cytosolic Ca2+, (Ca-c(2+)) and apoptosis induction by drugs that mobilize Ca2+ from different sources. We observed that thapsigargin (Thap), caffeine (Caff) and FCCP which caused similar increases in Ca-c(2+) levels (30-40%), also induced similar apoptotic rates (30-35%). On the other hand, antimycin (Anti), staurosporine (STS) and ethanol (Eth) promoted higher increases in Ca-c(2+) (55-65 %) and higher apoptotic rates (55-85%). Eth induced cell death in a concentration- and time-dependent manner. After treatment with Eth plus Caff for 6, 12 and 24 h, these effects were strongly potentiated. Results suggest that there might be a correlation between Ca-c(2+) increase and the rate of apoptosis. It is possible that Eth induces cell death by activation of more than one pathway and Ca-c(2+) might be one of the elements involved. the present work indicates that Ca-c(2+) can potentiate death by ethanol in rat astrocytes. (c) 2005 Elsevier Ireland Ltd. All rights reserved.
  • Nenhuma Miniatura disponível
    Item
    Somente Metadadados
    Bax affects intracellular Ca2+ stores and induces Ca2+ wave propagation
    (Nature Publishing Group, 2004-12-01) Carvalho, ACP; Sharpe, J.; Rosenstock, T. R.; Teles, AFV; Youle, R. J.; Smaili, Soraya Soubhi [UNIFESP]; Universidade Federal de São Paulo (UNIFESP); NINDS; Universidade de São Paulo (USP)
    In the present study, we evaluated proapoptotic protein Bax on mitochondria and Ca2+ homeostasis in primary cultured astrocytes. We found that recombinant Bax (rBax, 10 and 100 ng/ml) induces a loss in mitochondrial membrane potential (DeltaPsi(m)). This effect might be related to the inhibition of respiratory rates and a partial release of cytochrome c, which may change mitochondrial morphology. the loss of DeltaPsi(m) and a selective permeabilization of mitochondrial membranes contribute to the release of Ca2+ from the mitochondria. This was inhibited by cyclosporin A (5 muM) and Ruthenium Red (1 mug/ml), indicating the involvement of mitochondrial Ca2+ transport mechanisms. Bax-induced mitochondrial Ca2+ release evokes Ca2+ waves and wave propagation between cells. Our results show that Bax induces mitochondrial alteration that affects Ca2+ homeostasis and signaling. These changes show that Ca2+ signals might be correlated with the proapoptotic activities of Bax.
  • Imagem de Miniatura
    Item
    Acesso aberto (Open Access)
    Calcium and cell death signaling in neurodegeneration and aging
    (Academia Brasileira de Ciências, 2009-09-01) Smaili, Soraya Soubhi [UNIFESP]; Hirata, Hanako [UNIFESP]; Ureshino, Rodrigo Portes [UNIFESP]; Monteforte, Priscila T. [UNIFESP]; Morales, Ana P. [UNIFESP]; Muler, Mari Luminosa [UNIFESP]; Terashima, Juliana [UNIFESP]; Oseki, Karen Tubono [UNIFESP]; Rosenstock, Tatiana R. [UNIFESP]; Lopes, Guiomar Silva [UNIFESP]; Bincoletto, Claudia [UNIFESP]; Universidade Federal de São Paulo (UNIFESP)
    Transient increase in cytosolic (Cac2+) and mitochondrial Ca2+ (Ca m2+) are essential elements in the control of many physiological processes. However, sustained increases in Ca c2+ and Ca m2+ may contribute to oxidative stress and cell death. Several events are related to the increase in Ca m2+, including regulation and activation of a number of Ca2+ dependent enzymes, such as phospholipases, proteases and nucleases. Mitochondria and endoplasmic reticulum (ER) play pivotal roles in the maintenance of intracellular Ca2+ homeostasis and regulation of cell death. Several lines of evidence have shown that, in the presence of some apoptotic stimuli, the activation of mitochondrial processes maylead to the release of cytochrome c followed by the activation of caspases, nuclear fragmentation and apoptotic cell death. The aim of this review was to show how changes in calcium signaling can be related to the apoptotic cell death induction. Calcium homeostasis was also shown to be an important mechanism involved in neurodegenerative and aging processes.
  • Nenhuma Miniatura disponível
    Item
    Somente Metadadados
    Cell-Permeable Gomesin Peptide Promotes Cell Death by Intracellular Ca2+ Overload
    (Amer Chemical Soc, 2012-09-01) Paredes-Gamero, Edgar J. [UNIFESP]; Casaes-Rodrigues, Rafael L. [UNIFESP]; Moura, Gioconda E. D. D. [UNIFESP]; Domingues, Tatiana Moreira [UNIFESP]; Buri, Marcus V. [UNIFESP]; Ferreira, Victor H. C.; Trindade, Edvaldo S.; Moreno-Ortega, Ana J.; Cano-Abad, Maria F.; Nader, Helena B. [UNIFESP]; Ferreira, Alice T. [UNIFESP]; Miranda, Antonio [UNIFESP]; Justo, Giselle Z. [UNIFESP]; Tersariol, Ivarne L. S. [UNIFESP]; Universidade Federal de São Paulo (UNIFESP); Univ Fed Parana; Univ Autonoma Madrid; Univ Mogi das Cruzes
    In recent years, the antitumoral activity of antimicrobial peptides (AMPs) has been the goal of many research studies. Among AMPs, gomesin (Gm) displays antitumor activity by unknown mechanisms. Herein, we studied the cytotoxicity of Gm in the Chinese hamster ovary (CHO) cell line. Furthermore, we investigated the temporal ordering of organelle changes and the dynamics of Ca2+ signaling during Gm-induced cell death. the results indicated that Gm binds to the plasma membrane and rapidly translocates into the cytoplasm. Moreover, 20 mu M Gm increases the cytosolic Ca2+ and induces membrane permeabilization after 30 min of treatment. Direct Ca2+ measurements in CHO cells transfected with the genetically encoded D1-cameleon to the endoplasmic reticulum (ER) revealed that Gm induces ER Ca2+ depletion, which in turn resulted in oscillatory mitochondrial Ca2+ signal, as measured in cells expressing the genetically encoded probe to the mitochondrial matrix (mit)Pericam. This leads to mitochondria disruption, loss of mitochondrial membrane potential and increased reactive oxygen species prior to membrane permeabilization. Gm-induced membrane permeabilization by a Ca2+-dependent pathway involving Gm translocation into the cell, ER Ca2+ depletion and disruption, mitochondrial Ca2+ overload and oxidative stress.