Browsing by Author "Schalper Casanova, Kurt Alex"

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    Cell membrane permeabilization via connexin hemichannels in living and dying cells
    (2010) Sáez, Juan Carlos; Schalper Casanova, Kurt Alex; Orellana Roca, Juan Andrés; Shoji Sánchez, Kenji Fabricio
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    Connexin hemichannel composition determines the FGF-1-induced membrane permeability and free [Ca2+](i) responses
    (AMER SOC CELL BIOLOGY, 2008) Schalper Casanova, Kurt Alex; Palacios Prado, Nicolás; Retamal, Mauricio A.; Shoji Sánchez, Kenji Fabricio; Martinez, Agustin D.; Sáez, Juan Carlos
    Cell surface hemichannels (HCs) composed of different connexin (Cx) types are present in diverse cells and their possible role on FGF-1-induced cellular responses remains unknown. Here, we show that FGF-1 transiently (4-14 h, maximal at 7 h) increases the membrane permeability through HCs in HeLa cells expressing Cx43 or Cx45 under physiological extracellular Ca2+/Mg2+ concentrations. The effect does not occur in HeLa cells expressing HCs constituted of Cx26 or Cx43 with its C-terminus truncated at aa 257, or in parental nontransfected HeLa cells. The increase in membrane permeability is associated with a rise in HC levels at the cell surface and a proportional increase in HC unitary events. The response requires an early intracellular free Ca2+ concentration increase, activation of a p38 MAP kinase-dependent pathway, and a regulatory site of Cx subunit C-terminus. The FGF-1-induced rise in membrane permeability is also associated with a late increase in intracellular free Ca2+ concentration, suggesting that responsive HCs allow Ca2+ influx. The cell density of Cx26 and Cx43 HeLa transfectants cultured in serum-free medium was differentially affected by FGF-1. Thus, the FGF-1-induced cell permeabilization and derived consequences depend on the Cx composition of HCs.
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    Currently used methods for identification and characterization of hemichannels
    (2008) Schalper Casanova, Kurt Alex; Palacios Prado, Nicolás ; Orellana Roca, Juan Andrés; Sáez, Juan Carlos
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    Modulation of Brain Hemichannels and Gap Junction Channels by Pro-Inflammatory Agents and Their Possible Role in Neurodegeneration
    (Mary Ann Liebert, 2009) Orellana Roca, Juan Andrés; Sáez Pedraza, Pablo José; Shoji Sánchez, Kenji Fabricio; Schalper Casanova, Kurt Alex; Palacios Prado, Nicolás; Velarde Aliaga, María Victoria; Giaume, Christian; Bennett, Michael V. L.; Sáez, Juan Carlos
    In normal brain, neurons, astrocytes, and oligodendrocytes, the most abundant and active cells express pannexins and connexins, protein subunits of two families forming membrane channels. Most available evidence indicates that in mammals endogenously expressed pannexins form only hemichannels and connexins form both gap junction channels and hemichannels. Whereas gap junction channels connect the cytoplasm of contacting cells and coordinate electric and metabolic activity, hemichannels communicate the intra-and extracellular compartments and serve as a diffusional pathway for ions and small molecules. A subthreshold stimulation by acute pathological threatening conditions (e. g., global ischemia subthreshold for cell death) enhances neuronal Cx36 and glial Cx43 hemichannel activity, favoring ATP release and generation of preconditioning. If the stimulus is sufficiently deleterious, microglia become overactivated and release bioactive molecules that increase the activity of hemichannels and reduce gap junctional communication in astroglial networks, depriving neurons of astrocytic protective functions, and further reducing neuronal viability. Continuous glial activation triggered by low levels of anomalous proteins expressed in several neurodegenerative diseases induce glial hemichannel and gap junction channel disorders similar to those of acute inflammatory responses triggered by ischemia or infectious diseases. These changes are likely to occur in diverse cell types of the CNS and contribute to neurodegeneration during inflammatory process. Antiox. Redox Signal. 11, 369-399.