Browsing by Author "Ramirez, Marco A."

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    Escherichia coli Heat-Stable Enterotoxin Mediates Na+/H+ Exchanger 4 Inhibition Involving cAMP in T-84 Human Intestinal Epithelial Cells
    (2015) Beltrán, Ana R.; Carraro Lacroix, Luciene R.; Bezerra, Camila N. A.; Cornejo, Marcelo; Norambuena, Katrina; Toledo, Fernando; Araos, Joaquín; Pardo, Fabián; Leiva Mendoza, Andrea Alejandra; Sanhueza, Carlos; Malnic, Gerhard; Sobrevía Luarte, Luis Alberto; Ramirez, Marco A.
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    Functional Link Between Adenosine and Insulin: A Hypothesis for Fetoplacental Vascular Endothelial Dysfunction in Gestational Diabetes
    (BENTHAM SCIENCE PUBL LTD, 2011) Guzman Gutierrez, Enrique; Abarzua, Fernando; Belmar, Cristian; Nien, Jyh K.; Ramirez, Marco A.; Arroyo, Pablo; Salomon, Carlos; Westermeier, Francisco; Puebla, Carlos; Leiva, Andrea; Casanello, Paola; Sobrevia, Luis
    Gestational diabetes mellitus (GDM) is a syndrome compromising the health of the mother and the fetus. Endothelial damage and reduced metabolism of the vasodilator adenosine occur and fetal hyperinsulinemia associated with deficient insulin response and a metabolic rather than mitogenic phenotype is characteristic of this pathology. These phenomena lead to endothelial dysfunction of the fetoplacental unit. Major databases were searched for the relevant literature in the field. Special attention was placed on publications related with diabetes and hormone/metabolic disorders. We aimed to summarize the information regarding insulin sensitivity changes in GDM and the role of adenosine in this phenomenon. Evidence supporting the possibility that fetal endothelial dysfunction involves a functional link between adenosine and insulin signaling in the fetal endothelium from GDM pregnancies is summarized. Since insulin acts via membrane receptors type A (preferentially associated with mitogenic responses) or type B (preferentially associated with metabolic responses), a differential activation of these receptors in this syndrome is proposed.
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    Potential Role of Sodium-Proton Exchangers in the Low Concentration Arsenic Trioxide-Increased Intracellular pH and Cell Proliferation
    (PUBLIC LIBRARY SCIENCE, 2012) Aravena, Carmen; Beltran, Ana R.; Cornejo, Marcelo; Torres, Viviana; Diaz, Emilce S.; Guzman Gutierrez, Enrique; Pardo, Fabian; Leiva, Andrea; Sobrevia, Luis; Ramirez, Marco A.
    Arsenic main inorganic compound is arsenic trioxide (ATO) presented in solution mainly as arsenite. ATO increases intracellular pH (pHi), cell proliferation and tumor growth. Sodium-proton exchangers (NHEs) modulate the pHi, with NHE1 playing significant roles. Whether ATO-increased cell proliferation results from altered NHEs expression and activity is unknown. We hypothesize that ATO increases cell proliferation by altering pHi due to increased NHEs-like transport activity. Madin-Darby canine kidney (MDCK) cells grown in 5 mmol/L D-glucose-containing DMEM were exposed to ATO (0.05, 0.5 or 5 mu mol/L, 0-48 hours) in the absence or presence of 5-N, N-hexamethylene amiloride (HMA, 5-100 mu mol/L, NHEs inhibitor), PD-98059 (30 mu mol/L, MAPK1/2 inhibitor), Go6976 (10 mu mol/L, PKC alpha, beta I and mu inhibitor), or Schering 28080 (10 mu mol/L, H+/K(+)ATPase inhibitor) plus concanamycin (0.1 mu mol/L, V type ATPases inhibitor). Incorporation of [H-3]thymidine was used to estimate cell proliferation, and counting cells with a hemocytometer to determine the cell number. The pHi was measured by fluorometry in 2,7-bicarboxyethyl-5,6-carboxyfluorescein loaded cells. The Na+-dependent HMA-sensitive NHEs-like mediated proton transport kinetics, NHE1 protein abundance in the total, cytoplasm and plasma membrane protein fractions, and phosphorylated and total p42/44 mitogen-activated protein kinases (p42/44(mapk)) were also determined. Lowest ATO (0.05 mu mol/L, similar to 0.01 ppm) used in this study increased cell proliferation, pHi, NHEs-like transport and plasma membrane NHE1 protein abundance, effects blocked by HMA, PD-98059 or Go6976. Cell-buffering capacity did not change by ATO. The results show that a low ATO concentration increases MDCK cells proliferation by NHEs (probably NHE1)-like transport dependent-increased pHi requiring p42/44(mapk) and PKC alpha, beta I and/or mu activity. This finding could be crucial in diseases where uncontrolled cell growth occurs, such as tumor growth, and in circumstances where ATO, likely arsenite, is available at the drinking-water at these levels. Citation: Aravena C, Beltran AR, Cornejo M, Torres V, Diaz ES, et al. (2012) Potential Role of Sodium-Proton Exchangers in the Low Concentration Arsenic Trioxide-Increased Intracellular pH and Cell Proliferation. PLoS ONE 7(12): e51451. doi:10.1371/journal.pone.0051451
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    Sodium/proton exchanger isoform 1 regulates intracellular pH and cell proliferation in human ovarian cancer
    (2017) Sanhueza, Carlos; Araos, Joaquín; Naranjo, Luciano; Toledo, Fernando; Beltrán, Ana R.; Ramirez, Marco A.; Gutiérrez, Jaime; Pardo, Fabián; Leiva Mendoza, Andrea Alejandra; Sobrevía Luarte, Luis Alberto