Literature DB >> 19328800

Ca2+-dependent K+ efflux regulates deoxycholate-induced apoptosis of BHK-21 and Caco-2 cells.

Andrea Gerbino1, Marianna Ranieri, Stefania Lupo, Rosa Caroppo, Lucantonio Debellis, Isabella Maiellaro, Mariano F Caratozzolo, Francesco Lopez, Matilde Colella.   

Abstract

BACKGROUND & AIMS: Deoxycholate (DC) has proapoptotic and tumorigenic effects in different cell types of the gastrointestinal tract. Exposure of BHK-21 (stromal) cells to DC induces Ca(2+) entry at the plasma membrane, which affects intracellular Ca(2+) signaling. We assessed whether DC-induced increases in [Ca(2+)] can impinge on plasma membrane properties (eg, ionic conductances) involved in cell apoptosis.
METHODS: Single- and double-barreled microelectrodes were used to measure membrane potential (V(m)) and extracellular [K(+)] in BHK-21 fibroblasts and Caco-2 colon carcinoma cells. Apoptosis was assessed by Hoechst labeling, propidium iodide staining, and caspase-3 and caspase-7 assays.
RESULTS: DC-induced cell membrane hyperpolarization was directly measured with intracellular microelectrodes in both cell lines. Diverse Ca(2+) mobilizing agents, such as membrane receptor agonists, an inhibitor of the sarco/endoplasmic reticulum Ca(2+) adenosine triphosphatase and a Ca(2+) ionophore, also induced increases in V(m). Removal of extracellular Ca(2+) reduced the agonist- and DC-induced membrane hyperpolarization by approximately 15% and 60%, respectively. These findings indicate a prominent role for Ca(2+) entry at the plasma membrane in the action of this bile salt. Blockade of Ca(2+)-activated K(+) conductances by charybdotoxin and apamin reduced DC-induced hyperpolarization by 75% and 64% in BHK-21 and Caco-2 cells, respectively. These inhibitors also reduced the DC-induced increase in extracellular [K(+)] by 75% and cell apoptosis by approximately 50% in both cell lines.
CONCLUSIONS: Ca(2+)-dependent K(+) conductance is an important regulator of DC-induced apoptosis in stromal and colon cancer cells.

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Year:  2009        PMID: 19328800     DOI: 10.1053/j.gastro.2009.03.038

Source DB:  PubMed          Journal:  Gastroenterology        ISSN: 0016-5085            Impact factor:   22.682


  4 in total

1.  Deoxycholic acid mediates non-canonical EGFR-MAPK activation through the induction of calcium signaling in colon cancer cells.

Authors:  Sara M Centuori; Cecil J Gomes; Jesse Trujillo; Jamie Borg; Joshua Brownlee; Charles W Putnam; Jesse D Martinez
Journal:  Biochim Biophys Acta       Date:  2016-04-13

2.  Contributions of bile acids to gastrointestinal physiology as receptor agonists and modifiers of ion channels.

Authors:  Stephen J Keely; Andreacarola Urso; Alexandr V Ilyaskin; Christoph Korbmacher; Nigel W Bunnett; Daniel P Poole; Simona E Carbone
Journal:  Am J Physiol Gastrointest Liver Physiol       Date:  2021-11-10       Impact factor: 4.052

3.  The Na+/H+ exchanger controls deoxycholic acid-induced apoptosis by a H+-activated, Na+-dependent ionic shift in esophageal cells.

Authors:  Aaron Goldman; HwuDauRw Chen; Mohammad R Khan; Heather Roesly; Kimberly A Hill; Mohammad Shahidullah; Amritlal Mandal; Nicholas A Delamere; Katerina Dvorak
Journal:  PLoS One       Date:  2011-08-22       Impact factor: 3.240

4.  Activation of the Calcium-Sensing Receptor Corrects the Impaired Mitochondrial Energy Status Observed in Renal Polycystin-1 Knockdown Cells Modeling Autosomal Dominant Polycystic Kidney Disease.

Authors:  Annarita Di Mise; Marianna Ranieri; Mariangela Centrone; Maria Venneri; Grazia Tamma; Daniela Valenti; Giovanna Valenti
Journal:  Front Mol Biosci       Date:  2018-08-24
  4 in total

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