Mei-Yin Yeh

Tzu Hui Institute of Technology, P’ing-tung-chieh, Taiwan, Taiwan

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Publications (3)5.17 Total impact

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    ABSTRACT: The effect of capsaicin, a transient receptor potential vanniloid-1 (TRPV1) receptor agonist, on cytosolic free Ca2+ concentrations ([Ca2+]i) in Madin Darby canine kidney (MDCK) cells is unclear. This study explored whether capsaicin changed basal [Ca2+]i levels in suspended MDCK cells by using fura-2 as a Ca2+-sensitive fluorescent dye. Capsaicin at concentrations between 10–100 µM increased [Ca2+]i in a concentration-dependent manner. The Ca2+ signal was reduced by 80% by removing extracellular Ca2+. Capsacin induced Mn2+ influx, leading to quench of fura-2 fluorescence suggesting Ca2+ influx. This Ca2+ influx was inhibited by phospholipase A2 inhibitor aristolochic acid and the non-selective Ca2+ entry blocker La3+, but not by store-operated Ca2+ channel blockers nifedipine, econazole, and SK&F96365, and protein kinase C/A modulators. In Ca2+-free medium, pretreatment with the endoplasmic reticulum Ca2+ pump inhibitor thapsigargin abolished capsaicin-induced Ca2+ release. Conversely, pretreatment with capsaicin partly reduced thapsigargin-induced [Ca2+]i rise. Inhibition of phospholipase C with U73122 did not alter capsaicin-induced [Ca2+]i rise. The TRPV1 receptor antagonist capsazepine also induced significant Ca2+ entry and Ca2+ release. Collectively, in MDCK cells, capsaicin induced [Ca2+]i rises by causing phospholipase C-independent Ca2+ release from the endoplasmic reticulum and Ca2+ influx via phospholipase A2-regulated, La3+-sensitive Ca2+ channels in a manner dissociated from stimulation of TRPV1 receptors. Drug Dev Res, 2009. © 2009 Wiley-Liss, Inc.
    Drug Development Research 09/2009; 71(2):112 - 119. · 0.87 Impact Factor
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    ABSTRACT: Cadmium (Cd2+) is an industrial and environmental metal. The effect of Cd2+ on intracellular free-Ca2+ levels ([Ca2+](i)) and viability in Madin Darby canine kidney cells was explored. Cd2+increased [Ca2+](i) in a concentration-dependent manner with an EC50 of 85 microM. Cd2+-induced Mn2+ entry demonstrated Ca2+ influx. Removal of extracellular Ca2+ decreased the [Ca2+](i) signal by 60%. The [Ca2+](i) signal was inhibited by La3+ but not by L-type Ca2+ channel blockers. In Ca2+-free medium, Cd2+-induced [Ca2+]i signal was abolished by pre-treatment with 1 microM thapsigargin (an endoplasmic reticulum Ca2+pump inhibitor) and 2 microM carbonylcyanide m-chlorophenylhydrazone (CCCP; a mitochondrial uncoupler). Cd2+-induced Ca2+ release was not altered by inhibition of phospholipase C. At concentrations between 10 and 100 microM, Cd2+killed cells in a concentration-dependent manner. The cytotoxic effect of 100 microM Cd2+was reversed by pre-chelating cytosolic Ca2+with BAPTA. Cd2+-induced apoptosis was demonstrated by propidium iodide. Collectively, this study shows that Cd2+ induced a [Ca2+](i) increase in Madin Darby canine kidney cells via evoking Ca2+ entry through non-selective Ca2+ channels, and releasing stored Ca2+ from endoplasmic reticulum and mitochondria in a phospholipase C-independent manner.
    Basic & Clinical Pharmacology & Toxicology 06/2009; 104(5):345-51. · 2.18 Impact Factor
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    ABSTRACT: The effect of the endogenous cannabinoid anandamide on cytosolic free Ca(2+) concentration ([Ca(2+)](i)) and proliferation is largely unknown. This study examined whether anandamide altered Ca(2+) levels and caused Ca(2+)-dependent cell death in Madin-Darby canine kidney (MDCK) cells. [Ca(2+)](i) and cell death were measured using the fluorescent dyes fura-2 and WST-1 respectively. Anandamide at concentrations above 5 muM increased [Ca(2+)](i) in a concentration-dependent manner. The Ca(2+) signal was reduced by 78% by removing extracellular Ca(2+). The anandamide-induced Ca(2+) influx was insensitive to L-type Ca(2+) channel blockers and the cannabinoid receptor antagonist AM 251, but was inhibited differently by aristolochic acid, WIN 55,212-2 (a cannabinoid receptor agonist), phorbol ester, GF 109203X and forskolin. After pretreatment with thapsigargin (an endoplasmic reticulum Ca(2+) pump inhibitor), anandamide-induced Ca(2+) release was inhibited. Inhibition of phospholipase C with U73122 did not change anandamide-induced Ca(2+) release. At concentrations of 100 muM and 200 muM, anandamide killed 50% and 95% cells, respectively. The cytotoxic effect of 100 muM anandamide was completely reversed by pre-chelating cytosolic Ca(2+) with BAPTA. Collectively, in MDCK cells, anandamide induced [Ca(2+)](i) rises by causing Ca(2+) release from endoplasmic reticulum and Ca(2+) influx from extracellular space. Furthermore, anandamide can cause Ca(2+)-dependent cytotoxicity in a concentration-dependent manner.
    Basic &amp Clinical Pharmacology &amp Toxicology 05/2006; 98(4):416-22. · 2.12 Impact Factor