Endothelin-induced calcium signaling in cultured mouse microglial cells is mediated through ETB receptors
Thomas Möller, Oliver Kann, Marco Prinz, Frank Kirchhoff, Alexei Verkhratsky, Helmut Kettenmann
Abstract
Thomas Möller, Oliver Kann, Marco Prinz, Frank Kirchhoff, Alexei Verkhratsky, Helmut Kettenmann
Abstract
Microglial cells are the intrinsic immunocompetent cells of the central nervous system, which are activated by brain tissue damage. In this paper we investigated the ability of endothelins (ETs), which are potent vasoconstrictors, to induce intracellular calcium signals in cultured microglia cells. Both endothelin-1 and endothelin-3 increased intracellular Ca2+ concentration ([Ca2+]i). These [Ca2+]i transients were mimicked by BQ3020, an ETB receptor agonist and blocked by BQ788, a selective ETB antagonist, respectively. The calcium signals induced by the endothelins persisted in Ca(2+)-free media. Transcripts encoding the ETB receptor were detected in purified microglial cultures and cDNA fragments derived from ETB receptor mRNA were amplified from 9% of electrophysiologically characterized microglial cells by the use of single-cell RT-PCR.
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Microglial cells are the intrinsic immunocompetent cells of the central nervous system, which are activated by brain tissue damage. In this paper we investigated the ability of endothelins (ETs), which are potent vasoconstrictors, to induce intracellular calcium signals in cultured microglia cells. Both endothelin-1 and endothelin-3 increased intracellular Ca2+ concentration ([Ca2+]i). These [Ca2+]i transients were mimicked by BQ3020, an ETB receptor agonist and blocked by BQ788, a selective ETB antagonist, respectively. The calcium signals induced by the endothelins persisted in Ca(2+)-free media. Transcripts encoding the ETB receptor were detected in purified microglial cultures and cDNA fragments derived from ETB receptor mRNA were amplified from 9% of electrophysiologically characterized microglial cells by the use of single-cell RT-PCR.
Key concepts: Endothelins, Endothelin receptor, Agonist, Receptor, Endothelin 3, Fura-2, Endocrinology, Biology