Article abstract
Nature Cell Biology 3, 121 - 127 (2001)
Published online: 10 January 2001 | doi:10.1038/35055019
Lack of an endothelial store-operated Ca2+ current impairs agonist-dependent vasorelaxation in TRP4-/- mice
Marc Freichel1,
Suk Hyo Suh2,
Alexander Pfeifer3,
Ulli Schweig1,
Claudia Trost1,
Petra Wei
gerber1,
Martin Biel3,
Stephan Philipp1,
Doris Freise1,
Guy Droogmans2,
Franz Hofmann3,
Veit Flockerzi1
&
Bernd Nilius2
Abstract
Agonist-induced Ca2+ entry into cells by both store-operated channels and channels activated independently of Ca2+-store depletion has been described in various cell types. The molecular structures of these channels are unknown as is, in most cases, their impact on various cellular functions. Here we describe a store-operated Ca2+ current in vascular endothelium and show that endothelial cells of mice deficient in TRP4 (also known as CCE1) lack this current. As a consequence, agonist-induced Ca2+ entry and vasorelaxation is reduced markedly, showing that TRP4 is an indispensable component of store-operated channels in native endothelial cells and that these channels directly provide an Ca2+-entry pathway essentially contributing to the regulation of blood vessel tone.
- Institut für Pharmakologie und Toxikologie, Universität des Saarlandes, D-66421 Homburg, Germany
- Laboratorium voor Fysiologie, Campus Gasthuisberg, KU Leuven, B-3000 Leuven, Belgium
- Institut für Pharmakologie und Toxikologie, TU München, Biedersteinerstrasse 29, D-80808 München, Germany
Correspondence to: Veit Flockerzi1 e-mail: veit.flockerzi@med-rz.uni-saarland.de
Correspondence to: Bernd Nilius2 e-mail: bernd.nilius@med.kuleuven.ac.be
