Connexins and M3 muscarinic receptors contribute to heterogeneous Ca(2+) signaling in mouse aortic endothelium.

Détails

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Etat: Public
Version: Final published version
Licence: CC BY-NC-ND 4.0
ID Serval
serval:BIB_855794F06456
Type
Article: article d'un périodique ou d'un magazine.
Collection
Publications
Titre
Connexins and M3 muscarinic receptors contribute to heterogeneous Ca(2+) signaling in mouse aortic endothelium.
Périodique
Cellular physiology and biochemistry
Auteur(s)
Boittin F.X., Alonso F., Le Gal L., Allagnat F., Bény J.L., Haefliger J.A.
ISSN
1421-9778 (Electronic)
ISSN-L
1015-8987
Statut éditorial
Publié
Date de publication
2013
Peer-reviewed
Oui
Volume
31
Numéro
1
Pages
166-178
Langue
anglais
Notes
Publication types: Journal Article ; Research Support, Non-U.S. Gov't
Publication Status: ppublish
Résumé
Smooth muscle tone is controlled by Ca(2+) signaling in the endothelial layer. Mouse endothelial cells are interconnected by gap junctions made of Connexin40 (Cx40) and Cx37, which allow the exchange of signaling molecules to coordinate their activity. Here, we investigated the role of Cx40 in the endothelial Ca(2+) signaling of the mouse aorta.
Ca(2+) imaging was performed on intact aortic endothelium from both wild type (Cx40+/+) and Connexin40-deficient (Cx40 -/-) mice.
Acetylcholine (ACh) induced early fast and high amplitude Ca(2+) transients in a fraction of endothelial cells expressing the M3 muscarinic receptors. Inhibition of intercellular communication using carbenoxolone or octanol fully blocked the propagation of ACh-induced Ca(2+) transients toward adjacent cells in WT and Cx40-/- mice. As compared to WT, Cx40-/- mice displayed a reduced propagation of ACh-induced Ca(2+) waves, indicating that Cx40 contributes to the spreading of Ca(2+) signals. The propagation of those Ca(2+) responses was not blocked by suramin, a blocker of purinergic ATP receptors, indicating that there is no paracrine effect of ATP release on the Ca(2+) waves.
Altogether our data show that Cx40 and Cx37 contribute to the propagation and amplification of the Ca(2+) signaling triggered by ACh in endothelial cells expressing the M3 muscarinic receptors.
Mots-clé
Acetylcholine/pharmacology, Adenosine Triphosphate/metabolism, Animals, Anti-Ulcer Agents/pharmacology, Aorta/cytology, Calcium/metabolism, Calcium Signaling/drug effects, Carbenoxolone/pharmacology, Cell Communication/drug effects, Cells, Cultured, Connexins/genetics, Connexins/metabolism, Endothelial Cells/cytology, Endothelial Cells/drug effects, Endothelial Cells/metabolism, Gap Junctions/metabolism, Mice, Mice, Knockout, Octanols/pharmacology, Receptor, Muscarinic M3/metabolism
Pubmed
Web of science
Open Access
Oui
Création de la notice
10/05/2019 10:12
Dernière modification de la notice
20/08/2019 15:44
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