Role of RYR3 splice variants in calcium signaling in mouse nonpregnant and pregnant myometrium

Fabrice Dabertrand, Nicolas Fritz, Jean Mironneau, Nathalie Macrez, Jean-Luc Morel
American Journal of Physiology-Cell Physiology. 2007-09-01; 293(3): C848-C854
DOI: 10.1152/ajpcell.00069.2007

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1. Am J Physiol Cell Physiol. 2007 Sep;293(3):C848-54. Epub 2007 Jun 27.

Role of RYR3 splice variants in calcium signaling in mouse nonpregnant and
pregnant myometrium.

Dabertrand F(1), Fritz N, Mironneau J, Macrez N, Morel JL.

Author information:
(1)Centre de Neurosciences Intégratives et Cognitives, UMR5228 CNRS, Université
Bordeaux 1 and Université Bordeaux 2, Ave. des Facultés, Talence 33405, France.

Alternative splicing of ryanodine receptor subtype 3 (RYR3) may generate a short
isoform (RYR3S) without channel function and a functional full-length isoform
(RYR3L). The RYR3S isoform has been shown to negatively regulate the native RYR2
subtype in smooth muscle cells as well as the RYR3L isoform when both isoforms
were coexpressed in HEK-293 cells. Mouse myometrium expresses only the RYR3
subtype, but the role of RYR3 isoforms obtained by alternative splicing and their
activation by cADP-ribose during pregnancy have never been investigated. Here, we
show that both RYR3S and RYR3L isoforms are differentially expressed in
nonpregnant and pregnant mouse myometrium. The use of antisense oligonucleotides
directed against each isoform indicated that only RYR3L was activated by caffeine
and cADP-ribose in nonpregnant myometrium. These RYR3L-mediated Ca(2+) releases
were negatively regulated by RYR3S expression. At the end of pregnancy, the
relative expression of RYR3L versus RYR3S and its ability to respond to
cADP-ribose were increased. Therefore, our results suggest that physiological
regulation of RYR3 alternative splicing may play an essential role at the end of

DOI: 10.1152/ajpcell.00069.2007
PMID: 17596299 [Indexed for MEDLINE]

Auteurs Bordeaux Neurocampus