Effect of aging on calcium signaling in C57Bl6J mouse cerebral arteries

Carole Georgeon-Chartier, Céline Menguy, Anne Prévot, Jean-Luc Morel
Pflugers Arch - Eur J Physiol. 2012-12-14; 465(6): 829-838
DOI: 10.1007/s00424-012-1195-7

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1. Pflugers Arch. 2013 Jun;465(6):829-38. doi: 10.1007/s00424-012-1195-7. Epub 2012
Dec 14.

Effect of aging on calcium signaling in C57Bl6J mouse cerebral arteries.

Georgeon-Chartier C(1), Menguy C, Prévot A, Morel JL.

Author information:
(1)Institut des Maladies Neurodégénératives, UMR 5293, Universite Bordeaux,
33076, Bordeaux Cedex, France.

In cerebral arteries, alterations of vascular reactivity have been observed but
not well molecularly characterized. Therefore, we have hypothesized that
cerebrovascular reactivity could be modified by aging via a modification of
Ca(2+) signaling in smooth muscle cells. Ca(2+) signals and gene expression
implicated in contraction have been measured in posterior and middle cerebral
arteries from young (2-3 months) and old (20-22 months) C57Bl6/J mice. Aging
induced a decrease of KCl- and caffeine-induced contraction as well as a decrease
of the amplitudes and an increase of the durations of KCl- and caffeine-induced
Ca(2+) signals. These results could be linked with the decrease of gene
expression coding for Cav1.2, RyR2, SERCA2, PLB, STIM1, TRIC-B, and the increase
of FKBP12.6 and TPCN1 gene expression. Finally, aging induced a modification of
InsP3 subtype expression pattern responsible for a modification of the InsP3
affinity to activate Ca(2+) signals. These results show that aging induces a
decrease of contractility correlated with modifications of the expression of
genes encoding Ca(2+) signaling toolkit. Globally, the amplitude of Ca(2+)
signals was decreased, whereas their duration was increased by a defection of
Ca(2+) store refilling.

DOI: 10.1007/s00424-012-1195-7
PMID: 23238969 [Indexed for MEDLINE]

Auteurs Bordeaux Neurocampus