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Effect of aging on calcium signaling in C57Bl6J mouse cerebral arteries

  • Georgeon-Chartier, Carole Institut des Maladies Neurodégénératives, UMR 5293, Universite Bordeaux, France
  • Menguy, Céline Génétique des Maladies Vasculaires, UMR S 740, Universite Paris Diderot Paris, France - Génétique des Maladies Vasculaires, UMR S 740, INSERM, 75010 Paris, France
  • Prévot, Anne Department of Medicine Physiology, Universite de Fribourg, Switzerland
  • Morel, Jean-Luc Institut des Maladies Neurodégénératives, UMR 5293, Universite Bordeaux, France
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  • Pflügers Archiv - European Journal of Physiology. - 2013, vol. 465, no. 6, p. 829–838
English 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 Ca²⁺ signaling in smooth muscle cells. Ca²⁺ 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 Ca²⁺ 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 Ca²⁺ signals. These results show that aging induces a decrease of contractility correlated with modifications of the expression of genes encoding Ca²⁺ signaling toolkit. Globally, the amplitude of Ca²⁺ signals was decreased, whereas their duration was increased by a defection of Ca²⁺ store refilling.
Faculté des sciences et de médecine
Département de Médecine
  • English
Biological sciences
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