title: Effect of aging on calcium signaling in C57Bl6J mouse cerebral arteries.
abstract: 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.
authors.affiliation: Institut des Maladies Neurodégénératives, UMR 5293, Universite Bordeaux, 33076, Bordeaux Cedex, France. carole.georgeon@u-bordeaux2.fr
authors.forename: Carole
authors.initials: C
authors.lastname: Georgeon-Chartier
authors.forename: Céline
authors.initials: C
authors.lastname: Menguy
authors.forename: Anne
authors.initials: A
authors.lastname: Prévot
authors.forename: Jean-Luc
authors.initials: JL
authors.lastname: Morel
mesh_terms: D000375:Aging / Q000378:metabolism* / Q000502:physiology; D000818:Animals; D015220:Calcium Channels / Q000235:genetics / Q000378:metabolism; D020013:Calcium Signaling; D002135:Calcium-Binding Proteins / Q000235:genetics / Q000378:metabolism; D002536:Cerebral Arteries / Q000166:cytology / Q000378:metabolism / Q000502:physiology*; D018507:Gene Expression Regulation, Developmental; D007473:Ion Channels / Q000235:genetics / Q000378:metabolism; D008562:Membrane Glycoproteins / Q000235:genetics / Q000378:metabolism; D051379:Mice; D008810:Mice, Inbred C57BL; D009119:Muscle Contraction; D032389:Myocytes, Smooth Muscle / Q000378:metabolism; D000071737:Stromal Interaction Molecule 1; D022021:Tacrolimus Binding Proteins / Q000235:genetics / Q000378:metabolism; D014158:Transcription, Genetic; D000099211:Phospholamban
chemical_list: D015220:Calcium Channels; D002135:Calcium-Binding Proteins; D007473:Ion Channels; D008562:Membrane Glycoproteins; D000071737:Stromal Interaction Molecule 1; D022021:Tacrolimus Binding Proteins; D000099211:Phospholamban; C100757:Stim1 protein, mouse; C522222:TRIC-B protein, mouse; C403484:tacrolimus binding protein 1B