Enhanced capacitative calcium entry and sarcoplasmic-reticulum calcium storage capacity with advanced age in murine mesenteric arterial smooth muscle cells.
Enhanced capacitative calcium entry and sarcoplasmic-reticulum calcium storage capacity with advanced age in murine mesenteric arterial smooth muscle cells.
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随着年龄的增长，小鼠肠系膜动脉平滑肌细胞的钙进入能力和肌浆网钙储存能力增强。
DOI：
10.1016/j.exger.2008.10.007
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发表时间：
2009-03
影响因子：
3.9
通讯作者：
Wilson, Sean M.
中科院分区：
文献类型：
--
作者：
Goyal, Ravi;Angermann, Jeff E.;Ostrovskaya, Olga;Buchholz, John N.;Smith, Gregory D.;Wilson, Sean M.
Intracellular Ca2+ signaling is important to perfusion pressure related arterial reactivity and to vascular disorders including hypertension, angina and ischemic stroke. We have recently shown that advancing age leads to calcium signaling adaptations in mesenteric arterial myocytes from C57 BL/6 mice (Mech Ageing Dev, 127 (2006) 315–323), which may contribute to decrements in perfusion pressure related arterial contractility others have shown occur. Even still, the mechanisms underlying the changes in Ca2+ signaling and arterial reactivity are unresolved. Ca2+ transport and storage capabilities are thought to contribute to age-related Ca2+ signaling dysfunctions in other cell types. The present studies were therefore designed to test the hypothesis that cytosolic and compartmental Ca2+ homeostasis in mesenteric arterial myocytes changes with advanced age. The hypothesis was tested by performing digitalized fluorescence microscopy on mesenteric arterial myocytes isolated from 5–6 month and 29–30 month old C57Bl/6 mice. The data provide evidence that with advanced age capacitative Ca2+ entry and sarcoplasmic reticulum Ca2+ storage are increased although sarcoplasmic reticulum Ca2+ uptake and plasma membrane Ca2+ extrusion are unaltered. Overall, the studies begin to resolve the mechanisms associated with age-related alterations in mesenteric arterial smooth muscle Ca2+ signaling and their physiological consequences.
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DOI：
10.1152/ajplung.1997.273.2.l322
发表时间：
1997-08-01
影响因子：
4.9
作者：
Janssen, LJ;Walters, DK;Wattie, J
通讯作者：
Wattie, J
影响因子：
4
作者：
KEIZER, J;DEYOUNG, G
通讯作者：
DEYOUNG, G
影响因子：
3.3
作者：
KEIZER, J;LI, YX;RINZEL, J
通讯作者：
RINZEL, J
影响因子：
5
作者：
Poburko, D;Lhote, P;Ruegg, UT
通讯作者：
Ruegg, UT
影响因子：
3.3
作者：
DELP, MD;BROWN, M;HASSER, EM
通讯作者：
HASSER, EM