2015
DOI: 10.1097/fjc.0000000000000225
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Contrasting Patterns of Agonist-induced Store-operated Ca2+ Entry and Vasoconstriction in Mesenteric Arteries and Aorta With Aging

Abstract: Abstract:Ca2+ is a crucial factor in the regulation of smooth muscle contraction. Store-operated Ca2+ entry (SOCE) is one pathway that mediates Ca2+ influx and smooth muscle contraction. Vessel contraction function usually alters with aging to cause severe vascular-related diseases. However, the underlying mechanism is still not fully understood. Here, we assessed intracellular Ca2+ and vessel tension and found that SOCE and SOCE-mediated contraction of vascular smooth muscle cells (VSMCs) was reduced in aorta… Show more

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Cited by 16 publications
(20 citation statements)
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“…Previous studies have suggested that the depletion of ER Ca 2+ stores leads to cell apoptosis and growth arrest [ 21 , 22 ]. The Ca 2+ stores can be depleted by both ATP and thapsigargin (TG), an ER Ca 2+ -ATPase inhibitor [ 20 , 23 ]. Therefore, we examined the effect of CLIC4 on the ATP- and TG-induced Ca 2+ release from ER Ca 2+ stores.…”
Section: Resultsmentioning
confidence: 99%
“…Previous studies have suggested that the depletion of ER Ca 2+ stores leads to cell apoptosis and growth arrest [ 21 , 22 ]. The Ca 2+ stores can be depleted by both ATP and thapsigargin (TG), an ER Ca 2+ -ATPase inhibitor [ 20 , 23 ]. Therefore, we examined the effect of CLIC4 on the ATP- and TG-induced Ca 2+ release from ER Ca 2+ stores.…”
Section: Resultsmentioning
confidence: 99%
“…Here we report that a maternal age-related deterioration in Ca 2+ influx occurs in eggs. Reductions in store-operated Ca 2+ entry (SOCE) activity and expression of key SOCE-specific proteins, Stim1 and Orai1, are a characteristic feature of naturally-aged mitotic cells 48 49 , however their behaviour during egg aging is not known. We speculate that an age-related deterioration in SOCE channel expression or activity likely explains our observation of impaired influx in aged eggs following ER store depletion.…”
Section: Discussionmentioning
confidence: 99%
“…This may explain why we observed increased clustering (indicated by increased puncta size) between Orai1 and STIM1 in response to store depletion in transiently cultured mesenteric VSMC even though Orai1 did not significantly contribute to SOCE responses in freshly isolated tissue. Together these data suggest there may be a minimal contribution of vascular Orai1-dependent SOCE to normal vascular homeostasis; however, SOCE may become a more important mechanism of Ca 2+ influx in cardiovascular diseases involving VSMC dysfunction leading to a more proliferative, synthetic state of the VSMC [46,55].…”
Section: Plos Onementioning
confidence: 89%
“…Similarly, the mRNA and protein levels of STIM1 and Orai1 were significantly higher and there was a significant increase in SOCE and force generation in aortic rings in stoke-prone spontaneously hypertensive rats (SHRSP) compared to Wistar-Kyoto (WKY) controls [47]. In addition, SOCE-induced contraction was dramatically increased in mesenteric arteries from aged (22 months) compared to young (3 months) rats [46]. These data suggest SOCE plays a larger role in vascular function in diseased/aged states.…”
Section: Plos Onementioning
confidence: 98%