ArticleAmerican journal of physiology. Cell physiology2012
Orai1 and Ca2+-independent phospholipase A2 are required for store-operated Icat-SOC current, Ca2+ entry, and proliferation of primary vascular smooth muscle cells.
Article in American journal of physiology. Cell physiology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 23 citations in OpenAlex.
- A computational model of mutual antagonism in the mechano-signaling network of RhoA and nitric oxide.BMC molecular and cell biology · 2021Article
- Ameliorated biomechanical properties of carotid arteries by puerarin in spontaneously hypertensive rats.BMC complementary medicine and therapies · 2021Article
- ORAI1 CaFrontiers in cell and developmental biology · 2021Review
- Insights into Activation Mechanisms of Store-Operated TRPC1 Channels in Vascular Smooth Muscle.Cells · 2020Review
- The structure of iPLANature communications · 2018Article
- Store depletion induces Gαq-mediated PLCβ1 activity to stimulate TRPC1 channels in vascular smooth muscle cells.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2016Article
- Orai1 forms a signal complex with BKCa channel in mesenteric artery smooth muscle cells.Physiological reports · 2016Article
- Severe disturbance in the Ca2+ signaling in astrocytes from mouse models of human infantile neuroaxonal dystrophy with mutated Pla2g6.Human molecular genetics · 2012Article
- Orai1 calcium channels in the vasculature.Pflugers Archiv : European journal of physiology · 2012Review
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Authors and funding
4 authors at 1 institution in 1 country.
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Abstract
Store-operated Ca(2+) entry (SOCE) is important for multiple functions of vascular smooth muscle cells (SMC), which, depending of their phenotype, can resemble excitable and nonexcitable cells. Similar to nonexcitable cells, Orai1 was found to mediate Ca(2+)-selective (CRAC-like) current and SOCE in dedifferentiated cultured SMC and smooth muscle-derived cell lines. However, the role of Orai1 in cation-selective store-operated channels (cat-SOC), which are responsible for SOCE in primary SMC, remains unclear. Here we focus on primary SMC, and assess the role of Orai1 and Ca(2+)-independent phospholipase A(2) (iPLA(2)β, or PLA2G6) in activation of cat-SOC current (I(cat-SOC)), SOCE, and SMC proliferation. Using molecular, electrophysiological, imaging, and functional approaches, we demonstrate that molecular knockdown of either Orai1 or iPLA(2)β leads to similar inhibition of the whole cell cat-SOC current and SOCE in primary aortic SMC and results in significant reduction in DNA synthesis and impairment of SMC proliferation. This is the first demonstration that Orai1 and iPLA(2)β are equally important for cat-SOC, SOCE, and proliferation of primary aortic SMC.
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