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- W2294029632 abstract "The present study aimed to determine if TRPC1 and STIM1 mediate capacitative Ca2+ entry (CCE) in mouse pulmonary arterial smooth muscle cells (PASMCs). In primary cultured PASMCs loaded with fura-2, cyclopiazonic acid (CPA) caused a transient followed by a sustained rise in intracellular Ca2+ concentration ([Ca2+]i). The transient but not sustained rise in [Ca2+]i was partially inhibited by nifedipine but they were both inhibited by SKF 96365, Ni2+, La3+ and Gd3+. In addition, CPA increased the rate of Mn2+ quench of fura-2 fluorescence that was also inhibited by these blockers, exhibiting pharmacological properties characteristic of CCE. The nifedipine-insensitive rise in [Ca2+]i and the increase in Mn2+ quench rate were both inhibited in cells pretreated with antibodies raised against extracellular epitopes of TRPC1 and STIM1. Moreover, overexpression of STIM1 resulted in a marked increase in [Ca2+]i and Mn2+ quench rate caused by CPA, and they were reduced by TRPC1 antibody. RT-PCR and Western blot analysis revealed TRPC1 and STIM1 mRNAs and proteins. Furthermore, TRPC1 was found to co-immunoprecipitate with STIM1. Taken together, store-depletion causes activation of voltage-operated Ca2+ entry and CCE. These data provide direct evidence that TRPC1 channel mediates CCE through activation of STIM1 in mouse PASMCs. [Supported by HL49254, NCRR P20RR15581 (JR Hume) and AHA Scientist Development Grant (LC Ng)]" @default.
- W2294029632 created "2016-06-24" @default.
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- W2294029632 date "2009-04-01" @default.
- W2294029632 modified "2023-10-18" @default.
- W2294029632 title "TRPC1 Mediates Capacitative Calcium Entry through Activation of STIM1 in Mouse Pulmonary Arterial Smooth Muscle Cells" @default.
- W2294029632 doi "https://doi.org/10.1096/fasebj.23.1_supplement.999.10" @default.
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