TRPC1 and STIM1 mediate capacitative Ca<sup>2+</sup> entry in mouse pulmonary arterial smooth muscle cells

Ng, Lih Chyuan; McCormack, Mary D.; Airey, Judith A.; Singer, Cherie A.; Keller, Phillip S.; Xiang‐dong, Shen; Hume, Joseph R.

doi:10.1113/jphysiol.2009.172254

Cited by 86 publications

(91 citation statements)

References 59 publications

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“…The tissue was then transferred to an enzyme-free, low-Ca 2ϩ PSS and triturated with a fire-polished Pasteur pipette. The resulting dispersed PASMCs were subjected to cell culture as previously described (32). Freshly dispersed PASMCs were plated onto a 60-mm cell culture dish and incubated with DMEM cell culture medium containing 10% newborn calf serum (NCS), penicillin (100 U/ml), and streptomycin (100 g/ml).…”

Section: Methodsmentioning

confidence: 99%

“…The cytosolic Ca 2ϩ concentration was estimated in PASMCs loaded with fura-2 acetoxymethyl ester (fura-2 AM) (Molecular Probes, Eugene, OR) using a dual excitation digital Ca 2ϩ imaging system (IonOptix, Milton, MA) equipped with an intensified charge-coupled device (CCD) camera as previously described (31,32). PASMCs were loaded with 10 M fura-2 AM for 1 h in the dark at room temperature and placed on the coverslip of a 0.2-ml perfusion chamber mounted on an inverted epifluorescence microscope (Nikon) outfitted with a ϫ40 oil immersion objective (numerical aperture 1.3, Nikon).…”

Section: Methodsmentioning

confidence: 99%

“…On the other hand, STIM1 and Orai1 were recently found to mediate store-operated currents in cultured rat aorta smooth muscle cells (37). Our recent study in cultured mouse PASMCs reveals two Ca 2ϩ components of CCE, a transient followed by a sustained Ca 2ϩ component, and TRPC1 was shown to associate with STIM1 to mediate the sustained component (32). However, the molecular mechanism underlying the transient Ca 2ϩ component has not been identified.…”

mentioning

confidence: 99%

“…To date, there is very little evidence for the roles of Orai1 and STIM1 in vascular smooth muscle cells. STIM1 was shown to express in cultured coronary artery smooth muscle cells (47), saphenous vein cells (18), mesenteric artery smooth muscle cells (5), aorta smooth muscle cells (5,7,37), and PASMCs (24,32). siRNA targeting STIM1 resulted in reduction of Ca 2ϩ entry and whole cell current activated by CPA or thapsigargin (18,25,32,37,47).…”

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confidence: 99%

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Orai1 interacts with STIM1 and mediates capacitative Ca²⁺ entry in mouse pulmonary arterial smooth muscle cells

Ng¹,

Ramduny²,

Airey³

et al. 2010

American Journal of Physiology-Cell Physiology

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quench of fura-2 fluorescence caused by CPA, and these responses were reduced in cells treated with Orai1 siRNA. RT-PCR revealed Orai1 and STIM1 mRNAs, and Western blot analysis identified Orai1 and STIM1 proteins in mouse PASMCs. Furthermore, Orai1 was found to coimmunoprecipitate with STIM1, and the precipitation level of Orai1 was increased in cells subjected to store-depletion. Immunostaining revealed colocalization of Orai1 and STIM1 proteins, and the colocalization of these proteins was more apparent after storedepletion. These data provide direct evidence that the transient component of CCE is mediated by Orai1 channel as a result of STIM1 activation in mouse PASMCs.stromal interaction molecule 1; store-depletion; intracellular Ca 2ϩ

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Section: Methodsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

mentioning

confidence: 99%

mentioning

confidence: 99%

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Orai1 interacts with STIM1 and mediates capacitative Ca²⁺ entry in mouse pulmonary arterial smooth muscle cells

Ng¹,

Ramduny²,

Airey³

et al. 2010

American Journal of Physiology-Cell Physiology

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“…Several studies show that association between TRPC1 and STIM1 increases following store depletion (6,16,19,20), although a recent study was unable to demonstrate this (21). While the ezrin/radixin/moesin (ERM) domain of STIM1 appears to bind to TRPC1, the C-terminal 684 KK 685 residues are involved in gating the channel via electrostatic interaction with TRPC1( 639 DD 640 ) (8,13).…”

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confidence: 99%

Activation of TRPC1 by STIM1 in ER-PM microdomains involves release of the channel from its scaffold caveolin-1

Pani

Ong

Brazer

et al. 2009

Proc. Natl. Acad. Sci. U.S.A.

120

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Store-operated Ca 2؉ entry (SOCE) is activated by redistribution of STIM1 into puncta in discrete ER-plasma membrane junctional regions where it interacts with and activates store-operated channels (SOCs). The factors involved in precise targeting of the channels and their retention at these specific microdomains are not yet defined. Here we report that caveolin-1 (Cav1) is a critical plasma membrane scaffold that retains TRPC1 within the regions where STIM1 puncta are localized following store depletion. This enables the interaction of TRPC1 with STIM1 that is required for the activation of TRPC1-SOCE. Silencing Cav1 in human submandibular gland (HSG) cells decreased plasma membrane retention of TRPC1, TRPC1-STIM1 clustering, and consequently reduced TRPC1-SOCE, without altering STIM1 puncta. Importantly, activation of TRPC1-SOCE was associated with an increase in TRPC1-STIM1 and a decrease in TRPC1-Cav1 clustering. Consistent with this, overexpression of Cav1 decreased TRPC1-STIM1 clustering and SOCE, both of which were recovered when STIM1 was expressed at higher levels relative to Cav1. Silencing STIM1 or expression of ⌬ERM-STIM1 or STIM1( 684 EE 685 ) mutant prevented dissociation of TRPC1-Cav1 and activation of TRPC1-SOCE. However expression of TRPC1-( 639 KK 640 ) with STIM1( 684 EE 685 ) restored function and the dissociation of TRPC1 from Cav1 in response to store depletion. Further, conditions that promoted TRPC1-STIM1 clustering and TRPC1-SOCE elicited corresponding changes in SOCE-dependent NFkB activation and cell proliferation. Together these data demonstrate that Cav1 is a critical plasma membrane scaffold for inactive TRPC1. We suggest that activation of TRPC1-SOC by STIM1 mediates release of the channel from Cav1. S tore-operated calcium entry (SOCE) is activated by depletion of endoplasmic reticulum (ER) Ca 2ϩ stores and regulates a variety of critical cellular functions (1). Ca 2ϩ depletion in the ER lumen is detected by the Ca 2ϩ -binding protein STIM1, which oligomerizes into puncta and relocates to discrete ERplasma membrane (ER-PM) junctional regions (2, 3) where it associates with and activates store-operated channels including Orai1 and TRPC1, which are components of CRAC and SOC channels, respectively (4-13). Therefore, the location of these channels in the plasma membrane is likely to be critical for their interaction with peripheral STIM1 and activation. However, mechanisms involved in the precise targeting and retention of the channels at the domains where STIM1 puncta are located are not well-understood.Distinct regions of STIM1 determine aggregation and targeting of the protein to ER-PM junctional domains as well as its clustering with and gating of Orai1 and TRPC1 at these sites. The SAM and coiled-coiled domains are involved in STIM1 aggregation while the polybasic C-terminal region of STIM1 is suggested to target STIM1 to ER-PM junctional regions, which is the likely site for SOCE in native cells (3,(9)(10)(11)14). Thus, it can be predicted that SOCs are either localized in this...

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Smooth Muscle Ion Channels and Regulation of Vascular Tone in Resistance Arteries and Arterioles

Tykocki

Boerman

Jackson

2017

Comprehensive Physiology

270

347

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Vascular tone of resistance arteries and arterioles determines peripheral vascular resistance, contributing to the regulation of blood pressure and blood flow to, and within the body’s tissues and organs. Ion channels in the plasma membrane and endoplasmic reticulum of vascular smooth muscle cells (SMCs) in these blood vessels importantly contribute to the regulation of intracellular Ca2+ concentration, the primary determinant of SMC contractile activity and vascular tone. Ion channels provide the main source of activator Ca2+ that determines vascular tone, and strongly contribute to setting and regulating membrane potential, which, in turn, regulates the open-state-probability of voltage gated Ca2+ channels (VGCCs), the primary source of Ca2+ in resistance artery and arteriolar SMCs. Ion channel function is also modulated by vasoconstrictors and vasodilators, contributing to all aspects of the regulation of vascular tone. This review will focus on the physiology of VGCCs, voltage-gated K+ (KV) channels, large-conductance Ca2+-activated K+ (BKCa) channels, strong-inward-rectifier K+ (KIR) channels, ATP-sensitive K+ (KATP) channels, ryanodine receptors (RyRs), inositol 1,4,5-trisphosphate receptors (IP3Rs), and a variety of transient receptor potential (TRP) channels that contribute to pressure-induced myogenic tone in resistance arteries and arterioles, the modulation of the function of these ion channels by vasoconstrictors and vasodilators, their role in the functional regulation of tissue blood flow and their dysfunction in diseases such as hypertension, obesity, and diabetes.

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TRPC1 and STIM1 mediate capacitative Ca²⁺ entry in mouse pulmonary arterial smooth muscle cells

Abstract: Previous studies in pulmonary arterial smooth muscle cells (PASMCs)

Cited by 86 publications

References 59 publications

Orai1 interacts with STIM1 and mediates capacitative Ca²⁺ entry in mouse pulmonary arterial smooth muscle cells

Orai1 interacts with STIM1 and mediates capacitative Ca²⁺ entry in mouse pulmonary arterial smooth muscle cells

Activation of TRPC1 by STIM1 in ER-PM microdomains involves release of the channel from its scaffold caveolin-1

Smooth Muscle Ion Channels and Regulation of Vascular Tone in Resistance Arteries and Arterioles

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TRPC1 and STIM1 mediate capacitative Ca2+ entry in mouse pulmonary arterial smooth muscle cells

Abstract: Previous studies in pulmonary arterial smooth muscle cells (PASMCs)

Cited by 86 publications

References 59 publications

Orai1 interacts with STIM1 and mediates capacitative Ca2+ entry in mouse pulmonary arterial smooth muscle cells

Orai1 interacts with STIM1 and mediates capacitative Ca2+ entry in mouse pulmonary arterial smooth muscle cells

Activation of TRPC1 by STIM1 in ER-PM microdomains involves release of the channel from its scaffold caveolin-1

Smooth Muscle Ion Channels and Regulation of Vascular Tone in Resistance Arteries and Arterioles

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TRPC1 and STIM1 mediate capacitative Ca²⁺ entry in mouse pulmonary arterial smooth muscle cells

Orai1 interacts with STIM1 and mediates capacitative Ca²⁺ entry in mouse pulmonary arterial smooth muscle cells

Orai1 interacts with STIM1 and mediates capacitative Ca²⁺ entry in mouse pulmonary arterial smooth muscle cells