Overexpression of transient receptor potential canonical type 1 (TRPC1) alters both store operated calcium entry and depolarization-evoked calcium signals in C2C12 cells

Oláh, Tamás; Fodor, János; Ruzsnavszky, Olga; Vincze, János; Berbey, Céline; Allard, Bruno; Csernoch, László

doi:10.1016/j.ceca.2011.03.012

Cited by 27 publications

(26 citation statements)

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“…The lanthanides Gd 3ϩ and La 3ϩ were used because of their high selectivity for SOCE at low concentration (7,26,47). BTP-2 is an organic SOCE inhibitor that has been shown to block TRPC channels (12,14,40,73), and SKF-96365 is a nonselective cation channel blocker that inhibits SOCE in PASMCs (36,58). The high potency of Gd 3ϩ (IC 50 ϭ 2.8 nM) for the inhibition of CPA-induced SOCE was verified in our preparation (Fig.…”

Section: C84 Trpc Channels and Soce In Mct-induced Pulmonary Hypertenmentioning

confidence: 99%

Enhanced store-operated Ca²⁺ entry and TRPC channel expression in pulmonary arteries of monocrotaline-induced pulmonary hypertensive rats

Liu

Zhang

Yang

et al. 2012

American Journal of Physiology-Cell Physiology

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Here we further examine the involvement of TRPC and SOCE in PH with a widely used rat model of monocrotaline (MCT)-induced PAH. Rats developed severe PAH, right ventricular hypertrophy, and significant increase in store-operated TRPC1 and TRPC4 mRNA and protein in endothelium-denuded pulmonary arteries (PAs) 3 wk after MCT injection. Contraction of PA and Ca 2ϩ influx in PASMC evoked by store depletion using cyclopiazonic acid (CPA) were enhanced dramatically, consistent with augmented SOCE in the MCT-treated group. The time course of increase in CPA-induced contraction corresponded to that of TRPC1 expression. Endothelin-1 (ET-1)-induced vasoconstriction was also potentiated in PAs of MCT-treated rats. The response was partially inhibited by SOCE blockers, including Gd 3ϩ , La 3ϩ , and SKF-96365, as well as the general TRPC inhibitor BTP-2, suggesting that TRPC-dependent SOCE was involved. Moreover, the ET-1-induced contraction and Ca 2ϩ response in the MCT group were more susceptible to the inhibition caused by the various SOCE blockers. Hence, our study shows that MCTinduced PAH is associated with increased TRPC expression and SOCE, which are involved in the enhanced vascular reactivity to ET-1, and support the hypothesis that TRPC-dependent SOCE is an important pathway for the development of PH.canonical transient receptor potential 1; store-operated calcium channels; monocrotaline; pulmonary hypertension; endothelin-1 PULMONARY HYPERTENSION (PH) is a pathophysiological condition associated with a board spectrum of diseases of different pathological features and etiological mechanisms (53). Among them, pulmonary arterial hypertension (PAH) is a severe progressive form characterized by vasoconstriction, plexiform formation, and vascular cell proliferation and remodeling, resulting in elevated pulmonary vascular resistance, right ventricular hypertrophy, and eventually right heart failure and death (16). There are different types of PAH, including idiopathic (IPAH) and heritable PAH (53). PH owing to lung diseases and hypoxia is another category of PH, which includes PH associated with chronic obstructive pulmonary disease, sleep disorders, and chronic exposure to high altitude. PH in this group is generally mild to moderate, but it worsens the prognosis of the diseases (9, 41). The etiologic mechanisms of the various forms of PH are different, but they all have the common features of abnormalities in pulmonary vascular function, vascular cell proliferation, and remodeling, suggesting that they may share some important downstream signaling mechanisms in the process of disease development.Intracellular Ca 2ϩ signaling plays pivotal roles in the regulation of numerous physiological and pathophysiological processes, including contraction, proliferation, hypertrophy, and migration, in pulmonary arterial smooth muscle cell (PASMC) (45). Previous studies indicate that there are major alterations in ion channel expression and Ca 2ϩ homeostasis, such as membrane depolarization, downregulation of voltage-gated K ϩ chan...

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Section: C84 Trpc Channels and Soce In Mct-induced Pulmonary Hypertenmentioning

confidence: 99%

Enhanced store-operated Ca²⁺ entry and TRPC channel expression in pulmonary arteries of monocrotaline-induced pulmonary hypertensive rats

Liu

Zhang

Yang

et al. 2012

American Journal of Physiology-Cell Physiology

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“…The activation mode is regulated by its interaction with the Orai1-STIM1 complex or hTRPC3, for store-dependent or -independent pathways, respectively [ 17 ] . The functional cooperation between STIM1, Orai1 and TRPC1 was further revealed by studies where the expression of TRPC1 was enhanced in the mouse myoblast cell line C2C12, which resulted in enhancement of SOCE and downregulation of the STIM1-Orai1 pathway [ 204 ] . Furthermore, a recent study has reported that Ca 2+ entry through Orai1-forming channels activates plasma membrane insertion of TRPC1, as demonstrated by knockdown of Orai1 and expression of the dominant negative mutant Orai1 lacking a functional pore Orai1(E106Q) in human salivary gland cells [ 234 ] .…”

Section: Interaction Between Stim and Orai And Trp Proteinsmentioning

confidence: 97%

“…Nevertheless, in addition to the involvement of TRP members in receptor-operated Ca 2+ entry (ROCE), there is a body of evidence supporting a role for mammalian TRP channels in the conduction of SOCE. Particular attention has been focused on the TRPC subfamily members, which have been found to be gated by Ca 2+ store depletion in different cell types by using distinct experimental manoeuvres, from overexpression of specifi c TRPC proteins to knockdown of endogenous TRPs and knockout studies [ 99,[197][198][199][200][201][202][203][204] . Reports for store depletion induced activation of TRPC channels have been presented for all TRPC subfamily members, including TRPC1 [ 71,197,198,204,205 ] , TRPC3 [ 206,207 ] , TRPC4 [ 208,209 ] , TRPC5 [ 209,210 ] , TRPC6 [ 17, 34, 211 ] and TRPC7 [ 212 ] .…”

Section: The Trp Proteinsmentioning

confidence: 99%

Store-Operated Ca2+ Entry

Berna‐Erro

Redondo

Rosado

2012

Advances in Experimental Medicine and Biology

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“…Namely, the extent of activation of IP 3 Rs by thimerosal -a widely used IP 3 R activator ( [30,32]; for review see eg. [8] [21]). Taken together, these results suggest that the main effect of Trisk 32 overexpression is not the alteration of the functionality of SOCE.…”

Section: Discussionmentioning

confidence: 99%

Trisk 32 regulates IP3 receptors in rat skeletal myoblasts

Oláh

Fodor

Oddoux

et al. 2011

Pflugers Arch - Eur J Physiol

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To date four isoforms of triadins have been identified in rat skeletal muscle. While the function of the 95 kDa isoform in excitation-contraction coupling has been studied in detail, the role of the 32 kDa isoform (Trisk 32) remains elusive. Here Trisk 32 overexpression was carried out by stable transfection in L6.G8 myoblasts. Co-localization of Trisk 32 and IP 3 receptors (IP 3 R) was demonstrated by immunocytochemistry and their association was shown by coimmunoprecipitation. Functional effects of Trisk 32 on IP 3 -mediated Ca 2+ release were assessed by measuring changes in [Ca 2+ ] i following the stimulation by bradykinin or vasopressin. The amplitude of the Ca 2+ transients evoked by 20 µM bradykinin was significantly higher in Trisk 32-overexpressing (p<0.01; 426±84 nM, n=27) as compared to control cells (76±12 nM, n=23). The difference remained significant (p<0.02; 217±41 nM, n=21 and 97±29 nM, n=31, respectively) in the absence of extracellular Ca 2+ . Similar observations were made when 0.1 µM vasopressin was used to initiate Ca 2+ release. Possible involvement of the ryanodine receptors (RyR) in these processes was excluded, after functional and biochemical experiments. Furthermore, Trisk 32 overexpression had no effect on store-operated Ca 2+ -entry, despite a decrease in the expression of STIM1. These results suggest that neither the increased activity of RyR, nor the amplification of SOCE are responsible for the differences observed in bradykinin-or vasopressin-evoked Ca 2+ transients, rather, they were due to the enhanced activity of IP 3 R. Thus Trisk 32 not only colocalizes with, but directly contributes to the regulation of Ca 2+ release via IP 3 R.

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Overexpression of transient receptor potential canonical type 1 (TRPC1) alters both store operated calcium entry and depolarization-evoked calcium signals in C2C12 cells

Abstract: Oláh et al. Western-blot analysis of TRPC1 in the transfected clones. The 87 kDa human isoform

Cited by 27 publications

References 50 publications

Enhanced store-operated Ca²⁺ entry and TRPC channel expression in pulmonary arteries of monocrotaline-induced pulmonary hypertensive rats

Enhanced store-operated Ca²⁺ entry and TRPC channel expression in pulmonary arteries of monocrotaline-induced pulmonary hypertensive rats

Store-Operated Ca2+ Entry

Trisk 32 regulates IP3 receptors in rat skeletal myoblasts

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Overexpression of transient receptor potential canonical type 1 (TRPC1) alters both store operated calcium entry and depolarization-evoked calcium signals in C2C12 cells

Abstract: Oláh et al. Western-blot analysis of TRPC1 in the transfected clones. The 87 kDa human isoform

Cited by 27 publications

References 50 publications

Enhanced store-operated Ca2+ entry and TRPC channel expression in pulmonary arteries of monocrotaline-induced pulmonary hypertensive rats

Enhanced store-operated Ca2+ entry and TRPC channel expression in pulmonary arteries of monocrotaline-induced pulmonary hypertensive rats

Store-Operated Ca2+ Entry

Trisk 32 regulates IP3 receptors in rat skeletal myoblasts

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Enhanced store-operated Ca²⁺ entry and TRPC channel expression in pulmonary arteries of monocrotaline-induced pulmonary hypertensive rats

Enhanced store-operated Ca²⁺ entry and TRPC channel expression in pulmonary arteries of monocrotaline-induced pulmonary hypertensive rats