Calcium Influx Factor Directly Activates Store-operated Cation Channels in Vascular Smooth Muscle Cells

Trepakova, Elena S.; Csutora, Péter; Hunton, Dacia L.; Marchase, Richard B.; Cohen, Richard A.; Bolotina, Victoria M.

doi:10.1074/jbc.m004666200

Cited by 106 publications

(83 citation statements)

References 25 publications

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“…After 32-36 h they were treated with TG, and CIF was extracted from cells, purified, and then injected into X. laevis oocytes, which we routinely use as a sensitive bioassay system in CIF studies (29,30,33). Injection of CIF extract from control cells (transfected with scrambled siRNA) caused a strong Ca 2ϩ influx propagating from the point of injection through the oocytes (Fig.…”

Section: Resultsmentioning

confidence: 99%

“…Calcium influx factor (CIF) is known to be produced in the cells upon depletion of Ca 2ϩ stores (25)(26)(27)(28)(29)(30)(31)(32)(33) and/or a drop in intraluminal free Ca 2ϩ concentration (33). Although the molecular identity of CIF is still unknown, its presence and biological activity was detected by numerous groups in a wide variety of cell types ranging from yeast to human (for review see Ref.…”

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confidence: 99%

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Novel Role for STIM1 as a Trigger for Calcium Influx Factor Production

Csutora¹,

Peter²,

Kilic

et al. 2008

Journal of Biological Chemistry

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STIM1 has been recently identified as a Ca 2؉ sensor in endoplasmic reticulum (ER) and an initiator of the store-operated Ca 2؉ entry (SOCE) pathway, but the mechanism of SOCE activation remains controversial. Here we focus on the early ERdelimited steps of the SOCE pathway and demonstrate that STIM1 is critically involved in initiating of production of calcium influx factor (CIF), a diffusible messenger that can deliver the signal from the stores to plasma membrane and activate SOCE. We discovered that CIF production is tightly coupled with STIM1 expression and requires functional integrity of its intraluminal sterile ␣-motif (SAM) domain. We demonstrate that 1) molecular knockdown or overexpression

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Section: Resultsmentioning

confidence: 99%

mentioning

confidence: 99%

Novel Role for STIM1 as a Trigger for Calcium Influx Factor Production

Csutora¹,

Peter²,

Kilic

et al. 2008

Journal of Biological Chemistry

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“…A clear alternative is the suggested diffusible messenger for CCE, termed calcium inf lux factor (9,10). Interestingly, there is recent evidence for such a mode of signaling in vascular smooth muscle cells (48), which is one of the cell types that expresses the nonselective cation channel version of CCE (18).…”

Section: Discussionmentioning

confidence: 99%

Human Trp3 forms both inositol trisphosphate receptor-dependent and receptor-independent store-operated cation channels in DT40 avian B lymphocytes

Vázquez

Lièvremont

Bird

et al. 2001

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

164

146

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Mammalian Trp proteins are candidates for plasma membrane calcium channels regulated by receptor activation or by intracellular calcium store depletion [capacitative calcium entry (CCE)]. One extensively investigated member of the Trp family, the human Trp3 (hTrp3), behaves as a receptor-activated, calcium-permeable, nonselective cation channel when expressed in cell lines and does not appear to be activated by store depletion. Nonetheless, there is good evidence that Trp3 can be regulated by interacting with inositol trisphosphate receptors (IP3Rs), reminiscent of the conformational coupling mode of CCE. To investigate the role of Trp3 in CCE, and its regulation by IP3R, we transiently expressed hTrp3 in the wild-type DT40 chicken B lymphocyte cell line and its variant lacking IP3R. Expression of hTrp3 in either wild-type or IP3R-knockout cells did not increase basal membrane permeability, but resulted in a substantially greater divalent cation entry after thapsigargin-induced store depletion. This hTrp3-dependent divalent cation entry was significantly greater in the wild type than in IP3R-knockout cells. Thus, it appears that in this cell line, hTrp3 forms channels that are store-operated by both IP3R-dependent and IP 3R-independent mechanisms. Trp3, or one of its structural relatives, is a candidate for the store-operated, nonselective cation channels observed in smooth muscle cells and other cell types.

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“…First described in nonexcitable cells, CCE has now been shown to coexist with L-type channels in smooth and skeletal muscle cells (17,35) and in both neonatal and adult cardiomyocytes (12,13,31). The TRPC protein family has been a prime candidate for CCE channel proteins (14) and TRPC1, -3, -4, -5, and -6 have all been identified in rat and mouse hearts (14,28,30).…”

Section: Discussionmentioning

confidence: 99%

Overexpression of TRPC3 increases apoptosis but not necrosis in response to ischemia-reperfusion in adult mouse cardiomyocytes

Shan

Marchase²,

Chatham

2008

American Journal of Physiology-Cell Physiology

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Shan D, Marchase RB, Chatham JC. Overexpression of TRPC3 increases apoptosis but not necrosis in response to ischemia-reperfusion in adult mouse cardiomyocytes. Am J Physiol Cell Physiol 294: C833-C841, 2008. First published January 9, 2008 doi:10.1152/ajpcell.00313.2007.-An increase in cytosolic Ca 2ϩ via a capacitative calcium entry (CCE)-mediated pathway, attributed to members of the transient receptor potential (TRP) superfamily, TRPC1 and TRPC3, has been reported to play an important role in regulating cardiomyocyte hypertrophy. Increased cytosolic Ca 2ϩ also plays a critical role in mediating cell death in response to ischemiareperfusion (I/R). Therefore, we tested the hypothesis that overexpression of TRPC3 in cardiomyocytes will increase sensitivity to I/R injury. Adult cardiomyocytes isolated from wild-type (WT) mice and from mice overexpressing TRPC3 in the heart were subjected to 90 min of ischemia and 3 h of reperfusion. After I/R, viability was 51 Ϯ 1% in WT mice and 42 Ϯ 5% in transgenic mice (P Ͻ 0.05). Apoptosis assessed by annexin V was significantly increased in the TRPC3 group compared with WT (32 Ϯ 1% vs. 21 Ϯ 3%; P Ͻ 0.05); however, there was no significant difference in necrosis between groups. Treatment of TRPC3 cells with the CCE inhibitor SKF-96365 (0.5 M) significantly improved cellular viability (54 Ϯ 4%) and decreased apoptosis (15 Ϯ 4%); in contrast, the L-type Ca 2ϩ channel inhibitor verapamil (10 M) had no effect. Calpain-mediated cleavage of ␣-fodrin was increased approximately threefold in the transgenic group following I/R compared with WT (P Ͻ 0.05); this was significantly attenuated by SKF-96365. The calpain inhibitor PD-150606 (25 M) attenuated the increase in both ␣-fodrin cleavage and apoptosis in the TPRC3 group. Increased TRPC3 expression also increased sensitivity to Ca 2ϩ overload stress, but it did not affect the response to TNF-␣-induced apoptosis. These results suggest that CCE mediated via TRPC may play a role in cardiomyocyte apoptosis following I/R due, at least in part, to increased calpain activation.

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Calcium Influx Factor Directly Activates Store-operated Cation Channels in Vascular Smooth Muscle Cells

Cited by 106 publications

References 25 publications

Novel Role for STIM1 as a Trigger for Calcium Influx Factor Production

Novel Role for STIM1 as a Trigger for Calcium Influx Factor Production

Human Trp3 forms both inositol trisphosphate receptor-dependent and receptor-independent store-operated cation channels in DT40 avian B lymphocytes

Overexpression of TRPC3 increases apoptosis but not necrosis in response to ischemia-reperfusion in adult mouse cardiomyocytes

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