Orai1–STIM1 formed store-operated Ca2+ channels (SOCs) as the molecular components needed for Pb2+ entry in living cells

Chang, Yu Fen; Teng, Hsiao Chuan; Cheng, Sha-Yen; Wang, Chin Tien; Chiou, Shi Hwa; Kao, Lung‐Sen; Kao, Fu-Jen; Chiou, Arthur; Yang, De‐Ming

doi:10.1016/j.taap.2007.11.025

Cited by 22 publications

(31 citation statements)

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“…Orai1/CRACM1 was recently found to be a critical channel component of SOCs (Feske et al, 2006; Vig et al, 2006). When ER Ca 2+ stores are depleted, Orai1 accumulates with another essential SOC player, the ER Ca 2+ sensor STIM1, to drive the large Ca 2+ influx (Chang et al, 2008; Chiu et al, 2009; Potier et al, 2009). Orai1 with STIM1 has been proven to play a dominant role in the proliferation and migration of rat arterial SMCs (Potier et al, 2009), as well as in the activation of the aorta in hypertension rats (Giachini et al, 2009).…”

Section: Discussionmentioning

confidence: 99%

“…RNA samples for RT‐PCR were incubated for 30 min at 37°C with RNase‐free DNase I, and then for 10 min at 100°C to inactivate the DNase I. With Finnzymes PCR reagents (Finnzymes OY, Finland), RT‐PCR of Orai and STIM isoforms from the A10 cells was performed according to previously described procedures, including primer design, the general protocol for RNA extraction, and cDNA synthesis (Chang et al, 2008; Chiu et al, 2009).…”

Section: Methodsmentioning

confidence: 99%

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Potential effect of resistin on the ET‐1‐increased reactions of blood pressure in rats and Ca²⁺ signaling in vascular smooth muscle cells

Chuang¹,

Au²,

Wang³

et al. 2012

Journal Cellular Physiology

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Resistin and endothelin-1 (ET-1) are upregulated in people with type II diabetes mellitus, central obesity, and hypertension. ET-1 signaling is involved in Ca(2+)-contraction coupling and related to blood pressure regulation. The aim of this study is to investigate the role of resistin on ET-1-increased blood pressure and Ca(2+) signaling. The blood pressure and cytosolic Ca(2+) of vascular smooth muscle cells (VSMCs) of Sprague-Dawley rats were detected. The data demonstrated that resistin accelerated and prolonged ET-1-induced increases in blood pressure and had significant effects on ET-1-increased Ca(2+) reactions. Resistin-enhanced ET-1-increased Ca(2+) reactions were reversed by blockers of store-operated Ca(2+) entry (SOCE) and extracellular-signal-regulated kinase (ERK). The endogenous expression of Orai and stromal interaction molecular (STIM) were characterized in the VSMCs. Furthermore, resistin-enhanced ET-1 Ca(2+) reactions and the resistin-dependent activation of SOCE were abolished under STIM1-siRNA treatment, indicating that STIM1 plays an important role in resistin-enhanced ET-1 Ca(2+) reactions in VSMCs. Resistin appears to exert effects on ET-1-induced Ca(2+) increases by enhancing the activity of ERK-dependent SOCE (STIM1-partcipated), and may accelerate and prolong ET-1-increased blood pressure via the same pathway.

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Section: Discussionmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

Potential effect of resistin on the ET‐1‐increased reactions of blood pressure in rats and Ca²⁺ signaling in vascular smooth muscle cells

Chuang¹,

Au²,

Wang³

et al. 2012

Journal Cellular Physiology

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“…RT-PCR of the P2Y receptor isoforms from CG3 cells was performed according to previously described procedures that included the primer design and the general protocol for RNA extraction and cDNA synthesis (Elia et al, 2003;Chang et al, 2008 (Palmer et al, 2004), RP-mito- (Nagai et al, 2001), and TMRE (10 nM)-stained/transfected PTC cells using a time-lapse microscopy system (IX-71; Olympus, Tokyo, Japan) equipped with a 40ϫ oil objective (numerical aperture, 1.35; U/340) and a monochromator (Polychrome II; TILL Photonics GmbH, Grä felfing, Germany) driven by SimplePCI 6.0 software (Compix Institute, Sewickly, PA). A high-speed cooled charge-coupled device camera (MicroMAX: 782YHS; Roper Scientific, Trenton, NJ) was used to illuminate/acquire emission imaging of these fluorescent probes (340 and 380/505-520 nm for fura, 440/535 long pass for D1ER, 440/500 -525 nm for RP-mito, and 540/560 long pass for TMRE).…”

Section: Methodsmentioning

confidence: 99%

Clodronate-Induced Cell Apoptosis in Human Thyroid Carcinoma Is Mediated via the P2 Receptor Signaling Pathway

Yang

Teng²,

Chen³

et al. 2009

J Pharmacol Exp Ther

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Clodronate, a halogenated bisphosphonate, can inhibit the growth of human thyroid carcinoma (TC) cells. Previously, we found that a clodronate-induced Ca 2ϩ transient was correlated with clodronate-induced growth inhibition in TC cells. However, the details of the signaling process underlying the antiproliferative effect of clodronate on TC cells are not clear. In this study, we investigated the antiproliferative mechanism of clodronate on papillary TC (PTC) cells and xenotransplanted animals using a combination of pharmacological drugs. Reverse transcription-polymerase chain reaction analysis confirmed the endogenous expression of P2Y receptor isoforms in PTC cells. The P2 antagonist suramin not only inhibited the antiproliferative effect of clodronate and ATP on TC cells but also blocked all the Ca 2ϩ transients induced by clodronate and ATP. The release of Ca 2ϩ from the endoplasmic reticulum and membrane depolarization of mitochondria was observed during the clodronate-induced Ca 2ϩ transients. The results of terminal deoxynucleotidyltransferase dUTP nick-end labeling assays and flow cytometry with annexin V and caspase-3 staining suggest that both ATP and clodronate induce apoptosis. Significant inhibition of tumor invasion and colony formation was also observed in clodronate-treated PTC cells. We further demonstrated that only the cAMP inhibitor 9-(tetrahydro-2-furanyl)-9H-purin-6-amine (SQ22536), and not inhibitors of phospho-or store-operated Ca 2ϩ entry (2-aminoethyl diphenylborinate), can significantly reverse the effect of clodronate. Finally, in vivo animal and green fluorescent protein imaging studies further proved that the tumor inhibitory effect of clodronate on xenotransplanted CG3 cells can be reversed by treatment with suramin. In conclusion, we demonstrated that clodronate-induced PTC cell apoptosis and tumor inhibition are partially mediated by the P2Y receptorcAMP cascade.Papillary thyroid carcinoma (PTC) is one of the most commonly differentiated thyroid carcinomas (TCs) (Kondo et al., 2006;Kung et al., 2006). Genomic research has revealed that RET rearrangement and BRAF mutation are important in the carcinogenesis of TC/PTC (Lee et al., 1998;Kondo et al., 2006). Thus far, the treatment choice for TC is surgery in combination with postoperative radioiodine therapy (Huang et al., 2005). However, in patients with postoperative recurrent or lymphoid metastatic lesions without radioiodative uptake, the success of TC therapy is limited (Huang et al., 2005;Muresan et al., 2008).Anticancer or chemotherapeutic drugs are limited in effect and duration of response for the treatment of TC (Muresan et al., 2008). Recently, bisphosphonates (BPs) were found to have a broad range of in vivo and in vitro antitumor effects

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“…Among its effects are changes in motor activity levels in rhesus monkeys [68], rats [109] and Drosophila [50] and impairments in learning and memory in tadpoles [106], mice [107] and rats [3,43,59,81,82]. Despite considerable progress in understanding the physiological mechanisms of how lead affects neuronal plasticity during development [16,76,111] and in the adult [45,100,113,116], the genetic mechanisms lead disturbs are not well understood.…”

Section: Introductionmentioning

confidence: 99%

Genetical toxicogenomics in Drosophila identifies master-modulatory loci that are regulated by developmental exposure to lead

et al. 2009

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The genetics of gene expression in recombinant inbred lines (RILs) can be mapped as expression quantitative trait loci (eQTLs). So-called "genetical genomics" studies have identified locally-acting eQTLs (cis-eQTLs) for genes that show differences in steady state RNA levels. These studies have also identified distantly-acting master-modulatory trans-eQTLs that regulate tens or hundreds of transcripts (hotspots or transbands). We expand on these studies by performing genetical genomics experiments in two environments in order to identify trans-eQTL that might be regulated by developmental exposure to the neurotoxin lead. Flies from each of 75 RIL were raised from eggs to adults on either control food (made with 250 µM sodium acetate), or lead-treated food (made with 250 µM lead acetate, PbAc). RNA expression analyses of whole adult male flies (5-10 days old) were performed with Affymetrix DrosII whole genome arrays (18,952 probesets). Among the 1,389 genes with cis-eQTL, there were 405 genes unique to control flies and 544 genes unique to leadtreated ones (440 genes had the same cis-eQTLs in both samples). There are 2,396 genes with trans-eQTL which mapped to 12 major transbands with greater than 95 genes. Permutation analyses of the strain labels but not the expression data suggests that the total number of eQTL and the number of transbands are more important criteria for validation than the size of the transband. Two transbands, one located on the 2 nd chromosome and one on the 3 rd chromosome, co-regulate 33 lead-induced genes, many of which are involved in neurodevelopmental processes. For these 33 genes, rather than allelic variation at one locus exerting differential effects in two environments, we found that variation at two different loci are required for optimal effects on lead-induced expression.

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Orai1–STIM1 formed store-operated Ca2+ channels (SOCs) as the molecular components needed for Pb2+ entry in living cells

Cited by 22 publications

References 31 publications

Potential effect of resistin on the ET‐1‐increased reactions of blood pressure in rats and Ca²⁺ signaling in vascular smooth muscle cells

Potential effect of resistin on the ET‐1‐increased reactions of blood pressure in rats and Ca²⁺ signaling in vascular smooth muscle cells

Clodronate-Induced Cell Apoptosis in Human Thyroid Carcinoma Is Mediated via the P2 Receptor Signaling Pathway

Genetical toxicogenomics in Drosophila identifies master-modulatory loci that are regulated by developmental exposure to lead

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Orai1–STIM1 formed store-operated Ca2+ channels (SOCs) as the molecular components needed for Pb2+ entry in living cells

Cited by 22 publications

References 31 publications

Potential effect of resistin on the ET‐1‐increased reactions of blood pressure in rats and Ca2+ signaling in vascular smooth muscle cells

Potential effect of resistin on the ET‐1‐increased reactions of blood pressure in rats and Ca2+ signaling in vascular smooth muscle cells

Clodronate-Induced Cell Apoptosis in Human Thyroid Carcinoma Is Mediated via the P2 Receptor Signaling Pathway

Genetical toxicogenomics in Drosophila identifies master-modulatory loci that are regulated by developmental exposure to lead

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Potential effect of resistin on the ET‐1‐increased reactions of blood pressure in rats and Ca²⁺ signaling in vascular smooth muscle cells

Potential effect of resistin on the ET‐1‐increased reactions of blood pressure in rats and Ca²⁺ signaling in vascular smooth muscle cells