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STIM-1 and ORAI-1 channel mediate angiotensin-II-induced expression of Egr-1 in vascular smooth muscle cells.
J Cell Physiol. 2017 Dec; 232(12):3496-3509.JC

Abstract

An upregulation of Egr-1 expression has been reported in models of atherosclerosis and intimal hyperplasia and, various vasoactive peptides and growth promoting stimuli have been shown to induce the expression of Egr-1 in vascular smooth muscle cells (VSMC). Angiotensin-II (Ang-II) is a key vasoactive peptide that has been implicated in the pathogenesis of vascular diseases. Ang-II elevates intracellular Ca2+ through activation of the store-operated calcium entry (SOCE) involving an inositol-3-phosphate receptor (IP3R)-coupled depletion of endoplasmic reticular Ca2+ and a subsequent activation of the stromal interaction molecule 1 (STIM-1)/Orai-1 complex. However, the involvement of IP3R/STIM-1/Orai-1-Ca2+ -dependent signaling in Egr-1 expression in VSMC remains unexplored. Therefore, in the present studies, we have examined the role of Ca2+ signaling in Ang-II-induced Egr-1 expression in VSMC and investigated the contribution of STIM-1 or Orai-1 in mediating this response. 2-aminoethoxydiphenyl borate (2-APB), a dual non-competitive antagonist of IP3R and inhibitor of SOCE, decreased Ang-II-induced Ca2+ release and attenuated Ang-II-induced enhanced expression of Egr-1 protein and mRNA levels. Egr-1 upregulation was also suppressed following blockade of calmodulin and CaMKII. Furthermore, RNA interference-mediated depletion of STIM-1 or Orai-1 attenuated Ang-II-induced Egr-1 expression as well as Ang-II-induced phosphorylation of ERK1/2 and CREB. In addition, siRNA-induced silencing of CREB resulted in a reduction in the expression of Egr-1 stimulated by Ang-II. In summary, our data demonstrate that Ang-II-induced Egr-1 expression is mediated by STIM-1/Orai-1/Ca2+ -dependent signaling pathways in A-10 VSMC.

Authors+Show Affiliations

Laboratory of Cellular Signaling, Montreal Diabetes Research Center, Quebec, Canada. CHUM-Research Center (CRCHUM), Quebec, Canada. Faculty of Medicine, Department of Nutrition, University of Montreal, Quebec, Canada.CHUM-Research Center (CRCHUM), Quebec, Canada.CHUM-Research Center (CRCHUM), Quebec, Canada. Faculty of Medicine, Department of Medicine, University of Montreal, Quebec, Canada.Laboratory of Cellular Signaling, Montreal Diabetes Research Center, Quebec, Canada. CHUM-Research Center (CRCHUM), Quebec, Canada. Faculty of Medicine, Department of Nutrition, University of Montreal, Quebec, Canada. Faculty of Medicine, Department of Medicine, University of Montreal, Quebec, Canada.

Pub Type(s)

Journal Article

Language

eng

PubMed ID

28105751

Citation

Simo-Cheyou, Estelle R., et al. "STIM-1 and ORAI-1 Channel Mediate angiotensin-II-induced Expression of Egr-1 in Vascular Smooth Muscle Cells." Journal of Cellular Physiology, vol. 232, no. 12, 2017, pp. 3496-3509.
Simo-Cheyou ER, Tan JJ, Grygorczyk R, et al. STIM-1 and ORAI-1 channel mediate angiotensin-II-induced expression of Egr-1 in vascular smooth muscle cells. J Cell Physiol. 2017;232(12):3496-3509.
Simo-Cheyou, E. R., Tan, J. J., Grygorczyk, R., & Srivastava, A. K. (2017). STIM-1 and ORAI-1 channel mediate angiotensin-II-induced expression of Egr-1 in vascular smooth muscle cells. Journal of Cellular Physiology, 232(12), 3496-3509. https://doi.org/10.1002/jcp.25810
Simo-Cheyou ER, et al. STIM-1 and ORAI-1 Channel Mediate angiotensin-II-induced Expression of Egr-1 in Vascular Smooth Muscle Cells. J Cell Physiol. 2017;232(12):3496-3509. PubMed PMID: 28105751.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - STIM-1 and ORAI-1 channel mediate angiotensin-II-induced expression of Egr-1 in vascular smooth muscle cells. AU - Simo-Cheyou,Estelle R, AU - Tan,Ju Jing, AU - Grygorczyk,Ryszard, AU - Srivastava,Ashok K, Y1 - 2017/02/21/ PY - 2016/12/14/received PY - 2017/01/18/revised PY - 2017/01/18/accepted PY - 2017/1/21/pubmed PY - 2017/10/3/medline PY - 2017/1/21/entrez KW - CREB KW - Egr-1 KW - Orai-1 KW - STIM-1 KW - angiotensin-II SP - 3496 EP - 3509 JF - Journal of cellular physiology JO - J Cell Physiol VL - 232 IS - 12 N2 - An upregulation of Egr-1 expression has been reported in models of atherosclerosis and intimal hyperplasia and, various vasoactive peptides and growth promoting stimuli have been shown to induce the expression of Egr-1 in vascular smooth muscle cells (VSMC). Angiotensin-II (Ang-II) is a key vasoactive peptide that has been implicated in the pathogenesis of vascular diseases. Ang-II elevates intracellular Ca2+ through activation of the store-operated calcium entry (SOCE) involving an inositol-3-phosphate receptor (IP3R)-coupled depletion of endoplasmic reticular Ca2+ and a subsequent activation of the stromal interaction molecule 1 (STIM-1)/Orai-1 complex. However, the involvement of IP3R/STIM-1/Orai-1-Ca2+ -dependent signaling in Egr-1 expression in VSMC remains unexplored. Therefore, in the present studies, we have examined the role of Ca2+ signaling in Ang-II-induced Egr-1 expression in VSMC and investigated the contribution of STIM-1 or Orai-1 in mediating this response. 2-aminoethoxydiphenyl borate (2-APB), a dual non-competitive antagonist of IP3R and inhibitor of SOCE, decreased Ang-II-induced Ca2+ release and attenuated Ang-II-induced enhanced expression of Egr-1 protein and mRNA levels. Egr-1 upregulation was also suppressed following blockade of calmodulin and CaMKII. Furthermore, RNA interference-mediated depletion of STIM-1 or Orai-1 attenuated Ang-II-induced Egr-1 expression as well as Ang-II-induced phosphorylation of ERK1/2 and CREB. In addition, siRNA-induced silencing of CREB resulted in a reduction in the expression of Egr-1 stimulated by Ang-II. In summary, our data demonstrate that Ang-II-induced Egr-1 expression is mediated by STIM-1/Orai-1/Ca2+ -dependent signaling pathways in A-10 VSMC. SN - 1097-4652 UR - https://www.unboundmedicine.com/medline/citation/28105751/STIM_1_and_ORAI_1_channel_mediate_angiotensin_II_induced_expression_of_Egr_1_in_vascular_smooth_muscle_cells_ L2 - https://doi.org/10.1002/jcp.25810 DB - PRIME DP - Unbound Medicine ER -