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Thromb Haemost 2017; 117(05): 1002-1005
DOI: 10.1160/TH16-09-0690
DOI: 10.1160/TH16-09-0690
Letter to the Editor
SGK1 up-regulates Orai1 expression and VSMC migration during neointima formation after arterial injury
Further Information
Publication History
Received:
07 September 2016
Accepted after major revision:
23 January 2017
Publication Date:
13 November 2017 (online)
Supplementary Material to this article is available online at www.thrombosis-online.com
* Both authors contributed equally.
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References
- 1 Willecke F, Tiwari S, Rupprecht B. et al. Interruption of classic CD40L-CD40 signalling but not of the novel CD40L-Mac-1 interaction limits arterial neointima formation in mice. Thromb Haemost 2014; 112: 379-389.
- 2 Kapopara PR, von Felden J, Soehnlein O. et al. Deficiency of MAPK-activated protein kinase 2 (MK2) prevents adverse remodelling and promotes endothelial healing after arterial injury. Thromb Haemost 2014; 112: 1264-1276.
- 3 Kenagy RD, Hart CE, Stetler-Stevenson WG. et al. Primate smooth muscle cell migration from aortic explants is mediated by endogenous platelet-derived growth factor and basic fibroblast growth factor acting through matrix metalloproteinases 2 and 9. Circulation 1997; 96: 3555-3560.
- 4 Caglayan E, Vantler M, Leppanen O. et al. Disruption of platelet-derived growth factor-dependent phosphatidylinositol 3-kinase and phospholipase Cgamma 1 activity abolishes vascular smooth muscle cell proliferation and migration and attenuates neointima formation in vivo. J Am Coll Cardiol 2011; 57: 2527-2538.
- 5 Holy EW, Jakob P, Eickner T. et al. PI3K/p110alpha inhibition selectively interferes with arterial thrombosis and neointima formation, but not re-endothelialization: potential implications for drug-eluting stent design. Eur Heart J 2014; 35: 808-820.
- 6 Borst O, Schmidt EM, Munzer P. et al. The serum- and glucocorticoid-inducible kinase 1 (SGK1) influences platelet calcium signaling and function by regulation of Orai1 expression in megakaryocytes. Blood 2012; 119: 251-261.
- 7 Yang M, Zheng J, Miao Y. et al. Serum-glucocorticoid regulated kinase 1 regulates alternatively activated macrophage polarization contributing to angiotensin II-induced inflammation and cardiac fibrosis. Arterioscl Thromb Vasc Biol 2012; 32: 1675-1686.
- 8 Cheng J, Wang Y, Ma Y. et al. The mechanical stress-activated serum-, glucocorticoid-regulated kinase 1 contributes to neointima formation in vein grafts. Circ Res 2010; 107: 1265-1274.
- 9 BelAiba RS, Djordjevic T, Bonello S. et al. The serum- and glucocorticoid-inducible kinase Sgk-1 is involved in pulmonary vascular remodeling: role in redox-sensitive regulation of tissue factor by thrombin. Circ Res 2006; 98: 828-836.
- 10 Borst O, Schaub M, Walker B. et al. Pivotal role of serum- and glucocorticoid-inducible kinase 1 in vascular inflammation and atherogenesis. Arterioscl Thromb Vasc Biol 2015; 35: 547-557.
- 11 Lang F, Munzer P, Gawaz M. et al. Regulation of STIM1/Orai1-dependent Ca2+ signalling in platelets. Thromb Haemost 2013; 110: 925-930.
- 12 Walker B, Schmid E, Russo A. et al. Impact of the serum- and glucocorticoid-inducible kinase 1 on platelet dense granule biogenesis and secretion. J Thromb Haemost 2015; 13: 1325-1334.
- 13 Bisaillon JM, Motiani RK, Gonzalez-Cobos JC. et al. Essential role for STIM1/Orai1-mediated calcium influx in PDGF-induced smooth muscle migration. Am J Physiol Cell Pphysiol 2010; 298: C993-1005.
- 14 Zhang W, Halligan KE, Zhang X. et al. Orai1-mediated I (CRAC) is essential for neointima formation after vascular injury. Circ Res 2011; 109: 534-542.
- 15 Aubart FC, Sassi Y, Coulombe A. et al. RNA interference targeting STIM1 suppresses vascular smooth muscle cell proliferation and neointima formation in the rat. Mol Therapy 2009; 17: 455-462.
- 16 Kumar A, Lindner V. Remodeling with neointima formation in the mouse carotid artery after cessation of blood flow. Arterioscl Thromb Vasc Biol 1997; 17: 2238-2244.
- 17 Furgeson SB, Simpson PA, Park I. et al. Inactivation of the tumour suppressor, PTEN, in smooth muscle promotes a pro-inflammatory phenotype and enhances neointima formation. Cardiovasc Res 2010; 86: 274-282.
- 18 Yoshida T, Yamashita M, Horimai C. et al. Smooth muscle-selective inhibition of nuclear factor-kappaB attenuates smooth muscle phenotypic switching and neointima formation following vascular injury. J Am Heart Assoc 2013; 02: e000230.
- 19 Schonberger T, Siegel-Axel D, Bussl R. et al. The immunoadhesin glycoprotein VI-Fc regulates arterial remodelling after mechanical injury in ApoE-/- mice. Cardiovasc Res 2008; 80: 131-137.
- 20 Zhong W, Oguljahan B, Xiao Y. et al. Serum and glucocorticoid-regulated kinase 1 promotes vascular smooth muscle cell proliferation via regulation of beta-catenin dynamics. Cell Signal 2014; 26: 2765-2772.
- 21 Sun JY, Li C, Shen ZX. et al. Mineralocorticoid Receptor Deficiency in Macrophages Inhibits Neointimal Hyperplasia and Suppresses Macrophage Inflammation Through SGK1-AP1/NF-kappaB Pathways. Arterioscl Thromb Vasc Biol 2016; 36: 874-885.
- 22 Eylenstein A, Schmidt S, Gu S. et al. Transcription factor NF-kappaB regulates expression of pore-forming Ca2+ channel unit, Orai1, and its activator, STIM1, to control Ca2+ entry and affect cellular functions. J Biol Chem 2012; 287: 2719-2730.
- 23 Cercek B, Yamashita M, Dimayuga P. et al. Nuclear factor-kappaB activity and arterial response to balloon injury. Atherosclerosis 1997; 131: 59-66.