Download PDF
Thromb Haemost 2017; 117(05): 1002-1005
DOI: 10.1160/TH16-09-0690
Letter to the Editor
Schattauer GmbH

SGK1 up-regulates Orai1 expression and VSMC migration during neointima formation after arterial injury

Britta Walker-Allgaier   *
1   Department of Cardiology and Cardiovascular Medicine, University of Tübingen, Germany
,
Malte Schaub   *
1   Department of Cardiology and Cardiovascular Medicine, University of Tübingen, Germany
,
Ioana Alesutan
2   Department of Physiology, University of Tübingen, Germany
3   Department of Internal Medicine and Cardiology, Charité University Medicine, Campus Virchow Klinikum, Charité-Center for Cardiovascular Research (CCR), Berlin, Germany
4   Berlin Institute of Health (BIH), Berlin, Germany
,
Jakob Voelkl
2   Department of Physiology, University of Tübingen, Germany
3   Department of Internal Medicine and Cardiology, Charité University Medicine, Campus Virchow Klinikum, Charité-Center for Cardiovascular Research (CCR), Berlin, Germany
,
Sascha Geue
1   Department of Cardiology and Cardiovascular Medicine, University of Tübingen, Germany
,
Patrick Münzer
1   Department of Cardiology and Cardiovascular Medicine, University of Tübingen, Germany
,
José M. Rodríguez
5   Laboratory of Biochemical Genetics and Metabolism, The Rockefeller University of New York, New York, USA
,
Dietmar Kuhl
6   Center for Molecular Neurobiology (ZMNH), Institute for Molecular and Cellular Cognition (IMCC), University Medical Center Hamburg-Eppendorf (UKE), Germany
,
Florian Lang
2   Department of Physiology, University of Tübingen, Germany
,
Meinrad Gawaz
1   Department of Cardiology and Cardiovascular Medicine, University of Tübingen, Germany
,
Oliver Borst
1   Department of Cardiology and Cardiovascular Medicine, University of Tübingen, Germany
› Author Affiliations
Further Information

Publication History

Received: 07 September 2016

Accepted after major revision: 23 January 2017

Publication Date:
13 November 2017 (online)

    Permissions and Reprints

Supplementary Material to this article is available online at www.thrombosis-online.com

* Both authors contributed equally.


 

  • 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.
    Article in Thieme ConnectPubMedGoogle Scholar
  • 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.
    Article in Thieme ConnectPubMedGoogle Scholar
  • 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.
    CrossrefPubMedGoogle Scholar
  • 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.
    CrossrefPubMedGoogle Scholar
  • 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.
    CrossrefPubMedGoogle Scholar
  • 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.
    CrossrefPubMedGoogle Scholar
  • 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.
    CrossrefPubMedGoogle Scholar
  • 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.
    CrossrefPubMedGoogle Scholar
  • 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.
    CrossrefPubMedGoogle Scholar
  • 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.
    CrossrefPubMedGoogle Scholar
  • 11 Lang F, Munzer P, Gawaz M. et al. Regulation of STIM1/Orai1-dependent Ca2+ signalling in platelets. Thromb Haemost 2013; 110: 925-930.
    Article in Thieme ConnectPubMedGoogle Scholar
  • 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.
    CrossrefPubMedGoogle Scholar
  • 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.
    PubMedGoogle Scholar
  • 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.
    CrossrefPubMedGoogle Scholar
  • 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.
    CrossrefPubMedGoogle Scholar
  • 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.
    CrossrefPubMedGoogle Scholar
  • 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.
    CrossrefPubMedGoogle Scholar
  • 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.
    PubMedGoogle Scholar
  • 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.
    CrossrefPubMedGoogle Scholar
  • 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.
    CrossrefPubMedGoogle Scholar
  • 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.
    CrossrefPubMedGoogle Scholar
  • 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.
    CrossrefPubMedGoogle Scholar
  • 23 Cercek B, Yamashita M, Dimayuga P. et al. Nuclear factor-kappaB activity and arterial response to balloon injury. Atherosclerosis 1997; 131: 59-66.
    CrossrefPubMedGoogle Scholar