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Cell Calcium. 2019 Jan;77:39-48. doi: 10.1016/j.ceca.2018.11.005. Epub 2018 Nov 23.

Store-operated calcium entry in thrombosis and thrombo-inflammation.

Author information

1
Institute of Experimental Biomedicine, University Hospital and Rudolf Virchow Centre, University of Würzburg, Würzburg, Germany.
2
Department of Biochemistry, Cardiovascular Research Institute Maastricht (CARIM), Maastricht University, Maastricht, the Netherlands.
3
Institute of Experimental Biomedicine, University Hospital and Rudolf Virchow Centre, University of Würzburg, Würzburg, Germany. Electronic address: bernhard.nieswandt@virchow.uni-wuerzburg.de.
4
Institute of Experimental Biomedicine, University Hospital and Rudolf Virchow Centre, University of Würzburg, Würzburg, Germany. Electronic address: attila.braun@virchow.uni-wuerzburg.de.

Abstract

Cytosolic free calcium (Ca2+) is a second messenger regulating a wide variety of functions in blood cells, including adhesion, activation, proliferation and migration. Store-operated Ca2+ entry (SOCE), triggered by depletion of Ca2+ from the endoplasmic reticulum, provides a main mechanism of regulated Ca2+ influx in blood cells. SOCE is mediated and regulated by isoforms of the ion channel proteins ORAI and TRP, and the transmembrane Ca2+ sensors stromal interaction molecules (STIMs), respectively. This report provides an overview of the (patho)physiological importance of SOCE in blood cells implicated in thrombosis and thrombo-inflammation, i.e. platelets and immune cells. We also discuss the physiological consequences of dysregulated SOCE in platelets and immune cells and the potential of SOCE inhibition as a therapeutic option to prevent or treat arterial thrombosis as well as thrombo-inflammatory disease states such as ischemic stroke.

KEYWORDS:

Arterial thrombosis; Immune cells; Ischemic stroke; Platelets; SOCE; Thrombo-inflammation

PMID:
30530092
DOI:
10.1016/j.ceca.2018.11.005

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