Store-operated calcium entry in thrombosis and thrombo-inflammation

Elmina Mammadova-Bach; Magdolna Nagy; Johan W. M. Heemskerk; Bernhard Nieswandt; Attila Braun

doi:10.1016/j.ceca.2018.11.005

Store-operated calcium entry in thrombosis and thrombo-inflammation

Elmina Mammadova-Bach, Magdolna Nagy, Johan W. M. Heemskerk, Bernhard Nieswandt^*, Attila Braun^*

^*Corresponding author for this work

Research output: Contribution to journal › (Systematic) Review article › peer-review

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.

Original language	English
Pages (from-to)	39-48
Number of pages	10
Journal	Cell Calcium
Volume	77
DOIs	https://doi.org/10.1016/j.ceca.2018.11.005
Publication status	Published - Jan 2019

Keywords

SOCE
Platelets
Immune cells
Arterial thrombosis
Ischemic stroke
Thrombo-inflammation
REGULATORY T-CELLS
CA2+ ENTRY
ARTERIAL THROMBOSIS
HUMAN PLATELETS
CRAC CHANNEL
ISCHEMIC-STROKE
TRP CHANNELS
NEUTROPHIL RECRUITMENT
EFFECTOR FUNCTIONS
GLYCOPROTEIN VI

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10.1016/j.ceca.2018.11.005

Cite this

@article{b6b0f9eaa6444d7db09fbe8cb88c2fd0,

title = "Store-operated calcium entry in thrombosis and thrombo-inflammation",

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 = "SOCE, Platelets, Immune cells, Arterial thrombosis, Ischemic stroke, Thrombo-inflammation, REGULATORY T-CELLS, CA2+ ENTRY, ARTERIAL THROMBOSIS, HUMAN PLATELETS, CRAC CHANNEL, ISCHEMIC-STROKE, TRP CHANNELS, NEUTROPHIL RECRUITMENT, EFFECTOR FUNCTIONS, GLYCOPROTEIN VI",

author = "Elmina Mammadova-Bach and Magdolna Nagy and Heemskerk, {Johan W. M.} and Bernhard Nieswandt and Attila Braun",

note = "Funding Information: E.M.B., B.N. and A.B. are supported by the Deutsche Forschungsgemeinschaft (SFB/TR 240). M.N. and J.W.M.H. acknowledge support from the Cardiovascular Center (HVC) , Maastricht University Medical Center + , and the 5 th Meuse-Rhine Interregional Programme Polyvalve . Publisher Copyright: {\textcopyright} 2018 Elsevier Ltd",

year = "2019",

month = jan,

doi = "10.1016/j.ceca.2018.11.005",

language = "English",

volume = "77",

pages = "39--48",

journal = "Cell Calcium",

issn = "0143-4160",

publisher = "ELSEVIER SCI LTD",

}

TY - JOUR

T1 - Store-operated calcium entry in thrombosis and thrombo-inflammation

AU - Mammadova-Bach, Elmina

AU - Nagy, Magdolna

AU - Heemskerk, Johan W. M.

AU - Nieswandt, Bernhard

AU - Braun, Attila

N1 - Funding Information: E.M.B., B.N. and A.B. are supported by the Deutsche Forschungsgemeinschaft (SFB/TR 240). M.N. and J.W.M.H. acknowledge support from the Cardiovascular Center (HVC) , Maastricht University Medical Center + , and the 5 th Meuse-Rhine Interregional Programme Polyvalve . Publisher Copyright: © 2018 Elsevier Ltd

PY - 2019/1

Y1 - 2019/1

N2 - 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.

AB - 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.

KW - SOCE

KW - Platelets

KW - Immune cells

KW - Arterial thrombosis

KW - Ischemic stroke

KW - Thrombo-inflammation

KW - REGULATORY T-CELLS

KW - CA2+ ENTRY

KW - ARTERIAL THROMBOSIS

KW - HUMAN PLATELETS

KW - CRAC CHANNEL

KW - ISCHEMIC-STROKE

KW - TRP CHANNELS

KW - NEUTROPHIL RECRUITMENT

KW - EFFECTOR FUNCTIONS

KW - GLYCOPROTEIN VI

U2 - 10.1016/j.ceca.2018.11.005

DO - 10.1016/j.ceca.2018.11.005

M3 - (Systematic) Review article

C2 - 30530092

SN - 0143-4160

VL - 77

SP - 39

EP - 48

JO - Cell Calcium

JF - Cell Calcium

ER -