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The calcium sensor ...
The calcium sensor STIM1 is an essential mediator of arterial thrombosis and ischemic brain infarction
- Article/chapterEnglish2008
Publisher, publication year, extent ...
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2008-06-16
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Rockefeller University Press,2008
Numbers
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LIBRIS-ID:oai:prod.swepub.kib.ki.se:117493249
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http://kipublications.ki.se/Default.aspx?queryparsed=id:117493249URI
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https://doi.org/10.1084/jem.20080302DOI
Supplementary language notes
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Language:English
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Summary in:English
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Subject category:ref swepub-contenttype
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Subject category:art swepub-publicationtype
Notes
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Platelet activation and aggregation are essential to limit posttraumatic blood loss at sites of vascular injury but also contributes to arterial thrombosis, leading to myocardial infarction and stroke. Agonist-induced elevation of [Ca2+]i is a central step in platelet activation, but the underlying mechanisms are not fully understood. A major pathway for Ca2+ entry in nonexcitable cells involves receptor-mediated release of intracellular Ca2+ stores, followed by activation of store-operated calcium (SOC) channels in the plasma membrane. Stromal interaction molecule 1 (STIM1) has been identified as the Ca2+ sensor in the endoplasmic reticulum (ER) that activates Ca2+ release–activated channels in T cells, but its role in mammalian physiology is unknown. Platelets express high levels of STIM1, but its exact function has been elusive, because these cells lack a normal ER and Ca2+ is stored in a tubular system referred to as the sarcoplasmatic reticulum. We report that mice lacking STIM1 display early postnatal lethality and growth retardation. STIM1-deficient platelets have a marked defect in agonist-induced Ca2+ responses, and impaired activation and thrombus formation under flow in vitro. Importantly, mice with STIM1-deficient platelets are significantly protected from arterial thrombosis and ischemic brain infarction but have only a mild bleeding time prolongation. These results establish STIM1 as an important mediator in the pathogenesis of ischemic cardio- and cerebrovascular events.
Added entries (persons, corporate bodies, meetings, titles ...)
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Braun, A
(author)
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Kleinschnitz, C
(author)
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Bender, M
(author)
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Pleines, I
(author)
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Pham, M
(author)
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Renne, TKarolinska Institutet
(author)
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Stoll, G
(author)
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Nieswandt, B
(author)
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Karolinska Institutet
(creator_code:org_t)
Related titles
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In:The Journal of experimental medicine: Rockefeller University Press205:7, s. 1583-15911540-95380022-1007
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