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Article: CD44 sensitivity of platelet activation, membrane scrambling and adhesion under high arterial shear rates

TitleCD44 sensitivity of platelet activation, membrane scrambling and adhesion under high arterial shear rates
Authors
KeywordsThrombus formation
Platelet activation
CD44
Cytosolic Ca concentration 2+
Phosphatidylserine translocation
Issue Date2016
Citation
Thrombosis and Haemostasis, 2016, v. 115, n. 1, p. 99-108 How to Cite?
Abstract© Schattauer 2016. CD44 is required for signalling of macrophage migration inhibitory factor (MIF), an anti-apoptotic pro-inflammatory cytokine. MIF is expressed and released from blood platelets, key players in the orchestration of occlusive vascular disease. Nothing is known about a role of CD44 in the regulation of platelet function. The present study thus explored whether CD44 modifies degranulation (P-selectin exposure), integrin activation, caspase activity, phosphatidylserine exposure on the platelet surface, platelet volume, Orai1 protein abundance and cytosolic Ca2+-activity ([Ca2+]i). Platelets from mice lacking CD44 (cd44-/-) were compared to platelets from corresponding wild-type mice (cd44+/+). In resting platelets, P-selectin abundance, αIIbβ3 integrin activation, caspase-3 activity and phosphatidylserine exposure were negligible in both genotypes and Orai1 protein abundance, [Ca2+]i, and volume were similar in cd44-/- and cd44+/+ platelets. Platelet degranulation and αIIbβ3 integrin activation were significantly increased by thrombin (0.02 U/ml), collagen related peptide (CRP, 2 μg/ml and Ca2+-store depletion with thapsigargin (1 μM), effects more pronounced in cd44-/-than in cd44+/+ platelets. Thrombin (0.02 U/ml) increased platelet [Ca2+]i, caspase-3 activity, phosphatidylserine exposure and Orai1 surface abundance, effects again significantly stronger in cd44-/-than in cd44+/+ platelets. Thrombin further decreased forward scatter in cd44-/-and cd44+/+ platelets, an effect which tended to be again more pronounced in cd44-/-than in cd44+/+ platelets. Platelet adhesion and in vitro thrombus formation under high arterial shear rates (1,700 s-1) were significantly augmented in cd44-/-mice. In conclusion, genetic deficiency of CD44 augments activation, apoptosis and prothrombotic potential of platelets.
Persistent Identifierhttp://hdl.handle.net/10722/292921
ISSN
2023 Impact Factor: 5.0
2023 SCImago Journal Rankings: 1.248
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorLiu, Guilai-
dc.contributor.authorLiu, Guoxing-
dc.contributor.authorAlzoubi, Kousi-
dc.contributor.authorChatterjee, Madhumita-
dc.contributor.authorWalker, Britta-
dc.contributor.authorMünzer, Patrick-
dc.contributor.authorLuo, Dong-
dc.contributor.authorUmbach, Anja T.-
dc.contributor.authorElvira, Bernat-
dc.contributor.authorChen, Hong-
dc.contributor.authorVoelkl, Jakob-
dc.contributor.authorFöller, Michael-
dc.contributor.authorMak, Tak W.-
dc.contributor.authorBorst, Oliver-
dc.contributor.authorGawaz, Meinrad-
dc.contributor.authorLang, Florian-
dc.date.accessioned2020-11-17T14:57:30Z-
dc.date.available2020-11-17T14:57:30Z-
dc.date.issued2016-
dc.identifier.citationThrombosis and Haemostasis, 2016, v. 115, n. 1, p. 99-108-
dc.identifier.issn0340-6245-
dc.identifier.urihttp://hdl.handle.net/10722/292921-
dc.description.abstract© Schattauer 2016. CD44 is required for signalling of macrophage migration inhibitory factor (MIF), an anti-apoptotic pro-inflammatory cytokine. MIF is expressed and released from blood platelets, key players in the orchestration of occlusive vascular disease. Nothing is known about a role of CD44 in the regulation of platelet function. The present study thus explored whether CD44 modifies degranulation (P-selectin exposure), integrin activation, caspase activity, phosphatidylserine exposure on the platelet surface, platelet volume, Orai1 protein abundance and cytosolic Ca2+-activity ([Ca2+]i). Platelets from mice lacking CD44 (cd44-/-) were compared to platelets from corresponding wild-type mice (cd44+/+). In resting platelets, P-selectin abundance, αIIbβ3 integrin activation, caspase-3 activity and phosphatidylserine exposure were negligible in both genotypes and Orai1 protein abundance, [Ca2+]i, and volume were similar in cd44-/- and cd44+/+ platelets. Platelet degranulation and αIIbβ3 integrin activation were significantly increased by thrombin (0.02 U/ml), collagen related peptide (CRP, 2 μg/ml and Ca2+-store depletion with thapsigargin (1 μM), effects more pronounced in cd44-/-than in cd44+/+ platelets. Thrombin (0.02 U/ml) increased platelet [Ca2+]i, caspase-3 activity, phosphatidylserine exposure and Orai1 surface abundance, effects again significantly stronger in cd44-/-than in cd44+/+ platelets. Thrombin further decreased forward scatter in cd44-/-and cd44+/+ platelets, an effect which tended to be again more pronounced in cd44-/-than in cd44+/+ platelets. Platelet adhesion and in vitro thrombus formation under high arterial shear rates (1,700 s-1) were significantly augmented in cd44-/-mice. In conclusion, genetic deficiency of CD44 augments activation, apoptosis and prothrombotic potential of platelets.-
dc.languageeng-
dc.relation.ispartofThrombosis and Haemostasis-
dc.subjectThrombus formation-
dc.subjectPlatelet activation-
dc.subjectCD44-
dc.subjectCytosolic Ca concentration 2+-
dc.subjectPhosphatidylserine translocation-
dc.titleCD44 sensitivity of platelet activation, membrane scrambling and adhesion under high arterial shear rates-
dc.typeArticle-
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1160/TH14-10-0847-
dc.identifier.pmid26355696-
dc.identifier.scopuseid_2-s2.0-84951287078-
dc.identifier.volume115-
dc.identifier.issue1-
dc.identifier.spage99-
dc.identifier.epage108-
dc.identifier.isiWOS:000367265000012-
dc.identifier.issnl0340-6245-

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