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dc.contributor.author
Cao, Hang
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Qadri, Syed M.
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Lang, Elisabeth
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Pelzl, Lisann
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Umbach, Anja T.
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Leiss, Veronika
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Birnbaumer, Lutz
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Nürnberg, Bernd
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Pieske, Burkert
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Voelkl, Jakob
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Gawaz, Meinrad
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Bissinger, Rosi
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Lang, Florian
dc.date.available
2020-03-13T14:14:07Z
dc.date.issued
2018-09
dc.identifier.citation
Cao, Hang; Qadri, Syed M.; Lang, Elisabeth; Pelzl, Lisann; Umbach, Anja T.; et al.; Heterotrimeric G-protein subunit Gαi2 contributes to agonist-sensitive apoptosis and degranulation in murine platelets; American Physiological Society; Physiological Reports; 6; 17; 9-2018; 1-8
dc.identifier.issn
2051-817X
dc.identifier.uri
http://hdl.handle.net/11336/99447
dc.description.abstract
Gαi2, a heterotrimeric G-protein subunit, regulates various cell functions including ion channel activity, cell differentiation, proliferation and apoptosis. Platelet-expressed Gαi2 is decisive for the extent of tissue injury following ischemia/reperfusion. However, it is not known whether Gαi2 plays a role in the regulation of platelet apoptosis, which is characterized by caspase activation, cell shrinkage and cell membrane scrambling with phosphatidylserine (PS) translocation to the platelet surface. Stimulators of platelet apoptosis include thrombin and collagen-related peptide (CoRP), which are further known to enhance degranulation and activation of αII bβ3-integrin and caspases. Using FACS analysis, we examined the impact of agonist treatment on activation and apoptosis in platelets drawn from mice lacking Gαi2 and their wild-type (WT) littermates. As a result, treatment with either thrombin (0.01 U/mL) or CoRP (2 μg/mL or 5 μg/mL) significantly upregulated PS-exposure and significantly decreased forward scatter, reflecting cell size, in both genotypes. Exposure to CoRP triggered a significant increase in active caspase 3, ceramide formation, surface P-selectin, and αII bβ3-integrin activation. These molecular alterations were significantly less pronounced in Gαi2-deficient platelets as compared to WT platelets. In conclusion, our data highlight a previously unreported role of Gαi2 signaling in governing platelet activation and apoptosis.
dc.format
application/pdf
dc.language.iso
eng
dc.publisher
American Physiological Society
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dc.rights
info:eu-repo/semantics/openAccess
dc.rights.uri
https://creativecommons.org/licenses/by/2.5/ar/
dc.subject
APOPTOSIS
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DEGRANULATION
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G-PROTEIN
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GΑI2
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PLATELETS
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Biología Celular, Microbiología
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Ciencias Biológicas
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CIENCIAS NATURALES Y EXACTAS
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dc.title
Heterotrimeric G-protein subunit Gαi2 contributes to agonist-sensitive apoptosis and degranulation in murine platelets
dc.type
info:eu-repo/semantics/article
dc.type
info:ar-repo/semantics/artículo
dc.type
info:eu-repo/semantics/publishedVersion
dc.date.updated
2020-03-10T12:21:28Z
dc.journal.volume
6
dc.journal.number
17
dc.journal.pagination
1-8
dc.journal.pais
Estados Unidos
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dc.description.fil
Fil: Cao, Hang. Universität Tübingen; Alemania
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Fil: Qadri, Syed M.. Canadian Blood Services; Canadá. McMaster University; Canadá
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Fil: Lang, Elisabeth. Heinrich-heine-universität Düsseldorf; Alemania
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Fil: Pelzl, Lisann. Universität Tübingen; Alemania
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Fil: Umbach, Anja T.. Universität Tübingen; Alemania
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Fil: Leiss, Veronika. Universität Tübingen; Alemania
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Fil: Birnbaumer, Lutz. National Institutes of Health; Estados Unidos. Pontificia Universidad Católica Argentina "Santa María de los Buenos Aires". Instituto de Investigaciones Biomédicas. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Biomédicas; Argentina
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Fil: Nürnberg, Bernd. Universität Tübingen; Alemania
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Fil: Pieske, Burkert. Berlin Institute of Health; Alemania. Universitätsmedizin Berlin; Alemania
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Fil: Voelkl, Jakob. Berlin Institute of Health; Alemania. Universitätsmedizin Berlin; Alemania
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Fil: Gawaz, Meinrad. Universität Tübingen; Alemania
dc.description.fil
Fil: Bissinger, Rosi. Universität Tübingen; Alemania
dc.description.fil
Fil: Lang, Florian. Universität Tübingen; Alemania. Heinrich-heine-universität Düsseldorf; Alemania
dc.journal.title
Physiological Reports
dc.relation.alternativeid
info:eu-repo/semantics/altIdentifier/url/https://physoc.onlinelibrary.wiley.com/doi/full/10.14814/phy2.13841
dc.relation.alternativeid
info:eu-repo/semantics/altIdentifier/doi/http://dx.doi.org/10.14814/phy2.13841
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