Please use this identifier to cite or link to this item: https://repositorio.uca.edu.ar/handle/123456789/8687
Título : Heterotrimeric G-protein subunit Gαi2 contributes to agonist-sensitive apoptosis and degranulation in murine platelets
Autor : Cao, Hang 
Qadri, Syed M. 
Lang, Elisabeth 
Pelzl, Lisann 
Umbach, Anja T. 
Leiss, Veronika 
Birnbaumer, Lutz 
Nürnberg, Bernd 
Pieske, Burkert 
Voelkl, Jakob 
Gawaz, Meinrad 
Bissinger, Rosi 
Lang, Florian 
Palabras clave : APOPTOSISCELULAS DE LA SANGREREPERFUSION MIOCARDICA
Fecha de publicación : 2018
Editorial : Wiley Open Access
American Physiological Society
Physiological Society
Cita : Cao H, Qadri SM, Lang E, et al. Heterotrimeric G-protein subunit Gαi2 contributes to agonist-sensitive apoptosis and degranulation in murine platelets [en línea]. Physiological Reports. 2018;6(17):e13841. doi:10.14814/phy2.13841 Disponible en: https://repositorio.uca.edu.ar/handle/123456789/8687
Resumen : 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 αIIb β3-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 αIIb β3-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.
URI : https://repositorio.uca.edu.ar/handle/123456789/8687
ISSN : 2051-817X
Disciplina: MEDICINA
DOI: 10.14814/phy2.13841
Derechos: Acceso Abierto
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