Homozygous loss of mouse tetraspanin CD82 enhances integrin αIIbß3 expression and clot retraction in platelets.
Exp Cell Res
; 339(2): 261-9, 2015 Dec 10.
Article
en En
| MEDLINE
| ID: mdl-26562164
Integrin αIIbß3 is critical for platelet-mediated blood clotting. Tetraspanins are well-established regulators of integrins and genetic loss of tetraspanin CD151 or TSSC6 in mice leads to increased bleeding due to inadequate integrin αIIbß3 outside-in signaling. Conversely, mild but enhanced integrin αIIbß3 activation and hyperaggregation is observed in CD9 and CD63 null mice respectively. CD82 is reportedly expressed in platelets; however its function is unknown. Using genetically engineered CD82 null mice, we investigated the role of the tetraspanin CD82 in platelet activation. Loss of CD82 resulted in reduced bleed times in vivo. CD82 was present on the surface of both human and mouse platelets, and its levels did not change upon platelet activation or degranulation. No differences in platelet activation, degranulation, or aggregation in response to ADP or collagen were detected in CD82 null mice. However, the kinetics of clot retraction was enhanced, which was intrinsic to the CD82-null platelets. Integrin αIIbß3 surface expression was elevated on the platelets from CD82 null mice and they displayed enhanced adhesion and tyrosine kinase signaling on fibrinogen. This is the first report on CD82 function in platelets; which we found intrinsically modulates clot retraction, integrin αIIbß3 expression, cell adhesion, and tyrosine signaling.
Palabras clave
Texto completo:
1
Colección:
01-internacional
Base de datos:
MEDLINE
Asunto principal:
Plaquetas
/
Retracción del Coagulo
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Complejo GPIIb-IIIa de Glicoproteína Plaquetaria
/
Proteína Kangai-1
Límite:
Animals
/
Humans
Idioma:
En
Revista:
Exp Cell Res
Año:
2015
Tipo del documento:
Article
Pais de publicación:
Estados Unidos