Beta2 integrin modulates platelet caspase activation and life span in mice.
Eur J Cell Biol
; 80(2): 171-7, 2001 Feb.
Article
en En
| MEDLINE
| ID: mdl-11302522
We explored the role of CD18 (beta2 integrin) in platelet physiology, using mice genetically deficient in CD18 (CD18 -/-), or its main ligand CD54 (ICAM-1, CD54 -/-). CD18 and CD11a were evident in platelets from +/+, but not from CD18 -/- mice, as seen by immunofluorescence or Western blots. CD18 mRNA was also detectable by RT-PCR in platelets from +/+, but not from CD18 -/- mice. The life span of platelets was significantly shorter in CD18 -/- than in +/+ or CD54 -/- mice, as seen by in vivo biotinylation. When a local inflammation was elicited by the intra-tracheal injection of TNF, labeled platelets from +/+, but not from CD18 -/- donors, did localize in the lung. The content of Bcl-3 was about 20-fold higher in platelet from CD18 -/-, than in those from +/+ or CD54 -/- donors, as seen on Western blots or by immunofluorescence and flow cytometry, while the amount of pro-caspase-3 was decreased. An activation of caspases in platelets from CD18 -/- was also evidenced by protease assays. Accordingly, gelsolin, a protein cleaved by caspase-3, showed a low-molecular-weight band in platelets from CD18 -/- but not from +/+ donors. These results demonstrate that the beta2 integrin, present in mouse platelets, modulates caspase activation and consequently platelet life span and response to TNF.
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Colección:
01-internacional
Base de datos:
MEDLINE
Asunto principal:
Plaquetas
/
Antígenos CD18
/
Caspasas
Límite:
Animals
Idioma:
En
Revista:
Eur J Cell Biol
Año:
2001
Tipo del documento:
Article
País de afiliación:
Suiza
Pais de publicación:
Alemania