Thrombocytopenia in an animal model of malaria is associated with an increased caspase-mediated death of thrombocytes.
Apoptosis
; 7(2): 91-8, 2002 Apr.
Article
en En
| MEDLINE
| ID: mdl-11865192
Infection of mice with Plasmodium Berghei Anka (PbA) leads to a thrombocytopenia, due to a reduced platelet life span, eventually associated with a syndrome of severe or cerebral malaria (CM). Thrombocytopenia was associated with an increase in the number of microparticles (mcp) in plasma. More than >60% of these mcp were of platelet origin, as seen by staining with an anti-platelet antibody. The thrombocytopenia and the amount of mcp were decreased in mice treated with anti CD40L mAb, suggesting that CD40L is the main effector of the thrombocytopenia. Caspase-1, -3, -6, -8, -9 were activated in platelets from infected mice, as seen by the binding of labeled probes or the amount of pro-caspase-3. Treatment of infected mice with the caspases inhibitor ZVAD-fmk decreased the number of mcp and the thrombocytopenia, showing that platelet caspases are responsible for platelet fragmentation. In addition, the caspase inhibitor also caused a decrease in the mortality associated with CM, indicating a critical role of caspases in the expression of CM.
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Colección:
01-internacional
Base de datos:
MEDLINE
Asunto principal:
Trombocitopenia
/
Plaquetas
/
Malaria
Tipo de estudio:
Prognostic_studies
/
Risk_factors_studies
Límite:
Animals
Idioma:
En
Revista:
Apoptosis
Año:
2002
Tipo del documento:
Article
País de afiliación:
Suiza
Pais de publicación:
Países Bajos