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Membrane attack complex inhibitor CD59a protects against focal cerebral ischemia in mice.
Harhausen, Denise; Khojasteh, Uldus; Stahel, Philip F; Morgan, B Paul; Nietfeld, Wilfried; Dirnagl, Ulrich; Trendelenburg, George.
Afiliación
  • Harhausen D; Experimentelle Neurologie, Charité-Universitätsmedizin Berlin, CCM, Berlin, Germany.
J Neuroinflammation ; 7: 15, 2010 Mar 04.
Article en En | MEDLINE | ID: mdl-20202211
BACKGROUND: The complement system is a crucial mediator of inflammation and cell lysis after cerebral ischemia. However, there is little information about the exact contribution of the membrane attack complex (MAC) and its inhibitor-protein CD59. METHODS: Transient focal cerebral ischemia was induced by middle cerebral artery occlusion (MCAO) in young male and female CD59a knockout and wild-type mice. Two models of MCAO were applied: 60 min MCAO and 48 h reperfusion, as well as 30 min MCAO and 72 h reperfusion. CD59a knockout animals were compared to wild-type animals in terms of infarct size, edema, neurological deficit, and cell death. RESULTS AND DISCUSSION: CD59a-deficiency in male mice caused significantly increased infarct volumes and brain swelling when compared to wild-type mice at 72 h after 30 min-occlusion time, whereas no significant difference was observed after 1 h-MCAO. Moreover, CD59a-deficient mice had impaired neurological function when compared to wild-type mice after 30 min MCAO. CONCLUSION: We conclude that CD59a protects against ischemic brain damage, but depending on the gender and the stroke model used.
Asunto(s)

Texto completo: 1 Bases de datos: MEDLINE Asunto principal: Antígenos CD59 / Infarto Encefálico / Infarto de la Arteria Cerebral Media Tipo de estudio: Etiology_studies / Prognostic_studies Límite: Animals Idioma: En Revista: J Neuroinflammation Asunto de la revista: NEUROLOGIA Año: 2010 Tipo del documento: Article País de afiliación: Alemania

Texto completo: 1 Bases de datos: MEDLINE Asunto principal: Antígenos CD59 / Infarto Encefálico / Infarto de la Arteria Cerebral Media Tipo de estudio: Etiology_studies / Prognostic_studies Límite: Animals Idioma: En Revista: J Neuroinflammation Asunto de la revista: NEUROLOGIA Año: 2010 Tipo del documento: Article País de afiliación: Alemania