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Membrane attack complex inhibitor CD59a protects against focal cerebral ischemia in mice

MPG-Autoren
http://pubman.mpdl.mpg.de/cone/persons/resource/persons50445

Nietfeld,  W.
Dept. of Vertebrate Genomics (Head: Hans Lehrach), Max Planck Institute for Molecular Genetics, Max Planck Society;

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Harhausen.pdf
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Zitation

Harhausen, D., Khojasteh, U., Stahel, P. F., Morgan, B. P., Nietfeld, W., Dirnagl, U., et al. (2010). Membrane attack complex inhibitor CD59a protects against focal cerebral ischemia in mice. Journal of Neuroinflammation, 7, 7:15-7:15. doi:10.1186/1742-2094-7-15.


Zitierlink: http://hdl.handle.net/11858/00-001M-0000-0010-7C84-6
Zusammenfassung
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.