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Dimethylarginine dimethylaminohydrolase-1 transgenic mice are not protected from ischaemic stroke due to a ceiling effect of enzymatic activity in brain

F Leypoldt, M Gelderblom, CU Choe, EC von Leitner, D Atzler, E Schwedhelm, C Gerloff, C Sydow, R Böger, T Magnus · Aktuelle Neurologie · 2009 · Heft 10

Dokument
916473
CareLit-ID
Jahr
2009
Publikation
PDF
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Metadaten
DOI
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Bibliografische Angaben

Zeitschrift
Aktuelle Neurologie
Autor:innen
F Leypoldt, M Gelderblom, CU Choe, EC von Leitner, D Atzler, E Schwedhelm, C Gerloff, C Sydow, R Böger, T Magnus
Ausgabe
Heft 10 / 2009
Seiten
–
Erschienen: 2009-10-07 00:00:00
ISSN
0302-4350

Zusammenfassung

Background and Purpose: Methylated arginines are endogenous analogues of L-arginine, the substracte for NO synthase. Asymmetric dimethylarginine (ADMA) interferes with nitric oxide (NO) formation, causing endothelial dysfunction. ADMA is a predictor of cardiovascular events and mortality in humans. It is eliminated primarily by enzymatic activity of dimethylarginine dimethylaminohydrolase (DDAH). Methods: We investigated whether human DDAH-1 (hDDAH-1) transgenicity protects from ischemic tissue damage in temporary middle cerebral artery occlusion (tMCAO) in mice. Results: Infarct sizes did not significantly diff…

Schlagworte

Aktuelle Neurologie