Einfluss von Cyclooxygenase-2-abhängigen Prostanoiden und deren Rezeptoren auf die Hirnschädigung nach ischämischem Schlaganfall

• Antragsteller: Dr. Alexander Kunz
• Fachliche Zuordnung: Molekulare Biologie und Physiologie von Nerven- und Gliazellen
• Förderung: Förderung von 2005 bis 2006
• Projektkennung: Deutsche Forschungsgemeinschaft (DFG) - Projektnummer 5455980

• Erstellungsjahr: 2008

Zusammenfassung der Projektergebnisse

Keine Zusammenfassung vorhanden

Projektbezogene Publikationen (Auswahl)

• Biphasic temporal profile of free radical production after transient focal cerebral ischemia. Soc Neurosci Abstr. 2004;30
  Cho S, Kunz A, Kawano T, Park EM, Anrather J, Frys K, Iadecola C
  
• Cyclooxygenase-2 does not contribute to post-ischemic production of reactive oxygen species. Soc Neurosci Abstr. 2005;31
  Kunz A, Orio M, Anrather J, Zhou P, Iadecola C
  
• Mechanisms of cyclooxygenase-2 mediated neurotoxicity. In: Krieglstein J, Klumpp S, eds. Pharmacology of cerebral ischemia. Stuttgart, Germany: Medpharm Scientific Publishers; 2005:173-183
  Anrather J, Iadecola C, Kawano T, Kunz A, Ross ME, Wang G, Zhou P
  
• Lipopolysaccharide induces early tolerance to excitotoxicity via nitric oxide and cgmp. Soc Neurosci Abstr. 2006;32
  Orio M, Kunz A, Kawano T, Zhou P, Anrather J, Iadecola C
  
• No produced by inos mediates lipopolysaccharide-induced tolerance to excitotoxic brain injury in vivo. Soc Neurosci Abstr. 2006;32
  Kawano T, Anrather J, Kunz A, Zhou P, Iadecola C
  
• Prostaglandin e2 ep1 receptors: Downstream effectors of cox-2 neurotoxicity. Nat Med. 2006;12:225-229
  Kawano T, Anrather J, Zhou P, Park L, Wang G, Frys KA, Kunz A, Cho S, Orio M, Iadecola C
  
• Vasoprotective effect of inducible nitric oxide synthase in ischemic preconditioning. Soc Neurosci Abstr. 2006;32
  Kunz A, Park L, Abe T, Anrather J, Zhou P, Iadecola C
  
• Vasoprotective effect of inducible nitric oxide synthase in ischemic tolerance. Stroke. 2006;37:629
  Kunz A, Park L, Anrather J, Zhou P, Iadecola C
  
• Cyclooxygenase-2 does not contribute to postischemic production of reactive oxygen species. J Cereb Blood Flow Metab. 2007;27:545-551
  Kunz A, Anrather J, Zhou P, Orio M, Iadecola C
  
• Inos-derived no and nox2-derived superoxide confer tolerance to excitotoxic brain injury through peroxynitrite. J Cereb Blood Flow Metab. 2007;27:1453-1462
  Kawano T, Kunz A, Abe T, Girouard H, Anrather J, Zhou P, Iadecola C
  
• Key role of the scavenger receptor cd36 in post-ischemic inflammation and ischemic brain injury. Soc Neurosci Abstr. 2007;33
  Kunz A, Abe T, Hochrainer K, Anrather J, Zhou P, Iadecola C
  
• Lipopolysaccharide induces early tolerance to excitotoxicity via nitric oxide and cgmp. Stroke. 2007;38:2812-2817
  Orio M, Kunz A, Kawano T, Anrather J, Zhou P, Iadecola C
  
• Neurovascular protection by ischemic tolerance: Role of nitric oxide and reactive oxygen species. J Neurosci. 2007;27:7083-7093
  Kunz A, Park L, Abe T, Gallo EF, Anrather J, Zhou P, Iadecola C
  
• The neuroprotective effect of ep1 receptor inhibition is sustained in time, has a wide therapeutic window and is present both in male and female mice. Soc Neurosci Abstr. 2007;33
  Abe T, Kunz A, Shimamura M, Zhou P, Anrather J, Iadecola C
  
• Vasoprotective effects of inos-derived no and nox2-derived superoxide in ischemic preconditioning. 23rd International Symposium on Cerebral Blood Flow, Metabolism and Function. 2007
  Kunz A, Park L, Abe T, Anrather J, Zhou P, Iadecola C