Nitro-Fatty Acid Inhibition of Neointima Formation After Endoluminal Vessel Injury

RATIONALE:Fatty acid nitroalkenes are endogenously generated electrophilic byproducts of nitric oxide and nitrite-dependent oxidative inflammatory reactions. Existing evidence indicates nitroalkenes support posttranslational protein modifications and transcriptional activation that promote the resol...

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Veröffentlicht in:Circulation research 2009-11, Vol.105 (10), p.965-972
Hauptverfasser: Cole, Marsha P, Rudolph, Tanja K, Khoo, Nicholas K.H, Motanya, Uche N, Golin-Bisello, Franca, Wertz, Jeffrey W, Schopfer, Francisco J, Rudolph, Volker, Woodcock, Steven R, Bolisetty, Subhashini, Ali, Muhammad S, Zhang, Jifeng, Chen, Y Eugene, Agarwal, Anupam, Freeman, Bruce A, Bauer, Philip M
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Sprache:eng
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Zusammenfassung:RATIONALE:Fatty acid nitroalkenes are endogenously generated electrophilic byproducts of nitric oxide and nitrite-dependent oxidative inflammatory reactions. Existing evidence indicates nitroalkenes support posttranslational protein modifications and transcriptional activation that promote the resolution of inflammation. OBJECTIVE:The aim of this study was to assess whether in vivo administration of a synthetic nitroalkene could elicit antiinflammatory actions in vivo using a murine model of vascular injury. METHODS AND RESULTS:The in vivo administration (21 days) of nitro-oleic acid (OA-NO2) inhibited neointimal hyperplasia after wire injury of the femoral artery in a murine model (OA-NO2 treatment resulted in reduced intimal area and intima to media ratio versus vehicle- or oleic acid (OA)-treated animals, P
ISSN:0009-7330
1524-4571
DOI:10.1161/CIRCRESAHA.109.199075