Nitro-Fatty Acid Inhibition of Neointima Formation After Endoluminal Vessel Injury
| العنوان: | Nitro-Fatty Acid Inhibition of Neointima Formation After Endoluminal Vessel Injury |
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| المؤلفون: | Francisco J. Schopfer, Franca Golin-Bisello, Y. Eugene Chen, Bruce A. Freeman, Nicholas K.H. Khoo, Jifeng Zhang, Subhashini Bolisetty, Philip M. Bauer, Anupam Agarwal, Muhammad Ali, Marsha P. Cole, Tanja K. Rudolph, Volker Rudolph, Uche N Motanya, Steven R. Woodcock, Jeffrey W. Wertz |
| المصدر: | Circulation Research. 105:965-972 |
| بيانات النشر: | Ovid Technologies (Wolters Kluwer Health), 2009. |
| سنة النشر: | 2009 |
| مصطلحات موضوعية: | Neointima, Smooth muscle cell migration, Physiology, Oleic Acids, Inflammation, Pharmacology, Nitric Oxide, Article, Gene Expression Regulation, Enzymologic, Nitric oxide, Mice, chemistry.chemical_compound, Cell Movement, In vivo, medicine, Animals, Mice, Knockout, Platelet-Derived Growth Factor, Neointimal hyperplasia, Nitro Compounds, medicine.disease, Rats, Up-Regulation, Femoral Artery, Heme oxygenase, medicine.anatomical_structure, chemistry, Biochemistry, Heme Oxygenase (Decyclizing), medicine.symptom, Tunica Intima, Cardiology and Cardiovascular Medicine, Oxidation-Reduction, Blood vessel |
| الوصف: | 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-NO 2 ) inhibited neointimal hyperplasia after wire injury of the femoral artery in a murine model (OA-NO 2 treatment resulted in reduced intimal area and intima to media ratio versus vehicle- or oleic acid (OA)-treated animals, P 2 in both cultured aortic smooth muscle cells and in vivo. Inhibition of HO by Sn(IV)-protoporphyrin or HO-1 small interfering RNA reversed OA-NO 2 –induced inhibition of platelet-derived growth factor-stimulated rat aortic smooth muscle cell migration. The upregulation of HO-1 expression also accounted for the antistenotic actions of OA-NO 2 in vivo, because inhibition of neointimal hyperplasia following femoral artery injury was abolished in HO-1 −/− mice (OA-NO 2 –treated wild-type versus HO-1 −/− mice, P =0.016). Conclusions : In summary, electrophilic nitro-fatty acids induce salutary gene expression and cell functional responses that are manifested by a clinically significant outcome, inhibition of neointimal hyperplasia induced by arterial injury. |
| تدمد: | 1524-4571 0009-7330 |
| الوصول الحر: | https://explore.openaire.eu/search/publication?articleId=doi_dedup___::798b702081514a205c103b90d679989bTest https://doi.org/10.1161/circresaha.109.199075Test |
| حقوق: | OPEN |
| رقم الانضمام: | edsair.doi.dedup.....798b702081514a205c103b90d679989b |
| قاعدة البيانات: | OpenAIRE |
| تدمد: | 15244571 00097330 |
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