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dc.contributor.authorLi, Xinzhien_US
dc.contributor.authorBallantyne, Laurel L.en_US
dc.contributor.authorChe, Xinghuien_US
dc.contributor.authorMewburn, Jeffrey D.en_US
dc.contributor.authorKang, Jing X.en_US
dc.contributor.authorBarkley, Robert M.en_US
dc.contributor.authorMurphy, Robert C.en_US
dc.contributor.authorYu, Yingen_US
dc.contributor.authorFunk, Colin D.en_US
dc.date.accessioned2015-10-01T14:57:20Z
dc.date.issued2015en_US
dc.identifier.citationLi, Xinzhi, Laurel L. Ballantyne, Xinghui Che, Jeffrey D. Mewburn, Jing X. Kang, Robert M. Barkley, Robert C. Murphy, Ying Yu, and Colin D. Funk. 2015. “Endogenously Generated Omega‐3 Fatty Acids Attenuate Vascular Inflammation and Neointimal Hyperplasia by Interaction With Free Fatty Acid Receptor 4 in Mice.” Journal of the American Heart Association: Cardiovascular and Cerebrovascular Disease 4 (4): e001856. doi:10.1161/JAHA.115.001856. http://dx.doi.org/10.1161/JAHA.115.001856.en
dc.identifier.issn2047-9980en
dc.identifier.urihttp://nrs.harvard.edu/urn-3:HUL.InstRepos:22857001
dc.description.abstractBackground: Omega‐3 polyunsaturated fatty acids (ω3 PUFAs) suppress inflammation through activation of free fatty acid receptor 4 (FFAR4), but this pathway has not been explored in the context of cardiovascular disease. We aimed to elucidate the involvement of FFAR4 activation by ω3 PUFAs in the process of vascular inflammation and neointimal hyperplasia in mice. Methods and Results: We used mice with disruption of FFAR4 (Ffar4−/−), along with a strain that synthesizes high levels of ω3 PUFAs (fat‐1) and a group of crossed mice (Ffar4−/−/fat‐1), to elucidate the role of FFAR4 in vascular dysfunction using acute and chronic thrombosis/vascular remodeling models. The presence of FFAR4 in vascular‐associated cells including perivascular adipocytes and macrophages, but not platelets, was demonstrated. ω3 PUFAs endogenously generated in fat‐1 mice (n=9), but not in compound Ffar4−/−/fat‐1 mice (n=9), attenuated femoral arterial thrombosis induced by FeCl3. Neointimal hyperplasia and vascular inflammation in the common carotid artery were significantly curtailed 4 weeks after FeCl3 injury in fat‐1 mice (n=6). This included greater luminal diameter and enhanced blood flow, reduced intima:media ratio, and diminished macrophage infiltration in the vasculature and perivascular adipose tissue compared with control mice. These effects were attenuated in the Ffar4−/−/fat‐1 mice. Conclusions: These results indicate that ω3 PUFAs mitigate vascular inflammation, arterial thrombus formation, and neointimal hyperplasia by interaction with FFAR4 in mice. Moreover, the ω3 PUFA–FFAR4 pathway decreases inflammatory responses with dampened macrophage transmigration and infiltration.en
dc.language.isoen_USen
dc.publisherBlackwell Publishing Ltden
dc.relation.isversionofdoi:10.1161/JAHA.115.001856en
dc.relation.hasversionhttp://www.ncbi.nlm.nih.gov/pmc/articles/PMC4579939/pdf/en
dash.licenseLAAen_US
dc.subjectVascular Medicineen
dc.subjectadipose tissueen
dc.subjectfatty acidsen
dc.subjectinflammationen
dc.subjectomega‐3 fatty acid receptoren
dc.subjecttransgenic modelen
dc.titleEndogenously Generated Omega‐3 Fatty Acids Attenuate Vascular Inflammation and Neointimal Hyperplasia by Interaction With Free Fatty Acid Receptor 4 in Miceen
dc.typeJournal Articleen_US
dc.description.versionVersion of Recorden
dc.relation.journalJournal of the American Heart Association: Cardiovascular and Cerebrovascular Diseaseen
dash.depositing.authorKang, Jing X.en_US
dc.date.available2015-10-01T14:57:20Z
dc.identifier.doi10.1161/JAHA.115.001856*
dash.contributor.affiliatedKang, Jing


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