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dc.contributor.authorEndo, Jinen_US
dc.contributor.authorSano, Motoakien_US
dc.contributor.authorIsobe, Yosukeen_US
dc.contributor.authorFukuda, Keiichien_US
dc.contributor.authorKang, Jing X.en_US
dc.contributor.authorArai, Hiroyukien_US
dc.contributor.authorArita, Makotoen_US
dc.date.accessioned2015-02-02T15:33:05Z
dc.date.issued2014en_US
dc.identifier.citationEndo, Jin, Motoaki Sano, Yosuke Isobe, Keiichi Fukuda, Jing X. Kang, Hiroyuki Arai, and Makoto Arita. 2014. “18-HEPE, an n-3 fatty acid metabolite released by macrophages, prevents pressure overload–induced maladaptive cardiac remodeling.” The Journal of Experimental Medicine 211 (8): 1673-1687. doi:10.1084/jem.20132011. http://dx.doi.org/10.1084/jem.20132011.en
dc.identifier.issn0022-1007en
dc.identifier.urihttp://nrs.harvard.edu/urn-3:HUL.InstRepos:13890733
dc.description.abstractN-3 polyunsaturated fatty acids (PUFAs) have potential cardiovascular benefit, although the mechanisms underlying this effect remain poorly understood. Fat-1 transgenic mice expressing Caenorhabditis elegans n-3 fatty acid desaturase, which is capable of producing n-3 PUFAs from n-6 PUFAs, exhibited resistance to pressure overload–induced inflammation and fibrosis, as well as reduced cardiac function. Lipidomic analysis revealed selective enrichment of eicosapentaenoic acid (EPA) in fat-1 transgenic bone marrow (BM) cells and EPA-metabolite 18-hydroxyeicosapentaenoic acid (18-HEPE) in fat-1 transgenic macrophages. BM transplantation experiments revealed that fat-1 transgenic BM cells, but not fat-1 transgenic cardiac cells, contributed to the antiremodeling effect and that the 18-HEPE–rich milieu in the fat-1 transgenic heart was generated by BM-derived cells, most likely macrophages. 18-HEPE inhibited macrophage-mediated proinflammatory activation of cardiac fibroblasts in culture, and in vivo administration of 18-HEPE reproduced the fat-1 mice phenotype, including resistance to pressure overload–induced maladaptive cardiac remodeling.en
dc.language.isoen_USen
dc.publisherThe Rockefeller University Pressen
dc.relation.isversionofdoi:10.1084/jem.20132011en
dc.relation.hasversionhttp://www.ncbi.nlm.nih.gov/pmc/articles/PMC4113943/pdf/en
dash.licenseLAAen_US
dc.title18-HEPE, an n-3 fatty acid metabolite released by macrophages, prevents pressure overload–induced maladaptive cardiac remodelingen
dc.typeJournal Articleen_US
dc.description.versionVersion of Recorden
dc.relation.journalThe Journal of Experimental Medicineen
dash.depositing.authorKang, Jing X.en_US
dc.date.available2015-02-02T15:33:05Z
dc.identifier.doi10.1084/jem.20132011*
dash.contributor.affiliatedKang, Jing


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