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We examined the role of <jats:styled-content style=\"fixed-case\">PKC<\/jats:styled-content>\u03b7 in lipid metabolism and atherosclerosis using apolipoprotein E\u2010deficient (<jats:italic>Apoe<\/jats:italic><jats:sup><jats:italic>\u2212\/\u2212<\/jats:italic><\/jats:sup>) mice. <jats:styled-content style=\"fixed-case\">PKC<\/jats:styled-content>\u03b7 expression was augmented in the aortas of mice with atherosclerosis and exclusively detected in <jats:styled-content style=\"fixed-case\">MOMA<\/jats:styled-content>2\u2010positive macrophages within atherosclerotic lesions. <jats:italic>Prkch<\/jats:italic><jats:sup><jats:italic>+\/+<\/jats:italic><\/jats:sup><jats:italic>Apoe<\/jats:italic><jats:sup><jats:italic>\u2212\/\u2212<\/jats:italic><\/jats:sup> and <jats:italic>Prkch<\/jats:italic><jats:sup><jats:italic>\u2212\/\u2212<\/jats:italic><\/jats:sup><jats:italic>Apoe<\/jats:italic><jats:sup><jats:italic>\u2212\/\u2212<\/jats:italic><\/jats:sup> mice were fed a high\u2010fat diet (<jats:styled-content style=\"fixed-case\">HFD<\/jats:styled-content>), and the dyslipidemia observed in <jats:italic>Prkch<\/jats:italic><jats:sup><jats:italic>+\/+<\/jats:italic><\/jats:sup><jats:italic>Apoe<\/jats:italic><jats:sup><jats:italic>\u2212\/\u2212<\/jats:italic><\/jats:sup> mice was improved in <jats:italic>Prkch<\/jats:italic><jats:sup><jats:italic>\u2212\/\u2212<\/jats:italic><\/jats:sup><jats:italic>Apoe<\/jats:italic><jats:sup><jats:italic>\u2212\/\u2212<\/jats:italic><\/jats:sup> mice, with a particular reduction in serum <jats:styled-content style=\"fixed-case\">LDL<\/jats:styled-content> cholesterol and phospholipids. Liver steatosis, which developed in <jats:italic>Prkch<\/jats:italic><jats:sup><jats:italic>+\/+<\/jats:italic><\/jats:sup><jats:italic>Apoe<\/jats:italic><jats:sup><jats:italic>\u2212\/\u2212<\/jats:italic><\/jats:sup> mice, was improved in <jats:italic>Prkch<\/jats:italic><jats:sup><jats:italic>\u2212\/\u2212<\/jats:italic><\/jats:sup><jats:italic>Apoe<\/jats:italic><jats:sup><jats:italic>\u2212\/\u2212<\/jats:italic><\/jats:sup> mice, but glucose tolerance, adipose tissue and body weight, and blood pressure were unchanged. Consistent with improvements in <jats:styled-content style=\"fixed-case\">LDL<\/jats:styled-content> cholesterol, atherosclerotic lesions were decreased in <jats:styled-content style=\"fixed-case\">HFD<\/jats:styled-content>\u2010fed <jats:italic>Prkch<\/jats:italic><jats:sup><jats:italic>\u2212\/\u2212<\/jats:italic><\/jats:sup><jats:italic>Apoe<\/jats:italic><jats:sup><jats:italic>\u2212\/\u2212<\/jats:italic><\/jats:sup> mice. Immunoreactivity against 3\u2010nitrotyrosine in atherosclerotic lesions was dramatically decreased in <jats:italic>Prkch<\/jats:italic><jats:sup><jats:italic>\u2212\/\u2212<\/jats:italic><\/jats:sup><jats:italic>Apoe<\/jats:italic><jats:sup><jats:italic>\u2212\/\u2212<\/jats:italic><\/jats:sup> mice, accompanied by decreased necrosis and apoptosis in the lesions. <jats:styled-content style=\"fixed-case\">ARG<\/jats:styled-content>2 <jats:styled-content style=\"fixed-case\">mRNA<\/jats:styled-content> and protein levels were significantly increased in <jats:italic>Prkch<\/jats:italic><jats:sup><jats:italic>\u2212\/\u2212<\/jats:italic><\/jats:sup><jats:italic>Apoe<\/jats:italic><jats:sup><jats:italic>\u2212\/\u2212<\/jats:italic><\/jats:sup> macrophages. These data show that <jats:styled-content style=\"fixed-case\">PKC<\/jats:styled-content>\u03b7 deficiency improves dyslipidemia and reduces susceptibility to atherosclerosis in <jats:italic>Apoe<\/jats:italic><jats:sup><jats:italic>\u2212\/\u2212<\/jats:italic><\/jats:sup> mice, showing that <jats:styled-content style=\"fixed-case\">PKC<\/jats:styled-content>\u03b7 plays a role in atherosclerosis development.<\/jats:p>","DOI":"10.1111\/gtc.12402","type":"journal-article","created":{"date-parts":[[2016,8,22]],"date-time":"2016-08-22T11:12:54Z","timestamp":1471864374000},"page":"1030-1048","source":"Crossref","is-referenced-by-count":5,"title":["<scp>PKC<\/scp>\u03b7 deficiency improves lipid metabolism and atherosclerosis in apolipoprotein <scp>E<\/scp>\u2010deficient mice"],"prefix":"10.1111","volume":"21","author":[{"given":"Kumiko","family":"Torisu","sequence":"first","affiliation":[{"name":"Division of Neurofunctional Genomics Department of Immunobiology and Neuroscience Medical 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