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Junctional adhesion molecule A (<jats:styled-content style=\"fixed-case\">JAM<\/jats:styled-content>\u2010A) was recently described to regulate platelet activation. Specific deletion of <jats:styled-content style=\"fixed-case\">JAM<\/jats:styled-content>\u2010A from platelets resulted in increased reactivity and in accelerated progression of atherosclerosis. The aim of this study was to investigate the specific contribution of platelet\u2010derived <jats:styled-content style=\"fixed-case\">JAM<\/jats:styled-content>\u2010A to neointima formation after vascular injury. Mice with or without platelet\u2010specific (tr)<jats:styled-content style=\"fixed-case\">JAM<\/jats:styled-content>\u2010A\u2010deficiency in an apolipoprotein e (apoe<jats:sup>\u2212\/\u2212<\/jats:sup>) background underwent wire\u2010induced injury of the common carotid artery. <jats:italic>Ex vivo<\/jats:italic> imaging by two\u2010photon microscopy revealed increased platelet coverage at the site of injury in tr<jats:styled-content style=\"fixed-case\">JAM<\/jats:styled-content>\u2010A\u2010deficient mice. Cell recruitment assays showed increased adhesion of monocytic cells to activated <jats:styled-content style=\"fixed-case\">JAM<\/jats:styled-content>\u2010A\u2010deficient platelets than to control platelets. Inhibition of \u03b1<jats:sub>M<\/jats:sub>\u03b2<jats:sub>2<\/jats:sub> or <jats:styled-content style=\"fixed-case\">GPI<\/jats:styled-content>b\u03b1, but not of <jats:styled-content style=\"fixed-case\">CD<\/jats:styled-content>62P, suppressed those differences. Up to 4\u00a0weeks after wire injury, intimal neoplasia and neointimal cellular content were analysed. Neointimal lesion area was increased in tr<jats:styled-content style=\"fixed-case\">JAM<\/jats:styled-content>\u2010A<jats:sup>\u2212\/\u2212<\/jats:sup> apoe<jats:sup>\u2212\/\u2212<\/jats:sup> mice and the lesions showed an increased macrophage accumulation and proliferating smooth muscle cells compared with tr<jats:styled-content style=\"fixed-case\">JAM<\/jats:styled-content>\u2010A<jats:sup>+\/+<\/jats:sup> apoe<jats:sup>\u2212\/\u2212<\/jats:sup> littermates 2\u00a0weeks, but not 4\u00a0weeks after injury. Re\u2010endothelialization was decreased in tr<jats:styled-content style=\"fixed-case\">JAM<\/jats:styled-content>\u2010A<jats:sup>\u2212\/\u2212<\/jats:sup> apoe<jats:sup>\u2212\/\u2212<\/jats:sup> mice compared with controls 2\u00a0weeks after injury, yet it was complete in both groups after 4\u00a0weeks. A platelet gain of function by deletion of <jats:styled-content style=\"fixed-case\">JAM<\/jats:styled-content>\u2010A accelerates neointima formation only during earlier phases after vascular injury, through an increased recruitment of mononuclear cells. Thus, the contribution of platelets might become less important when neointima formation progresses to later stages.<\/jats:p>","DOI":"10.1111\/jcmm.13083","type":"journal-article","created":{"date-parts":[[2017,2,17]],"date-time":"2017-02-17T07:07:00Z","timestamp":1487315220000},"page":"1523-1531","source":"Crossref","is-referenced-by-count":18,"title":["Deletion of junctional adhesion molecule A from platelets increases early\u2010stage neointima formation after wire injury in hyperlipidemic mice"],"prefix":"10.1111","volume":"21","author":[{"given":"Zhen","family":"Zhao","sequence":"first","affiliation":[{"name":"Institute for Cardiovascular Prevention (IPEK) Ludwig\u2010Maximilians\u2010University Munich Munich Germany"},{"name":"Division of Vascular and Endovascular Surgery Ludwig\u2010Maximilians\u2010University Munich Munich 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