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The role of CD34\n                    <jats:sup>+<\/jats:sup>\n                    \/VEGF receptor (VEGFR) 2\n                    <jats:sup>+<\/jats:sup>\n                    progenitor cells (PCs) in vascular repair in HHcy is unknown. We studied the effect of HHcy on PCs and its role in vascular repair in severe HHcy (~150 \u03bcM), which was induced in cystathionine\u2010\u03b2 synthase heterozygous mice fed a high\u2010methionine diet for 8 weeks. Vascular injury was introduced by carotid air\u2010dry endothelium denudation. CD34\n                    <jats:sup>+<\/jats:sup>\n                    \/VEGFR2\n                    <jats:sup>+<\/jats:sup>\n                    cells were examined by flow cytometry. HHcy reduced bone marrow (BM) CD34\n                    <jats:sup>+<\/jats:sup>\n                    \/VEGFR2\n                    <jats:sup>+<\/jats:sup>\n                    cells and suppressed replenishment of postinjury CD34\n                    <jats:sup>+<\/jats:sup>\n                    \/VEGFR2\n                    <jats:sup>+<\/jats:sup>\n                    cells in peripheral blood (PB). Donor green fluorescent protein\u2010positive PC homing to the injured vessel was reduced in HHcy after CD34\n                    <jats:sup>+<\/jats:sup>\n                    PCs from enhanced green fluorescent protein mice were adoptively transferred following carotid injury. CD34\n                    <jats:sup>+<\/jats:sup>\n                    PC transfusion partially reversed HHcy\u2010suppressed re\u2010endothelialization and HHcy\u2010induced neointimal formation. Furthermore, homocysteine (Hcy) inhibited proliferation, adhesion, and migration and suppressed \u03b21\u2010integrin expression and activity in human CD34\n                    <jats:sup>+<\/jats:sup>\n                    endothelial colony\u2010forming cells (ECFCs) isolated from PBs in a dose\u2010dependent manner. A functional\u2010activating \u03b21\u2010integrin antibody rescued Hcy\u2010suppressed adhesion and migration in CD34\n                    <jats:sup>+<\/jats:sup>\n                    ECFCs. In conclusion, HHcy reduces BM CD34\n                    <jats:sup>+<\/jats:sup>\n                    \/VEGFR2\n                    <jats:sup>+<\/jats:sup>\n                    generation and suppresses CD34\n                    <jats:sup>+<\/jats:sup>\n                    \/VEGFR2\n                    <jats:sup>+<\/jats:sup>\n                    cell mobilization and homing to the injured vessel\n                    <jats:italic>via<\/jats:italic>\n                    \u03b21\u2010integrin inhibition, which partially contributes to impaired re\u2010endothelialization and vascular remodeling.\u2014Nelson, J., Wu, Y., Jiang, X., Berretta, R., Houser, S., Choi, E., Wang, J., Huang, J., Yang, X., Wang, H. Hyperhomocysteinemia suppresses bone marrow CD34\n                    <jats:sup>+<\/jats:sup>\n                    \/VEGF receptor 2\n                    <jats:sup>+<\/jats:sup>\n                    cells and inhibits progenitor cell mobilization and homing to injured vasculature\u2014a role of \u03b21\u2010integrin in progenitor cell migration and adhesion.\n                    <jats:italic>FASEB J<\/jats:italic>\n                    . 29, 3085\u20103099 (2015).\n                    <jats:ext-link xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" xlink:href=\"http:\/\/www.fasebj.org\">www.fasebj.org<\/jats:ext-link>\n                  <\/jats:p>","DOI":"10.1096\/fj.14-267989","type":"journal-article","created":{"date-parts":[[2015,4,8]],"date-time":"2015-04-08T21:52:36Z","timestamp":1428529956000},"page":"3085-3099","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":26,"title":["Hyperhomocysteinemia suppresses bone marrow CD34\n                    <sup>+<\/sup>\n                    \/VEGF receptor 2\n                    <sup>+<\/sup>\n                    cells and inhibits progenitor cell mobilization and homing to injured vasculature\u2014a role of \u03b21\u2010integrin in progenitor cell migration and adhesion"],"prefix":"10.1096","volume":"29","author":[{"given":"Jun","family":"Nelson","sequence":"first","affiliation":[{"name":"Center for Metabolic Disease Research, Temple University School of Medicine Philadelphia Pennsylvania USA"},{"name":"Department of Pharmacology Temple University School of Medicine Philadelphia Pennsylvania USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Yi","family":"Wu","sequence":"additional","affiliation":[{"name":"Thrombosis Research Center, Temple University School of Medicine Philadelphia Pennsylvania USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Xiaohua","family":"Jiang","sequence":"additional","affiliation":[{"name":"Center for Metabolic Disease Research, Temple University School of Medicine Philadelphia Pennsylvania USA"},{"name":"Department of Pharmacology Temple University School of Medicine Philadelphia Pennsylvania USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Remus","family":"Berretta","sequence":"additional","affiliation":[{"name":"Cardiovascular Research Center, Temple University School of Medicine Philadelphia Pennsylvania USA"},{"name":"Department of Physiology Temple University School of Medicine Philadelphia Pennsylvania USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Steven","family":"Houser","sequence":"additional","affiliation":[{"name":"Cardiovascular Research Center, Temple University School of Medicine Philadelphia Pennsylvania USA"},{"name":"Department of Physiology Temple University School of Medicine Philadelphia Pennsylvania 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