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In the present study, the role of interleukin\u201017A (\n                    <jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\n                    \u201017A) in angiogenesis in the process of ocular\n                    <jats:styled-content style=\"fixed-case\">NV<\/jats:styled-content>\n                    both\n                    <jats:italic>in vivo<\/jats:italic>\n                    and\n                    <jats:italic>in vitro<\/jats:italic>\n                    was investigated. Also, a paracrine role of\n                    <jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\n                    \u201017A was demonstrated in the crosstalk between endothelial cells and macrophages in angiogenesis. In the retinas of mice with retinopathy of prematurity, the\n                    <jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\n                    \u201017A expression increased significantly at postnatal day 15 (P15) and P18 during retinal\n                    <jats:styled-content style=\"fixed-case\">NV<\/jats:styled-content>\n                    . Mice given\n                    <jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\n                    \u201017A neutralizing antibody (\n                    <jats:styled-content style=\"fixed-case\">NA<\/jats:styled-content>\n                    b) developed significantly reduced choroidal\n                    <jats:styled-content style=\"fixed-case\">NV<\/jats:styled-content>\n                    and retinal\n                    <jats:styled-content style=\"fixed-case\">NV<\/jats:styled-content>\n                    . Studies on vascular endothelial growth factor (\n                    <jats:styled-content style=\"fixed-case\">VEGF<\/jats:styled-content>\n                    ) over\u2010expressing mice suggested that\n                    <jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\n                    \u201017A modulated\n                    <jats:styled-content style=\"fixed-case\">NV<\/jats:styled-content>\n                    through the\n                    <jats:styled-content style=\"fixed-case\">VEGF<\/jats:styled-content>\n                    pathway. Furthermore,\n                    <jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\n                    \u201017A deficiency shifted macrophage polarization toward an M2 phenotype during retinal\n                    <jats:styled-content style=\"fixed-case\">NV<\/jats:styled-content>\n                    with significantly reduced M1 cytokine expression compared with wild\u2010type controls.\n                    <jats:italic>In vitro<\/jats:italic>\n                    assays revealed that\n                    <jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\n                    \u201017A treated macrophage supernatant gave rise to elevated human umbilical vascular endothelial cell proliferation, tube formation and\n                    <jats:styled-content style=\"fixed-case\">VEGF<\/jats:styled-content>\n                    receptor 1 and receptor 2 expression. Therefore,\n                    <jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\n                    \u201017A could potentially serve as a novel target for treating ocular\n                    <jats:styled-content style=\"fixed-case\">NV<\/jats:styled-content>\n                    diseases. The limitation of this study involved the potential mechanisms, such as which transcription accounted for macrophage polarization and how the subsequent cytokines were modulated when macrophages were polarized. Further studies need to be undertaken to definitively determine the extent to which\n                    <jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\n                    \u201017A neutralizing anti\u2010angiogenic activity depends on macrophage modulation compared with anti\u2010\n                    <jats:styled-content style=\"fixed-case\">VEGF<\/jats:styled-content>\n                    treatment.\n                  <\/jats:p>","DOI":"10.1111\/imm.12571","type":"journal-article","created":{"date-parts":[[2015,12,23]],"date-time":"2015-12-23T03:27:34Z","timestamp":1450841254000},"page":"414-428","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":57,"title":["Interleukin\u201017A neutralization alleviated ocular neovascularization by promoting M2 and mitigating M1 macrophage polarization"],"prefix":"10.1111","volume":"147","author":[{"given":"Yanji","family":"Zhu","sequence":"first","affiliation":[{"name":"The Department of Ophthalmology Ruijin Hospital Shanghai Jiao Tong University School of Medicine Shanghai China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Wei","family":"Tan","sequence":"additional","affiliation":[{"name":"The Department of Ophthalmology The First People's Hospital The Third Affiliated Hospital of Zunyi Medical University Zunyi Guizhou China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Anna M.","family":"Demetriades","sequence":"additional","affiliation":[{"name":"The Department of Ophthalmology Presbyterian Hospital\u2010Cornell New York NY USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yujuan","family":"Cai","sequence":"additional","affiliation":[{"name":"The Department of Ophthalmology Ruijin Hospital Shanghai Jiao Tong University School of Medicine Shanghai 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