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Neointimal thickening is a prominent feature of early atherogenesis. This study aimed to examine the role of GM\u2010CSF in neointimal formation induced by endothelial injury using a GM\u2010CSF<jats:sup>\u2212\/\u2212<\/jats:sup> mouse model. Neointimal thickening was induced by endothelial damage in the common iliac arteries of normolipidemic C57Bl\/6 (wild\u2010type) and GM\u2010CSF<jats:sup>\u2212\/\u2212<\/jats:sup> mice. Arteries were collected weekly for 3\u20137 weeks following surgery. A significant delay in neointimal formation in the GM\u2010CSF<jats:sup>\u2212\/\u2212<\/jats:sup> compared with wild\u2010type mice was detected by morphometric analysis of the intimal area. Neointimal size was \u223c10% smaller in GM\u2010CSF<jats:sup>\u2212\/\u2212<\/jats:sup> mice at 4\u20136 weeks post\u2010surgery, compared with wild\u2010type mice. The neointima was composed predominantly of smooth muscle cells and there was no difference in the extent of endothelial cell coverage between the wild\u2010type and GM\u2010CSF<jats:sup>\u2212\/\u2212<\/jats:sup> mice. Using immunohistochemistry, reduced macrophages (F4\/80<jats:sup>+<\/jats:sup> cells), proliferating cells (proliferating cell nuclear antigen (PCNA)<jats:sup>+<\/jats:sup> cells) and platelet\u2010derived growth factor\u2010B were detected within the arteries of GM\u2010CSF<jats:sup>\u2212\/\u2212<\/jats:sup> mice compared with wild types at 4 weeks post\u2010surgery. GM\u2010CSF<jats:sup>\u2212\/\u2212<\/jats:sup> mice had reduced connective tissue within the neointima compared with wild types at 5 weeks post\u2010surgery, determined by trichrome staining. We conclude that GM\u2010CSF deficiency reduces neointimal formation in a normolipidemic model, primarily due to reduced macrophage recruitment.<\/jats:p>","DOI":"10.1038\/icb.2008.73","type":"journal-article","created":{"date-parts":[[2008,10,7]],"date-time":"2008-10-07T09:41:04Z","timestamp":1223372464000},"page":"122-130","source":"Crossref","is-referenced-by-count":8,"title":["GM\u2010CSF deficiency delays neointima formation in a normolipidemic mouse model of endoluminal endothelial damage"],"prefix":"10.1111","volume":"87","author":[{"given":"Angie K","family":"Harris","sequence":"first","affiliation":[{"name":"Discipline of Pathology, School of Medical Sciences and Bosch Institute, University of Sydney  Sydney New South Wales Australia"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Jie","family":"Shen","sequence":"additional","affiliation":[{"name":"Discipline of Pathology, School of Medical Sciences and Bosch Institute, University of Sydney  Sydney New South Wales Australia"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Jane","family":"Radford","sequence":"additional","affiliation":[{"name":"Discipline of Pathology, School of Medical Sciences and Bosch Institute, University of Sydney  Sydney New South Wales Australia"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Shisan","family":"Bao","sequence":"additional","affiliation":[{"name":"Discipline of Pathology, School of Medical Sciences and Bosch Institute, University of Sydney  Sydney New South Wales Australia"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Brett D","family":"Hambly","sequence":"additional","affiliation":[{"name":"Discipline of Pathology, School of Medical Sciences and Bosch Institute, University of Sydney  Sydney New South Wales Australia"}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"311","published-online":{"date-parts":[[2008,10,7]]},"reference":[{"key":"e_1_2_7_1_1","doi-asserted-by":"publisher","DOI":"10.1016\/S0140-6736(96)07495-8"},{"key":"e_1_2_7_2_1","doi-asserted-by":"publisher","DOI":"10.1161\/hc4201.097835"},{"key":"e_1_2_7_3_1","doi-asserted-by":"publisher","DOI":"10.1161\/CIRCULATIONAHA.104.529552"},{"key":"e_1_2_7_4_1","doi-asserted-by":"publisher","DOI":"10.1002\/jcp.1041280311"},{"key":"e_1_2_7_5_1","doi-asserted-by":"publisher","DOI":"10.1080\/08977190412331279881"},{"key":"e_1_2_7_6_1","doi-asserted-by":"publisher","DOI":"10.1161\/01.ATV.17.11.2489"},{"key":"e_1_2_7_7_1","doi-asserted-by":"publisher","DOI":"10.1006\/exmp.1994.1030"},{"key":"e_1_2_7_8_1","doi-asserted-by":"publisher","DOI":"10.1182\/blood.V71.1.99.99"},{"key":"e_1_2_7_9_1","doi-asserted-by":"publisher","DOI":"10.1016\/0021-9150(93)90026-Q"},{"key":"e_1_2_7_10_1","doi-asserted-by":"crossref","first-page":"3799","DOI":"10.4049\/jimmunol.146.11.3799","article-title":"Release of the cytokines colony\u2010stimulating factor\u20101, granulocyte\u2010macrophage colony\u2010stimulating factor, and IL\u20106 by cloned murine vascular smooth muscle cells","volume":"146","author":"Schrader JW","year":"1991","journal-title":"J Immunol"},{"key":"e_1_2_7_11_1","doi-asserted-by":"publisher","DOI":"10.1172\/JCI113471"},{"key":"e_1_2_7_12_1","doi-asserted-by":"publisher","DOI":"10.1146\/annurev.iy.10.040192.001455"},{"key":"e_1_2_7_13_1","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.86.18.7169"},{"key":"e_1_2_7_14_1","doi-asserted-by":"publisher","DOI":"10.1161\/01.ATV.19.1.98"},{"key":"e_1_2_7_15_1","doi-asserted-by":"publisher","DOI":"10.1046\/j.1365-2567.2000.00117.x"},{"key":"e_1_2_7_16_1","doi-asserted-by":"publisher","DOI":"10.1016\/S0002-9440(10)64036-9"},{"key":"e_1_2_7_17_1","doi-asserted-by":"publisher","DOI":"10.1016\/S0891-5849(01)00711-0"},{"key":"e_1_2_7_18_1","doi-asserted-by":"publisher","DOI":"10.1016\/0021-9150(92)90066-P"},{"key":"e_1_2_7_19_1","doi-asserted-by":"publisher","DOI":"10.1161\/01.ATV.19.7.1658"},{"key":"e_1_2_7_20_1","doi-asserted-by":"publisher","DOI":"10.1161\/01.CIR.0000097001.79750.78"},{"key":"e_1_2_7_21_1","doi-asserted-by":"crossref","first-page":"2383","DOI":"10.4049\/jimmunol.150.6.2383","article-title":"Culture of human monocytes with granulocyte\u2010macrophage colony\u2010stimulating factor results in enhancement of IFN\u2010\u03b3 receptors but suppression of IFN\u2010\u03b3\u2010induced expression of the gene IP\u201010","volume":"150","author":"Finbloom DS","year":"1993","journal-title":"J Immunol"},{"key":"e_1_2_7_22_1","doi-asserted-by":"crossref","first-page":"4218","DOI":"10.4049\/jimmunol.147.12.4218","article-title":"Production of IL\u20101 receptor antagonist by human in vitro\u2010derived macrophages. 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