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Our previous studies have shown that constitutive expression of a locally acting insulin\u2010like growth factor\u20101 Ea (IGF\u20101Ea) propeptide promotes functional restoration after cardiac injury associated with decreased scar formation. In the current study, we investigated the underlying molecular and cellular mechanisms behind the enhanced functional recovery. We observed improved cardiac function in mice overexpressing cardiac\u2010specific IGF\u20101Ea as early as day 7 after myocardial infarction. Analysis of gene transcription revealed that supplemental IGF\u20101Ea regulated expression of key metalloproteinases (MMP\u20102 and MMP\u20109), their inhibitors (TIMP\u20101 and TIMP\u20102), and collagen types (Col 1<jats:italic>\u03b1<\/jats:italic>1 and Col 1<jats:italic>\u03b1<\/jats:italic>3) in the first week after injury. Infiltration of inflammatory cells, which direct the remodelling process, was also altered; in particular there was a notable reduction in inflammatory Ly6C+ monocytes at day 3 and an increase in anti\u2010inflammatory CD206+ macrophages at day 7. Taken together, these results indicate that the IGF\u20101Ea transgene shifts the balance of innate immune cell populations early after infarction, favouring a reduction in inflammatory myeloid cells. This correlates with reduced extracellular matrix remodelling and changes in collagen composition that may confer enhanced scar elasticity and improved cardiac function.<\/jats:p>","DOI":"10.1155\/2015\/484357","type":"journal-article","created":{"date-parts":[[2015,9,30]],"date-time":"2015-09-30T21:24:53Z","timestamp":1443648293000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":31,"title":["Cardiac\u2010Restricted IGF\u20101Ea Overexpression Reduces the Early Accumulation of Inflammatory Myeloid Cells and Mediates Expression of Extracellular Matrix Remodelling Genes after Myocardial Infarction"],"prefix":"10.1155","volume":"2015","author":[{"given":"Enrique","family":"Gallego-Colon","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Robert D.","family":"Sampson","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-9932-4109","authenticated-orcid":false,"given":"Susanne","family":"Sattler","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Michael D.","family":"Schneider","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Nadia","family":"Rosenthal","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Joanne","family":"Tonkin","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"311","published-online":{"date-parts":[[2015,9,30]]},"reference":[{"key":"e_1_2_8_1_2","doi-asserted-by":"publisher","DOI":"10.1161\/01.cir.0000441139.02102.80"},{"key":"e_1_2_8_2_2","doi-asserted-by":"publisher","DOI":"10.1161\/circresaha.111.243162"},{"key":"e_1_2_8_3_2","doi-asserted-by":"publisher","DOI":"10.1038\/nrcardio.2014.28"},{"key":"e_1_2_8_4_2","doi-asserted-by":"publisher","DOI":"10.1016\/j.ghir.2004.11.001"},{"key":"e_1_2_8_5_2","doi-asserted-by":"publisher","DOI":"10.1016\/S0021-9258(19)89179-2"},{"key":"e_1_2_8_6_2","doi-asserted-by":"publisher","DOI":"10.3109\/08977199309010833"},{"key":"e_1_2_8_7_2","doi-asserted-by":"publisher","DOI":"10.1093\/nar\/14.20.7873"},{"key":"e_1_2_8_8_2","doi-asserted-by":"publisher","DOI":"10.1371\/journal.pone.0051152"},{"key":"e_1_2_8_9_2","doi-asserted-by":"publisher","DOI":"10.1161\/circresaha.107.148791"},{"key":"e_1_2_8_10_2","doi-asserted-by":"publisher","DOI":"10.18632\/aging.100107"},{"key":"e_1_2_8_11_2","doi-asserted-by":"publisher","DOI":"10.1016\/j.cardiores.2005.10.002"},{"key":"e_1_2_8_12_2","first-page":"364","article-title":"The collagen network of the heart","volume":"40","author":"Caulfield J. 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