{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,10,9]],"date-time":"2025-10-09T00:50:09Z","timestamp":1759971009836,"version":"build-2065373602"},"reference-count":39,"publisher":"Wiley","issue":"2","license":[{"start":{"date-parts":[[2014,10,13]],"date-time":"2014-10-13T00:00:00Z","timestamp":1413158400000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"funder":[{"DOI":"10.13039\/100000002","name":"National Institutes of Health","doi-asserted-by":"publisher","award":["ro1 hl075446"],"award-info":[{"award-number":["ro1 hl075446"]}],"id":[{"id":"10.13039\/100000002","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["The Anatomical Record"],"published-print":{"date-parts":[[2015,2]]},"abstract":"<jats:title>ABSTRACT<\/jats:title><jats:p>Background: Coronary anomalies are frequently associated with congenital cardiac defects. Accordingly, we tested the hypothesis that the development of the tunica media of coronary arteries\/arterioles is compromised in mice with cardiac defects of the outflow tract (persistent truncus arteriosus, double outlet right ventricle and transposition of the great arteries) by studying hearts of G7\u20109 generation mice bred from mutagenized mice caused by N\u2010ethyl\u2010N\u2010nitrosourea. Mice were studied at embryonic days E16.5, E17.5, and postnatal days 1 and 11. Data were based on immunohistochemistry of serial sections. Results: In 21 of 24 mice with outflow tract defects, the development of smooth muscle in arteries and arterioles was retarded; most commonly arterioles had an incomplete layer of smooth muscle or in a few instances, lacked a tunica media. In this model, an absence of a coronary ostium occurred in only 2 mice, indicating that the mechanisms underlying the formation of coronary ostia and the recruitment and differentiation of vascular smooth muscle differ. Coronary fistulas were present in 20% and dilated vessels in 30% of the hearts with cardiac defects. Conclusions: The data suggest that vascular smooth muscle recruitment and differentiation are not necessarily linked to other coronary anomalies, such as absence of a main coronary artery or branching patterns. Anat Rec, 298:408\u2013417, 2015. \u00a9 2014 Wiley Periodicals, Inc.<\/jats:p>","DOI":"10.1002\/ar.23056","type":"journal-article","created":{"date-parts":[[2014,9,30]],"date-time":"2014-09-30T05:37:56Z","timestamp":1412055476000},"page":"408-417","source":"Crossref","is-referenced-by-count":1,"title":["Coronary Anomalies in Mice With Congenital Heart Defects"],"prefix":"10.1002","volume":"298","author":[{"given":"Robert J.","family":"Tomanek","sequence":"first","affiliation":[{"name":"Department of Anatomy and Cell Biology, Carver College of Medicine The University of Iowa Iowa City Iowa"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Qing","family":"Yu","sequence":"additional","affiliation":[{"name":"Laboratory of Developmental Biology National Institutes of Health Bethesda Maryland"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Cecilia W.","family":"Lo","sequence":"additional","affiliation":[{"name":"Laboratory of Developmental Biology National 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