DISTRIBUTION OF FIBRONECTIN, TYPE-I COLLAGEN, TYPE-IV COLLAGEN, AND LAMININ IN THE CARDIAC JELLY OF THE MOUSE EMBRYONIC HEART WITH RETINOICACID-INDUCED COMPLETE TRANSPOSITION OF THE GREAT-ARTERIES

Background: In the mouse model of complete transposition of the great arteries (TGA) produced by all-trans retinoic acid (RA), parietal and septal ridges in the outflow tract (OT) are hypoplastic. At first, the se ridges are generated by an expanded cardiac jelly (mainly myocardia l basement membrane), Thereafter, endothelial cells delaminate and inv ade into the adjacent cardiac jelly to form endocardial cushion tissue (formation of cushion ridge), During cushion tissue formation, baseme nt membrane antigens play an important role in the regulation of this endothelial-mesenchymal transformation. Methods: To examine whether th e myocardial basement membrane components are altered in the RA-treate d heart OT, immunohistochemistry for fibronectin, type I collagen, typ e IV collagen, and laminin was carried out in mouse embryonic hearts a t 9.5 and 10.5 ED (embryonic day; vaginal plug = day 0) with or withou t prior exposure to RA. Results: Particulate/fibrillar fibronectin and fibrillar type I collagen were observed in the thick cardiac jelly of the control heart at the onset of mesenchymal formation. In the RA-tr eated heart, an intermittent patchy staining for fibronectin and a spa rse distribution of type I collagen were observed in the thin cardiac jelly. Laminin and type IV collagen were distributed continuously on t he basal surface (layer adjacent to the basal plasma membrane) of endo cardium and myocardium in both control and RA-treated hearts. Conclusi ons: The alterations in the antigens of the myocardial basement membra ne (cardiac jelly) may be responsible for the hypoplasticity of pariet al and septal ridges that characterizes RA-induced TGA morphology. Thi s may be one of the reasons why mesenchymal cell formation is inhibite d in the RA-induced TGA. (C) 1997 Wiley-Liss, Inc.