The Distribution of Tenascin in Rat Embryos with Normal Heart and Cardiovascular Anomalies Induced by Bis‐Diamine

Abstract

AbstractThe mesenchyme in the truncal ridge and aortico‐pulmonary (A‐P) septum in the developing heart expresses tenascin (TN), a component of extracellular matrices. We observed immunohistochemically the localization of TN with reference to fibronectin (FN) distribution in rat embryonic hearts at gestation days 12. 13 and 14 and compared the results with those in bis‐diamine‐induced cardiovascular anomalies. In control rat embryonic hearts, TN was distributed in the dorsal mesocardium and the distal part of the truncal ridge at gestation day 12, and in part of the conal and truncal ridges, A‐P septum and proximal wall of aortic arch arteries at gestation days 13 and 14. The conotruncal regions with TN expression may correspond to the areas where cardiac neural crest cells migrate in the heart. In bis‐diamine‐treated rat hearts showing conotruncal anomalies, TN was localized in incompletely fused and hypoplastic conotruncal ridges, but the intensity and area of staining were decreased suggesting a decreased neural crest cell migration. FN was diffusely distributed in both the normal and anomalous embryonic hearts, including atrioventricular cushion tissue in addition to the region expressing TN. TN was densely distributed in the fusing area of the conal and truncal ridges in comparison to FN, suggesting that TN may be mainly expressed during the time of fusion of conal and truncal ridges to form the A‐P septum in the embryonic heart. In conclusion, bis‐diamine may cause the poor development of neural crest derived tissue, subsequently bringing about hypoplasia of the A‐P septum and truncal and conal ridges.