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Overgrowth and Enlarged Heart in Mouse Fetuses with Maternally Inherited T hP and t wLub2 : An Example of Genomic Imprinting in Animals
Author(s) -
MIYABARA Shinichi,
BOGART Mark H.,
WINKING Heinz,
SUGIHARA Hajime
Publication year - 1993
Publication title -
congenital anomalies
Language(s) - English
Resource type - Journals
eISSN - 1741-4520
pISSN - 0914-3505
DOI - 10.1111/j.1741-4520.1993.tb00512.x
Subject(s) - fetus , medicine , biology , anatomy , endocrinology , pregnancy , genetics
T hp/+ mouse is known to have differing phenotypes depending on gender of the T hP parent. In the present study, fetuses with maternally [Group A (until day 18 of pregnancy) and Group C (day 19)] and paternally [Group B] inherited T hP were examined with particular reference to the developmental abnormalities of hearts. In addition, a small number of fetuses with maternally inherited t wLub2 on day 19 were compared with T hp . Group A T hP fetuses had greater body weight, possibly larger body size, generalized edema (100%), marked enlargement of the hearts (100%) and hypoplastic pulmonary trunk (73.7%). There were no such malformations in Group B T hP fetuses or in the controls (+/+) for both groups. The bilaterally thickened ventricular wall of fetal hearts in Group A and C T hP fetuses bulged into ventricular cavity. The pulmonary valve was also thickened. The labeling indices of the ventricular myocardial cells by BrdU were inclined to be higher in Group A T hP than in the control (+/+) fetuses. Fetuses of t wLub2 had abnormalities of the cardiovascular system similar to Group C T hp . The results suggest that cardiac lesions in fetuses with maternally inherited T hP and t wLub2 correspond to cardiomyopathy. Overgrowth and enlarged heart indicate the possibility of T hP as an animal model for Wiedemann‐Beckwith syndrome.