Estrogen and androgen-receptor crosstalk with beta-catenin signaling and sex differences in myocardial hypertrophy

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The existence of sex-related differences in the manifestation and outcome of cardiovascular disease is well accepted. However, the molecular mechanisms involved in these differences are unknown. Sex hormones and their receptors appear to play an important role in this context. Based on the known role of -catenin in early embryonic cardiogenesis and in cardiac remodeling, the observation that during myocardial hypertrophy embryonal genetic programs are reactivated, and the finding that -catenin interacts with sex hormone receptors, we hypothesize that a crosstalk between -catenin and estrogen/androgen receptor signaling contributes to the observed differences. In this context, we will: (1) identify genes that are regulated by a crosstalk between estrogen or androgen receptor and the TCF/-catenin complex, (2) investigate whether or not these genes play a role in the sexspecific differences in myocardial hypertrophy, and (3) characterize the molecular mechanisms involved.