The pregnancy hormone relaxin has recently been shown to be cardio-protective. Despite its well-established anti-fibrotic actions in the heart, the effects of relaxin on cardiomyocytes (CM) remain to be determined. We investigated effects of isoform 2 of the human relaxin (H2-relaxin) on CM hypertrophy and apoptosis. In cultured neonatal rat CM, phenylephrine (50 microM) and cardiac fibroblast-conditioned medium (FCM) were used respectively to induce CM hypertrophy. The degree of hypertrophy was indicated by increased cell size, protein synthesis and gene expression of atrial natriuretic peptide (ANP). Whilst H2-relaxin (16.7 nM) alone failed to suppress hypertrophy induced by phenylephrine, it repressed the FCM-induced increase in protein synthesis by 24 (P
|Pages (from-to)||1582 - 1589|
|Number of pages||8|
|Publication status||Published - 2007|
Moore, X-L., Tan, S-L., Lo, C-Y., Fang, L., Su, Y-D., Gao, X-M., Woodcock, E. A., Summers, R. J., Tregear, G. W., Bathgate, R., & Du, X-J. (2007). Relaxin antagonizes hypertrophy and apoptosis in neonatal rat cardiomyocytes. Endocrinology, 148(4), 1582 - 1589.