{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,1,8]],"date-time":"2026-01-08T02:19:07Z","timestamp":1767838747538,"version":"3.49.0"},"reference-count":55,"publisher":"The Endocrine Society","issue":"4","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2007,4,1]]},"abstract":"<jats:p>The pregnancy hormone relaxin has recently been shown to be cardio-protective. Despite its well-established antifibrotic 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 \u03bcm) and cardiac fibroblast-conditioned medium 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. Although H2-relaxin (16.7 nm) alone failed to suppress hypertrophy induced by phenylephrine, it repressed the cardiac fibroblast-conditioned medium-induced increase in protein synthesis by 24% (P &amp;lt; 0.05) and reversed the increase in cell size (P &amp;lt; 0.001) and atrial natriuretic peptide expression (P&amp;lt;0.01). We further studied the effect of H2-relaxin on CM apoptosis induced by H2O2 (200 \u03bcm). Studies of DNA laddering and nuclear staining demonstrated that H2-relaxin treatment reduced H2O2-induced DNA fragmentation. Real-time PCR and Western blot analysis revealed a significant increase in the Bcl2\/Bax ratio in H2-relaxin-treated CM. Further analysis showed that activation of Akt (1.8-fold, P&amp;lt; 0.001) and ERK (2.0-fold, P&amp;lt;0.01) were involved in the antiapoptotic action of H2-relaxin in CM, and that Gi\/o coupling of relaxin receptors was associated with the H2-relaxin-induced Akt activation in CM. In conclusion, these results extend our current knowledge of the cardiac actions of relaxin by demonstrating that H2-relaxin indirectly inhibits CM hypertrophy and directly protects CM from apoptosis.<\/jats:p>","DOI":"10.1210\/en.2006-1324","type":"journal-article","created":{"date-parts":[[2007,1,5]],"date-time":"2007-01-05T01:55:50Z","timestamp":1167962150000},"page":"1582-1589","source":"Crossref","is-referenced-by-count":79,"title":["Relaxin Antagonizes Hypertrophy and Apoptosis in Neonatal Rat Cardiomyocytes"],"prefix":"10.1210","volume":"148","author":[{"given":"Xiao-lei","family":"Moore","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Su-ling","family":"Tan","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Chen-yi","family":"Lo","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Lu","family":"Fang","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Yi-Dan","family":"Su","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Xiao-Ming","family":"Gao","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Elizabeth A.","family":"Woodcock","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Roger J.","family":"Summers","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Geoffrey W.","family":"Tregear","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Ross A. 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