Clinical treatment with an inhibitor of histone deacetylase induces histone hyperacetylation in target cells and may restore sensitivity to the anti-leukemic effects of all-trans-retinoic acid in acute promyelocytic leukemia. Similar therapy may prove useful in other neoplastic diseases that are associated with oncogenic repression of gene transcription due to recruitment of histone deacetylases.

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Background-Corin is a transmembrane protease that processes natriuretic peptides in the heart. Like many membrane proteins, corin is shed from the cell surface. Methods and Results-In this study, we obtained plasma samples from healthy controls and patients with heart failure (HF) and acute myocardial infarction. Soluble corin levels in plasma were measured by an ELISA method. In healthy adults (nϭ198), plasma corin levels were 690 pg/mL (SD, 260 pg/mL). The corin levels did not differ significantly among different age groups. In patients with HF (nϭ291), plasma corin levels were significantly lower compared with that of healthy controls (365 pg/mL [SD, 259]; PϽ0.001). The reduction in plasma corin levels seemed to correlate with the severity of HF. In patients of New York Heart Association classes II, III, and IV, plasma corin levels were 450 pg/mL (SD, 281 pg/mL; nϭ69), 377 pg/mL (SD, 270 pg/mL; nϭ132), and 282 pg/mL (SD, 194 pg/mL; nϭ90), respectively (PϽ0.001 class II vs class IV; PϽ0.05 class III vs class IV). In contrast, plasma corin levels in patients with acute myocardial infarction (nϭ73) were similar to that of healthy controls (678 pg/mL [SD, 285 pg/mL]; PϾ0.05). Conclusions-Soluble corin was detected in human plasma. Plasma corin levels were reduced significantly in patients with HF but not in those with acute myocardial infarction. Our results indicate that corin deficiency may contribute to the pathogenesis of HF and that plasma corin may be used as a biomarker in the diagnosis of HF. (Circ Heart Fail. 2010;3:207-211.)