Homeodomain only protein x is down-regulated in human heart failure

Abstract

Homeodomain only protein x (Hopx) is an unusual homeodomain protein that has diverse effects on cardiac growth. Manipulation of Hopx function in murine models is associated with cardiac hypertrophy, dilation and fibrosis. In the present study, we examined the expression profile of Hopx in various models of pathologic cardiac hypertrophy and failure. Hopx expression is significantly reduced in neonatal rat cardiac myocytes after α/β adrenergic receptor agonist treatment. Cardiac hypertrophy and failure induced by transaortic constriction in mice causes marked down-regulation of Hopx expression. Interestingly, HOPX expression was significantly reduced in hearts of humans with end-stage heart failure when compared to non-failing control hearts, and HOPX levels remain low after LVAD support. Our findings suggest that HOPX/Hopx expression is reduced in multiple examples of human and murine cardiac hypertrophy and failure.