Cardiomyocyte-specific transgenic expression of lysyl oxidase-like protein-1 induces cardiac hypertrophy in mice.

Lysyl oxidase (LOX) and LOX-like protein-1 (LOXL-1) are extracellular matrix-embedded amine oxidases that have critical roles in the cross-linking of collagen and elastin. LOX family proteins are abundantly expressed in the remodeled heart of animals and humans and are implicated in cardiac fibrosis; however, their role in cardiac hypertrophy is unknown. In this study, in vitro stimulation with hypertrophic agonists significantly increased LOXL-1 expression, LOX enzyme activity and [(3)H] leucine incorporation in neonatal rat cardiomyocytes.

Comparison of gene expression profiling in pressure and volume overload-induced myocardial hypertrophies in rats.

Gene expression profiling has been conducted in rat hearts subjected to pressure overload (PO). However, pressure and volume overload produce morphologically and functionally distinct forms of cardiac hypertrophy. Surprisingly, gene expression profiling has not been reported for in an animal model of volume overload (VO).

Pheochromocytoma presenting as recurrent hypotension and syncope.

We report a case with pheochromocytoma presenting as recurrent syncope due to hypotension. A 71-year-old man was admitted because of recurrent syncope and paroxysmal hypotension. He was diagnosed as having pheochromocytoma.

Behavior of caveolae and caveolin-3 during the development of myocyte hypertrophy.

Recent studies have indicated that caveolae are enriched in a variety of signaling molecules, some of which are associated with cardiomyocyte hypertrophy. Caveolin-3, a major constituent of cardiac caveolae, has been suggested to interact with several signaling molecules. We investigated the morphologic changes of caveolae and caveolin-3 expression in hypertrophied cardiomyocytes induced by an alpha1-adrenergic agonist.