Surgical repair of severe mitral valve regurgitation complicated by incomplete cor triatriatum.

A 69-year-old woman with exertional dyspnea was referred emergently to our hospital for further evaluation. Transthoracic echocardiography showed severe mitral valve regurgitation and moderate tricuspid regurgitation, which were thought to be the main cause of her heart failure. An electrocardiogram showed paroxysmal atrial fibrillation.

Biological role of p300 in cardiac myocytes.

A cellular target of adenovirus E1A oncoprotein, p300 is a transcriptional coactivator required for the maintenance of differentiated phenotypes in cardiac myocytes. The full transcriptional activities of hypertrophy-responsive transcription factors such as GATA-4 and MEF2 require interaction with p300. A p300 protein also possesses intrinsic histone acetyl transferase activity, which promotes a transcriptionally active chromatin configuration.

Cardiac p300 is involved in myocyte growth with decompensated heart failure.

A variety of stresses on the heart initiate a number of subcellular signaling pathways, which finally reach the nuclei of cardiac myocytes and cause myocyte hypertrophy with heart failure. However, common nuclear pathways that lead to this state are unknown. A zinc finger protein, GATA-4, is one of the transcription factors that mediate changes in gene expression during myocardial-cell hypertrophy.

GATA-6 is involved in PPARgamma-mediated activation of differentiated phenotype in human vascular smooth muscle cells.

Objective: Peroxisome proliferator-activated receptor-gamma (PPARgamma) is a member of the nuclear receptor superfamily involved in the growth and differentiation of many cell types. Although the activation of PPARgamma in human vascular smooth muscle cells (VSMCs) inhibits the growth of these cells, the precise mechanism of this effect is unknown. PPARgamma-mediated growth inhibition of VSMCs is associated with the induction of the differentiated phenotype.

LOX-1 pathway affects the extent of myocardial ischemia-reperfusion injury.

Lectin-like oxidized low-density lipoprotein receptor-1 (LOX-1) was originally identified as a receptor for oxidized low-density lipoprotein predominantly expressed in endothelial cells. LOX-1 expression can be induced in cardiomyocytes and that activation of LOX-1 is involved in apoptosis. To investigate possible roles of LOX-1 in myocardial ischemia-reperfusion injury, rats were subjected to coronary artery ligation for 1h followed by reperfusion for 2h.

Calcineurin-GATA-6 pathway is involved in smooth muscle-specific transcription.

Intracellular calcium is one of the important signals that initiates the myogenic program. The calcium-activated phosphatase calcineurin is necessary for the nuclear import of the nuclear factor of activated T cell (NFAT) family members, which interact with zinc finger GATA transcription factors. Whereas GATA-6 plays a role in the maintenance of the differentiated phenotype in vascular smooth muscle cells (VSMCs), it is unknown whether the calcineurin pathway is associated with GATA-6 and plays a role in the differentiation of VSMCs.

Basic fibroblast growth factor protects cardiac myocytes from iNOS-mediated apoptosis.

Basic fibroblast growth factor (bFGF) is an important angiogenic factor produced by hearts subjected to ischemia. However, the direct effects of bFGF on myocardial cells are unknown. Primary cultured cardiac myocytes from neonatal rats were stimulated with lipopolysaccharide (LPS), a potent inducer of inducible nitric oxide synthase (iNOS), in the presence or the absence of bFGF.

Rho/ROCK pathway contributes to the activation of extracellular signal-regulated kinase/GATA-4 during myocardial cell hypertrophy.

The low molecular weight GTPase Rho mediates a variety of cytoskeleton-dependent cell functions and stretch- and G(q) protein-induced hypertrophic responses in cardiac myocytes. Although ROCK, one of Rho's effectors, has been suggested to mediate hypertrophic signals, the relationship of Rho/ROCK with downstream signals is unknown. A zinc finger transcription factor, GATA-4, is activated by extracellular signal-regulated kinase 1/2 and is required for the up-regulation of the endothelin-1 gene during myocardial cell hypertrophy.