Hypertrophy Expression Research Articles

Gene expression of prostacyclin receptor in the hypertrophied heart of spontaneously hypertensive rats.

1. Prostacyclin elicits potent vasodilation and inhibition of platelet aggregation through binding to its membrane receptor. The impairment of prostacyclin receptor activity is implicated in various human cardiovascular diseases. We recently succeeded in molecular cloning of cDNA for the mouse, rat, and human prostacyclin receptors. 2. In the present study, we examined the mRNA expression of the prostacyclin receptor in various rat tissues, and further investigated its gene expression in the hypertrophied cardiac ventricles of stroke-prone spontaneously hypertensive rats (SHRSP). 3. In rat tissues, a single RNA band of approximately 3.7 kb was detected by northern blotting analysis using rat prostacyclin receptor cDNA as a probe. In adult Wistar rats, abundant mRNA expression was observed in the aorta, lung and spleen. Substantial amounts of transcript were expressed in the heart, pancreas, thymus and stomach. In contrast, no mRNA expression was detected in the brain. 4. We further examined the mRNA expression of the prostacyclin receptor in the ventricles of 21 week old SHRSP. The ventricles of SHRSP showed remarkable hypertrophy, compared with those of age-matched Wistar-Kyoto (WKY) rats. The expression of prostacyclin receptor mRNA in the hypertrophied ventricles of SHRSP was almost equivalent to that in the ventricles of WKY. 5. The present study revealed the gene expression of the prostacyclin receptor in various rat tissues, and further demonstrated the receptor mRNA expression in hypertensive cardiac hypertrophy. The present study will give a clue to investigate the clinical implication of prostacyclin and its receptor.

Molecular remodelling in hypertrophied hearts from polyomavirus large T-antigen transgenic mice.

Polyomavirus large T-antigen transgenic mice develop cardiac hypertrophy characterized by an increase in atrial natriuretic factor and beta-myosin heavy chain isoform expression. The aim of this study was to examine changes in proto-oncogene expression in hypertrophied hearts from the transgenic mice. Expression of early growth response-1 (Egr-1) mRNA was detected in hearts from all 15 transgenic mice, but was not detectable in 13 control mice. Reverse transcriptase-polymerase chain reaction experiments using Egr-1-specific primers confirmed the increase in Egr-1 mRNA in enlarged hearts from the transgenic mice. Expression of c-jun, junD and Ha-ras mRNAs was increased in the transgenic hearts 3, 17 and 2.8-fold respectively. Western blots showed an increase in c-myc, c-jun and ras protein in hypertrophied transgenic hearts. Immunofluorescence analyses confirmed an increase in Egr-1 and c-jun protein in transgenic cardiomyocytes. Proliferating cell nuclear antigen, Ki-ras and HSP 90 mRNAs were decreased 22, 2.7 and 3-fold, respectively in the transgenic hearts. Not altered in most hypertrophied hearts was expression of c-fos, junB, p53, c-neu, c-myc, HSP70, HSP27, TGF-beta or IGF 1 mRNAs. Proto-oncogene and growth factor gene expression in hypertrophy induced by PVLT expression is modulated with some proto-oncogenes increased and others decreased in expression.

Cardiac catheterization and other imaging modalities in the evaluation of valvular heart disease.

This review describes recent publications using cardiac catheterization and diagnostic imaging modalities, excluding transesophageal and transthoracic echocardiography, to evaluate valvular heart disease. Radionuclide techniques and magnetic resonance imaging continue to be studied as to whether they can improve the quantification of valvular regurgitation. As yet, however, they are not justified in the routine evaluation of patients with valvular heart disease. Cardiac catheterization has been used by several authors to assess more completely the obstructive physiology of valve stenosis, including obtaining a better understanding of transvalvular pressure gradients; the phenomenon of downstream pressure recovery; and the utility of valve resistance in quantifying the severity of the valve stenosis, which complements the calculated valve area, especially in cases of low cardiac output. Traditional cardiac catheterization techniques have recently been used to show a sex difference in left ventricular systolic performance in aortic stenosis. Intracardiac ultrasound and electrocardiography are being studied as methods to guide percutaneous valvotomy. The analysis of myocardial tissue samples obtained by endocardial biopsy promises understanding gene-protein-function interactions. Specifically, myosin alterations in aortic valve disease and protooncogene expression in hypertrophy are exciting, emerging areas of investigation.

Cardiac myosin heavy and light chain gene expression in hypertrophy and heart failure

Cardiac myosin heavy and light chain gene expression in hypertrophy and heart failure

THE OCULAR COMPLICATIONS OF BRIGHT'S DISEASE

GENERAL STATEMENT. The eyes become involved as a result of the general systemic conditions arising in Bright's disease. These systemic conditions, briefly considered, are the result of faulty kidney excretion, leading to the retention of urea or other excrementitious substances in the blood. These retained products are either poisonous in themselves or secondarily lead to the formation of toxins, thus producing inflammatory and degenerative changes in the vessel walls and the tissues of the body; or they may interfere with the proper conversion of the elements of food into those favorable for assimilation by the cells of the body, thus producing anemia and hydremia. To this abnormal condition of the blood is attributed the general arteriofibrosis, which finds its expression in hypertrophy of the heart and general increased arterial tension, leading to exudation and hemorrhage or total occlusion of the arterioles, with subsequent death of the parts cut off. In