Ventricular remodeling and transforming growth factor-beta 1 mRNA expression after nontransmural myocardial infarction in rats: effects of angiotensin converting enzyme inhibition and angiotensin II type 1 receptor blockade

  title={Ventricular remodeling and transforming growth factor-beta 1 mRNA expression after nontransmural myocardial infarction in rats: effects of angiotensin converting enzyme inhibition and angiotensin II type 1 receptor blockade},
  author={Tae-Jin Youn and H.-S. Kim and Byung Hee Oh},
  journal={Basic Research in Cardiology},
  • T. YounH. KimB. Oh
  • Published 1 August 1999
  • Biology, Medicine
  • Basic Research in Cardiology
Abstract With the application of early reperfusion therapy after acute MI, the incidence and importance of nontransmural infarction is increasing. In a rat model with nontransmural infarction, we evaluated 1) the changes of LV dimension, LV interstitial fibrosis and transforming growth factor-β1 (TGF-β1) mRNA expression and 2) the effects of angiotensin converting enzyme (ACE) inhibitor and angiotensin II type 1 (AT1) receptor antagonist treatment. Female Sprague-Dawley rats were subjected to… 

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Cardiac Fibrogenesis Following Infarction in Mice With Deletion of Inducible Nitric Oxide Synthase

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The Possible Beneficial Effect of Angiotensin II Receptor Antagonist (Losartan) in Experimental- Hepatic Fibrosis in Albino Rats. Histological, Immunohistochemical and Biochemical Study

It is found that losartan has a benifical effect in liver fibrosis induced by BDL, however, further study for its usefulness in human hepatic fibrosis is recommended.

A potential role for angiotensin II in obesity induced cardiac hypertrophy and ischaemic/reperfusion injury

Current data suggest that angiotensin II may contribute to obesity induced cardiac remodelling and ischaemic/reperfusion injury, and blood pressure, and heart weight to body weight ratios.



Comparative effects of chronic angiotensin-converting enzyme inhibition and angiotensin II type 1 receptor blockade on cardiac remodeling after myocardial infarction in the rat.

It is demonstrated that inhibition of generation of angiotensin II and AT1 receptor blockade are equally effective in preventing important features of ventricular remodeling after myocardial infarction and failure and restores minimal coronary vascular resistance in postinfarction reactive hypertrophy.

Differential effects of kinins on cardiomyocyte hypertrophy and interstitial collagen matrix in the surviving myocardium after myocardial infarction in the rat.

Kinins inhibit the interstitial accumulation of collagen but do not modulate cardiomyocyte hypertrophy after MI, which is related to a reduced generation/receptor blockade of angiotensin II.

Transforming growth factor beta-1 in acute myocardial infarction in rats.

A significant role for TGF-beta in the response of the heart to injury is indicated, as shown by the results of immunohistochemical staining and Northern blot analysis of mRNA.

Effects of an AT1 receptor antagonist, an ACE inhibitor and a calcium channel antagonist on cardiac gene expressions in hypertensive rats

The results show that hypertension causes not only left ventricular hypertrophy but also molecular transition of myocardium to a foetal phenotype and interstitial fibrosis‐related molecular changes.

Hypertrophic stimuli induce transforming growth factor-beta 1 expression in rat ventricular myocytes.

The view that TGF-beta 1, released by myocytes and acting in an autocrine and/or paracrine manner, is involved in myocardial remodeling by hypertrophic stimuli is supported.

Angiotensin II stimulates extracellular matrix protein synthesis through induction of transforming growth factor-beta expression in rat glomerular mesangial cells.

Results indicate that Ang II induces mesangial cell synthesis of matrix proteins and show that these effects are mediated by Ang II induction of TGF-beta expression, which may well contribute to glomerulosclerosis in vivo.

Molecular characterization of angiotensin II--induced hypertrophy of cardiac myocytes and hyperplasia of cardiac fibroblasts. Critical role of the AT1 receptor subtype.

The phenotypic changes of cardiac cells in response to Ang II in vitro closely mimic those of growth factor response in vitro and of load-induced hypertrophy in vivo, and all biological effects of Ang II examined here are mediated primarily by the AT1 receptors.

Altered Left Ventricular Remodeling With βd‐Adrenergic Blockade and Exercise After Coronary Reperfusion in Rats

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Interactions of transforming growth factor-beta and angiotensin II in renal fibrosis.

The protective effect of inhibition of the renin-angiotensin system in experimental and human kidney diseases correlates closely with the suppression of transforming growth factor-beta production, suggesting that transforming growthfactor-beta, in addition to blood pressure, should be a therapeutic target.

Angiotensin II-induced mitogenesis of spontaneously hypertensive rat-derived cultured smooth muscle cells is dependent on autocrine production of transforming growth factor-beta.

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