The effect of streptozotocin-induced diabetes in rats on cardiac contractile proteins.

Malhotra, Ashwani; Penpargkul, Somsong; Fein, F. S.; Sonnenblick, Edmund H.; Scheuer, James

doi:10.1161/01.res.49.6.1243

Cited by 197 publications

(66 citation statements)

References 32 publications

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“…It has been shown that many other pathophysiological states, including exercise (52,53), diabetes (54,55), starvation (56), high carbohydrate diet (56), adrenalectomy (56), dwarfism (57), and gonadectomy (58), can also modulate the cardiac MHC isozyme distribution. It remains to be seen whether these stimuli act independently on the expression of the MHC genes or whether their effects are mediated by a common biochemical signal.…”

Section: Resultsmentioning

confidence: 99%

Myosin heavy chain messenger RNA and protein isoform transitions during cardiac hypertrophy. Interaction between hemodynamic and thyroid hormone-induced signals.

Izumo¹,

Lompré²,

Matsuoka³

et al. 1987

J. Clin. Invest.

431

198

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Expression of the cardiac myosin isozymes is regulated during development, by hormonal stimuli and hemodynamic load. In this study, the levels of expression of the two isoforms (a and ,j) of myosin heavy chain (MHC) during cardiac hypertrophy were investigated at the messenger RNA (mRNA) and protein levels. In normal control and sham-operated rats, the a-MHC mRNA predominated in the ventricular myocardium. In response to aortic coarctation, there was a rapid induction of the #-MHC mRNA followed by the appearance of comparable levels of the jN-MHC protein in parallel to an increase in the left ventricular weight. Administration of thyroxine to coarctated animals caused a rapid deinduction of 0-MHC and induction of a-MHC, both at the mRNA and protein levels, despite progression of left ventricular hypertrophy. These results suggest that the MHC isozyme transition during hemodynamic overload is mainly regulated by pretranslational mechanisms, and that a complex interplay exists between hemodynamic and hormonal stimuli in MHC gene expression.

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Section: Resultsmentioning

confidence: 99%

Myosin heavy chain messenger RNA and protein isoform transitions during cardiac hypertrophy. Interaction between hemodynamic and thyroid hormone-induced signals.

Izumo¹,

Lompré²,

Matsuoka³

et al. 1987

J. Clin. Invest.

431

198

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show abstract

“…In the early stages of the disease in either genetically diabetic mice [22] or streptozotocindiabetic rats [23], myocyte damage has been observed which involved mitochondria, myofilaments and sarcoplasmic reticulum; moreover, alterations have been found in myosin isotypes [24] as well as in a variety of cellular functions such as myosin-ATPase activity, calcium uptake, catecholamine sensitivity and Na +-K +-ATPase [24][25][26].…”

Section: Discussionmentioning

confidence: 99%

Increased rat myocardial type VI collagen in diabetes mellitus and hypertension

Spiro

Crowley

1993

Diabetologia

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Summary. Diabetic cardiomyopathy, a condition characterized by the accumulation of carbohYdrate-containing material surrounding the myocardial small blood vessels, has been studied in alloxan-diabetic normotensive and hypertensive rats. Immunochemical techniques were used to monitor several extracellular matrix constituents present in extracts of cardiac tissue, namely types I, IV and VI collagen, laminin and fibronectin, as well as myosin. These studies have indicated that after induction of diabetes, type VI collagen but none of the other matrix components studied, was significantly increased (from 2.29 + 0.04 mg/g in normal to 2.85 + 0.18 mg/g in diabetic ventricles, p < 0.01). Hypertension, whether induced by the clipping of one renal artery or genetically determined (spontaneously hypertensive rats), resulted in a similar elevation in type VI collagen (2.71 + 0.12 rag/g, p < 0.005 compared to normal rats). In the presence of diabetes plus hypertension the effect was not additive, the type VI collagen level being 2.93 + 0.15 (p < 0.001 compared to normal rats). Basement membrane collagen (type IV) in the myocardium appeared to be unaffected by diabetes or hypertension and the myosin contents of the hearts of the four experimental groups were similar. Quantitative determinations indicate that compared to type IV collagen, laminin or fibronectin, type VI collagen represents the major periodic acid-Schiff-reactive extracellular constituent of the rat ventricle. Its preferential increase in the heart in diabetes may provide insight into the molecular mechanisms of the diabetic microvascular disease.

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“…Male and female rats were used because although hypertensive hypertrophy occurs in both sexes with consequent depressed contractile protein ATPase levels, physical training by swimming is associated with physiologic hypertrophy only in the females (5 (6,7).…”

Section: Methodsmentioning

confidence: 99%

Physiologic cardiac hypertrophy corrects contractile protein abnormalities associated with pathologic hypertrophy in rats.

Scheuer¹,

Malhotra²,

Hirsch³

et al. 1982

J. Clin. Invest.

Self Cite

146

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A B S T R A C T To evaluate the combined effects of cardiac overload imposed by hypertension and by chronic exercise, male and female rats were made hypertensive by unilateral renal artery stenoses and made to exercise in an 8-10-wk swimming program. Sedentary normotensive animals, sedentary hypertensive animals and normotensive animals exposed to the swimming program were also studied. Hypertension was associated with the development of cardiac hypertrophy, and this was exaggerated in hypertensive swimmers. Actomyosin, Ca2`-myosin, and actin-activated Mg2 -myosin ATPase activities were enhanced in normotensive swimmers, depressed in hypertensives and were normal or increased in hypertensive swimmers. Myosin isoenzyme analysis showed a predominant VI pattern in normals; an increase in percent VI isoenzyme is swimmers; a predominant V3 pattern in hypertensives; and a return to the predominant V1 pattern in hypertensive swimmers. These findings suggest that the hypertrophy imposed by hypertension and hypertrophy imposed by physical training using a chronic swimming program are distinctly different biological phenomena. Physical training by swimming prevents the changes in cardiac myosin induced by hypertension despite the exaggeration of hypertrophy.A preliminary report of this work was presented at the

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The effect of streptozotocin-induced diabetes in rats on cardiac contractile proteins.

Cited by 197 publications

References 32 publications

Myosin heavy chain messenger RNA and protein isoform transitions during cardiac hypertrophy. Interaction between hemodynamic and thyroid hormone-induced signals.

Myosin heavy chain messenger RNA and protein isoform transitions during cardiac hypertrophy. Interaction between hemodynamic and thyroid hormone-induced signals.

Increased rat myocardial type VI collagen in diabetes mellitus and hypertension

Physiologic cardiac hypertrophy corrects contractile protein abnormalities associated with pathologic hypertrophy in rats.

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