Protein synthesis and degradation during regression of thyroxine-induced cardiac hypertrophy.
نویسندگان
چکیده
To characterize changes in rates of protein turnover during regression of thyroxine-induced left ventricular hypertrophy, New Zealand White rabbits received intravenous thyroxine (200 micrograms/kg/d) for 9 days. Thyroxine was withheld, and in vivo protein turnover was evaluated on the 10th, 15th and 20th days. Animals not receiving thyroxine served as controls. Heart rate, blood pressure, and rate-pressure product were measured to correlate changes in cardiac work with protein turnover rates during the development and regression of hypertrophy. Thyroxine administration produced left ventricular hypertrophy by increasing the rate of protein synthesis (from 37.9 +/- 8.9 to 64.1 +/- 15.3 mg/day; P less than 0.05) to a greater degree than protein degradation (from 29.8 +/- 8.9 to 48.2 +/- 15.3 mg/day for control and thyroxine-treated animals, respectively; P less than 0.05). Cessation of thyroxine administration resulted in an eventual return of left ventricular mass to that of normally growing control animals. The major observation noted during thyroxine withdrawal was a return of protein synthetic rates to normal. Absolute rates of protein degradation remained elevated, whereas fractional protein degradative rates (i.e. the fraction of total protein degraded per day) were unchanged by the administration and withdrawal of thyroxine. These results indicate that suppression of both physiological and hormone-induced growth following cessation of thyroxine resulted from a decrease in cardiac protein synthetic rates and an increased rate of flux through the protein degradative pathway(s), while fractional rates of protein degradation (and thus average protein half-life) remained unchanged. The development and regression of thyroxine-induced hypertrophy correlated with thyroxine-mediated alterations in cardiac work.
منابع مشابه
Synthesis and degradation of myocardial protein during the development and regression of thyroxine-induced cardiac hypertrophy in rats.
Cardiac hypertrophy was induced in rats by daily injections of L-thyroxine (1.0 mg/kg). Regression from hypertrophy was studied 4 days after discontinuing thyroxine. Isolated, Langendorff-perfused hearts were perfused with Krebs-Henseleit buffer, glucose, insulin, and amino acids. To measure protein synthesis, left ventricular tissue was assayed for incorporation of tritiated phenylalanine into...
متن کاملThe Effect of Aerobic Training on expression of some indices of myocardial hypertrophy and atrophy in rats
Background: Protein synthesis and degradation are dynamically regulated processes that to control the accretion or loss of muscle mass. However, the mechanisms responsible exercise-induced heart hypertrophy remains elusive. The aim of this study was to investigate the effect of aerobic training on expression of some indices of myocardial hypertrophy and atrophy in male rats. Materials and Meth...
متن کاملThe Possible Role of TNF-alpha in Physiological and Pathophysiological Cardiac Hypertrophy in Rats
Pathological cardiac hypertrophy was produced by partial abdominal aortic constriction (PAAC) for 4 wk, while physiological cardiac hypertrophy was produced by chronic swimming training (CST) for 8 wk in rats. Pentoxifylline (30 mg/kg, 300 mg/kg i.p., day-1) treatment was started three days before PAAC and CST and it was continued for 4 wk in PAAC and 8 wk in CST experimental model. The left ve...
متن کاملRole of oxidative stress in the aortic constriction-induced ventricular hypertrophy in rat
Introduction:Severe abdominal aortic constriction above the renal arteries induces arterial hypertension above the stenotic site that is the cause of cardiac hypertrophy. Previous studies have shown that high blood pressure induces myocardial oxidative stress with conflicting results. In the present study, we assessed the effects of acute hypertension on the myocardial oxidative stress an...
متن کاملEffect of 8 Weeks of Endurance Training on S6K1 and 4EBP1 Proteins Content in the Left Ventricle of the Heart of Diabetic Rats Induced by Streptozotocin and Nicotinamide
Introduction: Physiological hypertrophy of the heart is dependent on cellular pathways and important proteins such as the ribosomal protein S6 kinase beta-1 (S6K1) and eukaryotic translation intiation factor4E-binding protein-1(4EBP1). The aim of this study was to investigate the effect of 8 weeks of endurance training on ribosomal protein S6 kinase beta-1 and eukaryotic translation initiation...
متن کاملذخیره در منابع من
با ذخیره ی این منبع در منابع من، دسترسی به آن را برای استفاده های بعدی آسان تر کنید
برای دانلود متن کامل این مقاله و بیش از 32 میلیون مقاله دیگر ابتدا ثبت نام کنید
ثبت ناماگر عضو سایت هستید لطفا وارد حساب کاربری خود شوید
ورودعنوان ژورنال:
- Journal of molecular and cellular cardiology
دوره 21 9 شماره
صفحات -
تاریخ انتشار 1989