Increase in type I adenosine 3′,5′-monophosphate-dependent protein kinase during isoproterenol-induced cardiac hypertrophy

Byus, Craig V.; Chubb, James M.; Huxtable, Ryan J.; Russell, Diane Haddock

doi:10.1016/0006-291x(76)90866-4

Cited by 70 publications

(16 citation statements)

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“…This cell cycle-specific expression of type I and type II protein kinases suggests an orderly sequence of phosphorylation during the cell cycle, presumably catalyzed by a specific type of protein kinase. In isoproterenol stimulation of cardiac hypertrophy in the rat, type I protein kinase was increased in specific activity 2-fold after daily injection of the drug for 10 days (15 (1978) analogues of cyclic AMP, prostaglandins, and high concentrations of concanavalin A (16). The above studies emphasize the importance of the types of protein kinase present, their relative amounts, and their selective activation.…”

mentioning

confidence: 83%

“…This cell cycle-specific expression of type I and type II protein kinases suggests an orderly sequence of phosphorylation during the cell cycle, presumably catalyzed by a specific type of protein kinase. In isoproterenol stimulation of cardiac hypertrophy in the rat, type I protein kinase was increased in specific activity 2-fold after daily injection of the drug for 10 days (15). Recent reports indicate that the stimulation of mitogenesis in human lymphocytes by plant lectins such as phytohemagglutinin and concanavalin A is related to early activation of type I protein kinase and is inhibited by the simultaneous early activation of both type I and type II protein kinase that occurs in response to nonspecific stimuli such as 223 The costs of publication of this article were defrayed in part by the payment of page charges.…”

Section: Introductionmentioning

confidence: 99%

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Specific regulation by steroid hormones of the amount of type I cyclic AMP-dependent protein kinase holoenzyme.

Fuller¹,

Byus²,

Russell³

1978

Proc. Natl. Acad. Sci. U.S.A.

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The total amounts of type I and type II cytoplasmic cyclic AMP-dependent protein kinase activities were measured in various tissues of intact rats and rats subjected to castration, hypophysectomy, or adrenalectomy. After castration, the total amount of type I activity decreased rapidly in classically steroid-responsive tissues such as the ventral prostate and levator ani muscle and less rapidly in the liver. After hypophysectomy and adrenalectomy, type I activity in the liver de-creased to the same extent as after castration. Type I activity could be maintained in the ventral prostate and levator ani muscle at control levels by the daily injection of dihydrotestosterone. Furthermore, after post-castration regression of the prostate for 3 days, three daily subcutaneous injections of dihydrotestosterone resulted in a complete restoration of type I activity to the intact level. The amount of type II activity was not altered by any of the experimental ablations. This study provides evidence linking steroid action to the ability of steroid-responsive tissues to maintain a substantial activity of type I cyclic AMP-dependent protein kinase.Since the proposal of the second-messenger theory of hormone action (1), a rapidly expanding body of literature has confirmed the involvement of cyclic AMP in the regulation of anabolic events stimulated by trophic hormones. Indeed, cyclic AMPmediation of hypertrophy always seems to be expressed through a temporally linked series of events (2). Instrumental in the elucidation of this series of events has been the extensive substantiation of an earlier hypothesis of Kuo and Greengard (3) that all the effects of cyclic AMP are mediated through cyclic AMP-dependent protein kinases. Because certain tissues have sufficient cyclic AMP levels to activate these enzymes, at least partially, it now seems that the measurement of further activation, rather than measurement of detectable elevation of cyclic AMP, is the parameter of choice for study of the cellular events produced by trophic agents.The involvement of cyclic nucleotides in the action of steroid hormones has been less clear, with some controversy evident in the literature. Singhal et al. (4) Increasing evidence suggests that the total amount of type I and type II cyclic AMP-dependent protein kinase activity present in a tissue must be considered as well as the activation of varying pool sizes of protein kinases in response to specific stimuli. The relative amounts of type I and type II protein kinase vary among tissues; a striking example is the almost total lack of type I in bovine heart contrasted to type I predominating in rat heart (8, 9).Recent evidence suggests different biological roles for type I and type II cyclic AMP-dependent protein kinases. In rat testes, Lee et al. (10) were able to show an alteration in the amount of type I and type II as a function of ontogeny. Whereas testes from fetal and 2-day-old rats exhibit only type I protein kinase, type II protein kinase levels increase gradually during the first po...

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mentioning

confidence: 83%

“…This cell cycle-specific expression of type I and type II protein kinases suggests an orderly sequence of phosphorylation during the cell cycle, presumably catalyzed by a specific type of protein kinase. In isoproterenol stimulation of cardiac hypertrophy in the rat, type I protein kinase was increased in specific activity 2-fold after daily injection of the drug for 10 days (15). Recent reports indicate that the stimulation of mitogenesis in human lymphocytes by plant lectins such as phytohemagglutinin and concanavalin A is related to early activation of type I protein kinase and is inhibited by the simultaneous early activation of both type I and type II protein kinase that occurs in response to nonspecific stimuli such as 223 The costs of publication of this article were defrayed in part by the payment of page charges.…”

Section: Introductionmentioning

confidence: 99%

Specific regulation by steroid hormones of the amount of type I cyclic AMP-dependent protein kinase holoenzyme.

Fuller¹,

Byus²,

Russell³

1978

Proc. Natl. Acad. Sci. U.S.A.

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“…The kidney enzyme was separated into two peaks (PKI and PKII), as reported in the case of other tissues (14). It was also reported that the amounts of the isozymes were altered in pathological conditions of the experimental animals (23,24). Therefore, the isozyme distribution in the kidney of hypothyroid rats was compared with that of the normal.…”

Section: Discussionmentioning

confidence: 99%

Effects of phenylephrine and isoproterenol on the activity of cyclic AMP-dependent protein kinase of hypothyroid rat tissues.

1979

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Abstract-The present study was designed to examine the properties of cyclic AMP dependent protein kinase from normal and hypothyroid rat tissues. The activity of the liver enzyme decreased in hypothyroid rats and this reduced activity may be due to the decrease in synthesis of enzyme protein. The enzyme activity from the kidney of hypothyroid rats increased by 35% in the absence of cyclic AMP. Further, the enzyme from the kidney of hypothyroid animals responded to phenylephrine and isoproterenol.In the heart, the basal enzyme activity was the same in both groups, but the enzyme from the heart of hypothyroid animals did not respond to isoproterenol. When hypothyroid rats were treated with 3,3',5-triiodothyronine, the enzyme activities from those rat tissues showed essentially the same level as those of the corresponding normal ones. These results suggest that thyroid hormone regulates adrenergic agonists mediated responses both at the sites of adrenoceptors and that of protein phosphory lation. Furthermore, the dependence on thyroid hormone varies according to the tissue.Thyroid hormone plays an important role in the regulation of adrenergic agonists mediated responses in tissues from several species (1). There may be at least two sites of action of thyroid hormone in regard to this mechanism: one is the adrenoceptors including adenylate cyclase and the other the intracellular processes after the formation of the agonists receptor complex.In our laboratory, we found that the increased response of a-adrenoceptors of hearts from hypothyroid rats to phenylephrine and decreased response of jj-adrenoceptors of hearts and livers from hypothyroid rats to isoproterenol could not be explained by changes in intracellular contents of cyclic AMP. It has also been suggested that the decreased sensitivity of i3-adrenoceptor in the liver and heart might account for the change in enzyme activities involved in cyclic AMP metabolism (2-5).The present study was carried out to compare the cyclic AMP-dependent protein kinase activity of normal and hypothyroid rats and to examine the effects of adrenergic agonists on this enzyme. The possible physiological relationship between thyroid hormone and adrenergic agonists is discussed. MATERIALS AND METHODSMale Wistar strain rats were used throughout the experiments. Rats were made hypo

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“…Catecholamines have been repeatedly implicated in cardiac hypertrophy in studies of exogenously administered isoprenaline, adrenaline or noradrenaline (Fisher, Horst & Kopin, 1965;Nair, Cutilletta & Rabinowitz, 1968;Stanton, Brenner & Mayfield, 1969;Feldman & Russell, 1972;Laks, Morady & Swan, 1973;Byus, Chubb, Huxtable & Russell, 1976). Three fold elevations of the endogenous plasma catecholamine, adrenaline, have been shown to parallel cardiac hypertrophy in the dog (Womble, Haddox & Russell, 1978) whereas ablation of plasma adrenaline by adrenal medulla denervation prevents cardiac hypertrophy after aortic constriction (Womble, Larson, Copeland, Brown, Haddox & Russell, 1980).…”

Section: Introductionmentioning

confidence: 99%

“…Three fold elevations of the endogenous plasma catecholamine, adrenaline, have been shown to parallel cardiac hypertrophy in the dog (Womble, Haddox & Russell, 1978) whereas ablation of plasma adrenaline by adrenal medulla denervation prevents cardiac hypertrophy after aortic constriction (Womble, Larson, Copeland, Brown, Haddox & Russell, 1980). Since catecholamines possessing both a and 1 agonistic properties increase cyclic AMP and ODC in the heart (Keely, Corbin & Park, 1975;Warnica, Antony, Gibson & Harris, 1975;Byus et al, 1976;Bareis & Slotkin, 1978;Fuller & Hemrick, 1978;Keely, Lincoln & Corbin, 1978), the present study examined the specific nature of the receptor(s) coupled to the ODC response in foetal murine heart by evaluation with both a and P agonists and antagonists.…”

Section: Introductionmentioning

confidence: 99%

β₂‐ADRENOCEPTORS REGULATE INDUCTION OF MYOCARDIAL ORNITHINE DECARBOXYLASE IN MICE in vivo

Copeland¹,

Larson²,

Roeske³

et al. 1982

British J Pharmacology

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The pharmacological characteristics of the myocardial adrenoceptor of the mouse have been examined during embryogenesis by measuring ornithine decarboxylase (ODC, EC 4.1.1.17) induction. A four fold elevation of ODC activity was observed after isoprenaline (10 mg/kg, s.c), and enzyme activity was increased two to three fold following adrenaline (1 mg/kg, s.c.) or terbutaline given by direct injection to the foetus (10 μg/500 mg). Pretreatment with the β‐adrenoceptor antagonist, propranolol (10 mg/kg), totally blocked the increase in ODC activity. Elevation of myocardial ODC activity was not inhibited by metoprolol, a relatively specific β1‐adrenoceptor antagonist, at a dose of 10 mg/kg. Since the increase in ODC activity was blocked by a β‐adrenoceptor antagonist (propranolol) and enzyme activity was stimulated by terbutaline, a β2‐agonist, we conclude that β2‐adrenoceptors are selectively coupled to the regulation of murine cardiac ODC activity following catecholamine stimulation.

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Increase in type I adenosine 3′,5′-monophosphate-dependent protein kinase during isoproterenol-induced cardiac hypertrophy

Cited by 70 publications

References 10 publications

Specific regulation by steroid hormones of the amount of type I cyclic AMP-dependent protein kinase holoenzyme.

Specific regulation by steroid hormones of the amount of type I cyclic AMP-dependent protein kinase holoenzyme.

Effects of phenylephrine and isoproterenol on the activity of cyclic AMP-dependent protein kinase of hypothyroid rat tissues.

β₂‐ADRENOCEPTORS REGULATE INDUCTION OF MYOCARDIAL ORNITHINE DECARBOXYLASE IN MICE in vivo

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Increase in type I adenosine 3′,5′-monophosphate-dependent protein kinase during isoproterenol-induced cardiac hypertrophy

Cited by 70 publications

References 10 publications

Specific regulation by steroid hormones of the amount of type I cyclic AMP-dependent protein kinase holoenzyme.

Specific regulation by steroid hormones of the amount of type I cyclic AMP-dependent protein kinase holoenzyme.

Effects of phenylephrine and isoproterenol on the activity of cyclic AMP-dependent protein kinase of hypothyroid rat tissues.

β2‐ADRENOCEPTORS REGULATE INDUCTION OF MYOCARDIAL ORNITHINE DECARBOXYLASE IN MICE in vivo

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β₂‐ADRENOCEPTORS REGULATE INDUCTION OF MYOCARDIAL ORNITHINE DECARBOXYLASE IN MICE in vivo