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PubMedDate not supplied

[Study of the role of endogenous 3',5'-cyclic AMP in the radioresistance of the cell].

A survival period of irradiated rat thymocytes was studied after administration of several possible modifiers of intracellular 3',5'-cyclo AMP. Theophylline, which inhibits 3',5'-cyclo AMP phosphodiesterase, adrenaline, ATP and adenosine possessed a radioprotective effect if they were added before the irradiation or just immediately after it. Imidazole activated 3',5'-cyclo AMP phosphodiesterase and, being added within the above-mentioned periods, it shortened the survival period at the irradiated cells. When theophylline and imidazole were added within 30 min after the irradiation, their effect was completely altered: imidazole increased but theophylline decreased the survival period of the irradiated cells. 3',5'-cyclo AMP and N6-2'-0-dibutyryl-3',5'-cyclo AMP did not affect the viability of thymocytes after the irradiation.

3',5'-Cyclic-AMP Phosphodiesterases↗
PubMed1990

Dissociation between cyclic AMP rise and mucin secretion in response to a beta-adrenergic agonist.

A novel hypotonic swelling method has been used to introduce cyclic AMP phosphodiesterase (cAMP PDE) into intact rat submandibular acini. Acini swollen in the presence of cAMP PDE showed no cyclic AMP rise in response to the beta-agonist isoproterenol; however, stimulation of mucin secretion was not impaired. Control experiments showed that acini swollen in the absence of cAMP PDE showed normal cyclic AMP rise and mucin secretion responses. The results showing a dissociation between cyclic AMP rise and mucin secretion suggest that cyclic AMP is not the sole mediator of beta-adrenergic stimulation of epithelial cell secretion. The method of intracellular manipulation described will allow (i) investigation of key regulators of secretory events, shown to be defective in CF cells. (ii) determination of the biochemical function of proteins which are candidates for the biochemical defect in CF.

3',5'-Cyclic-AMP Phosphodiesterases↗
PubMed1978

Effect of the diuretic, 1,4-dimorpholino-7-phenylpyrido[3,4-d]-pyridazine (DS-511) and its derivatives on ADH-cyclic AMP system in rat renal medullary slices.

The effect of the diuretics, 1,4-dimorpholino-7-phenylpyrido[3,4-d]pyridazine (DS-511) and its 4'-hydroxy derivative [DS-511(4'-OH)] on the ADH-cyclic AMP system was studied in slices of rat renal medulla. These compounds alone did not affect the basal level of cyclic AMP in the slices. Preincubation with 10(-6) mol DS-511 or 10(-7) to 10(-5) mol DS-511-(4'-OH) in the presence of theophylline, inhibited arginine vasopressin stimulated formation of cyclic AMP, but after washing the slices the formation was restored. Etacrynic acid required higher concentrations such as 10(-5) and 10(4-) mol to cause inhibition. No effect was observed with furosemide and hydrochlorothiazide in concentrations up to 10(-4) mol. DS-511(4'-OH) at concentrations higher than 10(-6) mol inhibited the activity of cyclic AMP-phosphodiesterase in the medullary homogenate. These results suggest the water diuretic action of DS-511 is partly mediated by its inhibition of the ADH-cyclic AMP system.

3',5'-Cyclic-AMP Phosphodiesterases↗
PubMed1989

[The role of ADP-cyclic AMP system in horseshoe crab amebocytes aggregation and gel formation].

A study of the effects of ADP and cyclic AMP related drugs on gel formation induced by endotoxin and amebocytes aggregation was conducted. The gel formation induced by endotoxin could be inhibited by ADP, cyclic AMP, ATP and aminophylline. Conversely, Phosphodiesterase enhanced gelation rate. A calmodulin antagonist, trifluoperazine, also inhibited endotoxin-induced gel formation, but this agent was able to induce potentiation in amebocytes aggregation. These results suggest that the cyclic AMP phosphodiesterase system may play an important role in endotoxin-induced gel formation, and it was concluded that, in the presence of both Ca++ and endotoxin, the calmodulin-like protein will activate the cyclic AMP phosphodiesterase system and decrease the concentration of cyclic AMP, thus promoting gel formation.

3',5'-Cyclic-AMP Phosphodiesterases↗
PubMed1985

A possible cyclic AMP-mediated regulation of microsomal fatty acyl-CoA desaturation system in Tetrahymena microsomes.

Profound alterations in the microsomal fatty acyl-CoA desaturase activities and cyclic AMP production of a unicellular eukaryote, Tetrahymena pyriformis NT-1, originally grown in the glucose-deficient medium, were observed, following the administration of glucose or beta-adrenergic agonists such as epinephrine and isoproterenol. There was a great increase of stearoyl-CoA (delta 8) desaturase activity coincident with a 2-fold decrease of oleoyl-CoA (delta 12) desaturase activity over the first 2 h after administration of these compounds. During this period of time, it was found that the production in vivo of labeled oleic acid from [14C]acetic or [3H]palmitic acid increases 2-fold and the formation in vivo of each labeled linoleic and gamma-linolenic acids drastically decreases. Glucose or beta-adrenergic agonists caused an increase of stearoyl-CoA-stimulated reoxidation rate of NADH-reduced cytochrome b5 but depressed oleoyl-CoA-stimulated reoxidation rate of b5, indicating that both desaturase activities are controlled by the respective terminal components of the desaturase system. A significant and reproducible increase of adenylate cyclase activity and a slight decrease of cyclic AMP phosphodiesterase activity were observed to occur within the first 2 h after the addition of these compounds, when cyclic AMP content in Tetrahymena cell rose by 3-4-fold. Propranolol, a beta-adrenergic blocker, abolished the effects of glucose or beta-adrenergic agonists on the activities of fatty acyl-CoA desaturases and the terminal components as well as cyclic AMP production of cells. These results suggest that glucose and beta-adrenergic agonists may modulate the microsomal fatty acyl-CoA desaturase system in Tetrahymena by acting through the increase of intracellular cyclic AMP content.

3',5'-Cyclic-AMP Phosphodiesterases↗
PubMedDate not supplied

[Effect of training and physical load on 3':5'-AMP content and activity fo the enzymes of its metabolism in rat muscle].

It is established tha in skeletal muscles of dormant animals under the influence of training the 3':5'-AMP content and the activity of adenylate cyclase increase; that of phosphodiesterase remains unchanged. A long physical load causes no changes in the 3':5"-AMP content in the skeletal muscles of the trained rats as compared to its content in the intact animals but evokes a decrease as compared to its level in the trained rats muscles. The activity of adenylate cyclase in the skeletal muscles of the trained rats under long physical load lowers, that of 3':5'-AMP phosphodiesterase also decreases but to a less extent. The found changes in the 3':5'-AMP metabolism in the trained animals skeletal muscles evidence for a possible participation of the 3':5'-AMP system in development of the organism adaptation to higher physical loads.

3',5'-Cyclic-AMP Phosphodiesterases↗
PubMed2002

Cyclic AMP-receptor proteins in human salivary glands.

In mammalian species, cyclic AMP receptor proteins (cARP) are the regulatory (R) subunits of cyclic AMP-dependent protein kinase (PKA), the cellular effector of cyclic AMP-mediated signal transduction. An isoform of the PKA type II R subunit (RII), cARP, is a polyfunctional protein, present in most tissues and cells. It is expressed in salivary and other glands of rodents, and secreted into the saliva of rats and Man. The aim of the present study was to determine the expression of cARP in human salivary glands using immunoelectron microscopy. Thin sections of normal salivary glands embedded in LR Gold resin were labeled with anti-cARP primary antibody, then with gold-conjugated secondary antibody. Labeling was present in the secretory granules and cytoplasm of parotid, submandibular (SMG) and sublingual gland serous cells. Quantitative analysis showed considerable variability in granule labeling from sample to sample, indicating shifts in expression and cellular location of cARP. Unlike rodent salivary glands, the granules of intercalated and striated duct cells also were labeled. The cytoplasm and granules of mucous cells of the SMG and sublingual glands were unlabeled, while the Golgi complex and filamentous bodies in these cells showed moderate reactivity. Mitochondria and nuclei of both serous and mucous cells were unlabeled. Labeling also was present in the connective tissue adjacent to the epithelial cells. The results indicate that serous cells of the parotid and SMG are the major source of salivary cARP. They also reveal significant species differences in the glandular distribution of RII. RII binds to cytoskeletal and nuclear proteins, and may function to regulate extracellular cyclic AMP levels. Thus, the tissue and cellular distribution of RII may serve as an index of regulation of gene expression and cell differentiation.

Antibodies↗
PubMed1975

Effect of surgical trauma on plasma concentrations of cyclic AMP and cortisol.

The response of plasma cortisol and cyclic AMP concentrations to surgical trauma was examined in 7 general surgical patients. Five patients made uncomplicated recoveries and showed peak cortisol levels at 6 hours postoperatively, returning to normal by 24 hours. On patient developed postoperative pneumonia and the plasma cortisol remained elevated up to 48 hours, and the final patient showed no cortisol response at all. The plasma cyclic AMP concentrations showed a consistent rise during the operation itself, which was statistically significant when compared with preoperative levels (P less than 0.0125). Concentrations had fallen to normal by 6 hours in all the cases, except in the patient who developed pneumonia, where the plasma cyclic AMP also showed a prolonged elevation. The significance of these findings requires further elucidation, but the temporal relationship of the cyclic AMP and cortisol peaks would support the hypothesis that cyclic AMP may play a part in the mediation of ACTH release following surgical trauma.

Adrenocorticotropic Hormone↗
PubMed1978

Cyclic AMP, adrenaline and noradrenaline in plasma during surgery.

Plasma concentrations of cyclic AMP, adrenaline and noradrenaline were measured in 6 patients undergoing hysterectomy from before induction of anaesthesia to 6 h after skin incision. Noradrenaline did not vary significantly during the observation period, whereas cyclic AMP and adrenaline increased after skin incision. A significant correlation was found between plasma concentrations of cyclic AMP and adrenaline (r = 0.84, P less than 0.01), suggesting that the latter is responsible for the increase in plasma cyclic AMP which is observed in relation to surgical procedures. Peak concentrations of cyclic AMP and adrenaline were seen in the early postoperative phase. This indicates that the most pronounced acute endocrine stress response to surgery of moderate severity occurs after termination of anaesthesia.

Adult↗
PubMed1988

New synthesis of cyclic AMP-dependent protein kinases during liver regeneration.

As has been previously reported one surge in cytosolic calmodulin is produced between 4 and 12 h after a partial hepatectomy. Moreover, a surge in cytosolic cyclic AMP and another in cyclic AMP-dependent protein kinase activity can be detected during the late period of the prereplicative phase of liver regeneration after a partial hepatectomy. It is known that these three surges are involved in triggering DNA synthesis. By kinetic studies and by injecting transcription (actinomycin D) and translation (cycloheximide) inhibitors into hepatectomized rats we have demonstrated that the cyclic AMP-dependent protein kinase surge is produced by new synthesis of the enzyme. In thyroparathyroidectomized rats subjected to a partial hepatectomy the calmodulin surge was similar to that observed in normal hepatectomized rats whereas the surge in cyclic AMP-dependent protein kinase activity was strongly decreased suggesting that the cyclic AMP-dependent protein kinase surge is not generated by the previous surge in calmodulin.

Calmodulin↗
PubMed1975

The effect of insulin on basal and hormone-induced elevations of cyclic AMP content in cultured human fibroblasts.

Studies were carried out on confluent cultures of human fibroblasts to explore the effect of insulin on basal and hormone-induced elevations of intracellular cyclic AMP content during short-term incubations in serum-free medium. Insulin tended to decrease basal levels of cyclic AMP but this was not statistically significant. Similarly, insulin was unable to block the elevations of intracellular cyclic AMP content induced by PGE1, epinephrine and glucagon. Paradoxically, when cells were preincubated with insulin, PGE1-stimulated cyclic AMP elevation was potentiated, possibly because insulin was conserving factors needed for a maximal PGE1 stimulus or retarding the leakage of cAMP itself. The results indicate that insulin has little or no direct effect on cyclic AMP metabolism in cultured human fibroblasts and is consistent with the known insensitivity of these cells to insulin for other parameters.

Adult↗
PubMed1979

Evidence suggesting that a cyclic AMP-dependent protein kinase is a positive regulator of proliferation in Cloudman S91 melanoma cells.

Wild-type Cloudman S91 melanoma cells have a retarded rate of division when agents which raise cyclic AMP levels such as melanotropin, protaglandin E1, or cholera toxin are supplemented to the culture medium. A mutant cell line was isolated which had the opposite response, i.e., the mutant grew very slowly unless agents which raised cyclic AMP levels were present (Pawelek et al., '75a). In this report evidence is presented indicating that the molecular basis for the mutant phenotype resides in the major cyclic AMP-dependent protein kinase found in the cells. The mutant kinase had increased thermolability and an elevated activation constant for cyclic AMP over the corresponding wild-type kinase. It is proposed that the elevated requirement for cyclic AMP for the proliferation of cAdep cells is related to the elevated activation constant of the kinase, suggesting that the kinase is a positive regulator of proliferation in Cloudman S91 cells.

Animals↗
PubMed1982

Increases in cyclic AMP potentiate competence formation in BALB/c-3T3 cells.

The ability of platelet-derived growth factor and fibroblast growth factor to stimulate the initiation of DNA synthesis in quiescent BALB/c-3T3 cells was enhanced by cholera toxin. However, the addition of cholera toxin to unsupplemented medium was not mitogenic, nor did cholera toxin increase the mitogenic potential of medium supplemented with platelet-poor plasma. The enhancement of serum-induced DNA synthesis by cholera toxin was due to a specific effect on competence formation and not plasma-controlled progression. Cholera toxin increased the rate of competence formation during a transient exposure of quiescent cells to platelet-derived growth factor; this rate was further increased by the addition of isobutylmethylxanthine, a cyclic nucleotide phosphodiesterase inhibitor. Intracellular cyclic AMP concentrations in quiescent BALB/c-3T3 cells were increased 2- to 3-fold after the addition of cholera toxin., The addition of cholera toxin plus 30 microM isobutylmethylxanthine caused an even greater (7- to 8-fold) increase in the cellular levels of cyclic AMP. That these increases in cyclic AMP concentrations mediated at least part of the increased sensitivity of quiescent cells to competence factors was substantiated by the observation that 0.01 to 1 mM monobutrylcyclic AMP or 8-bromocyclic AMP also caused a concentration-dependent potentiation of competence formation in quiescent cells during a transient exposure to platelet-derived growth factor.

8-Bromo Cyclic Adenosine Monophosphate↗
PubMed1982

Cyclic AMP does not modulate hexose uptake of serum-deprived BHK-21 fibroblasts.

We have studied the uptakes of the glucose analogs, 2-deoxyglucose (2DG), and 3-O-methylglucose (3OMG) in serum-deprived BHK-21 fibroblasts. Incubation for 4 hours with 0.25 mM 1-methyl-3-isobutylxanthine (MIX) increased cellular cyclic AMP 3 to 15 fold, without affecting the initial rates of uptake of these sugars. Incubation with 100 nM insulin, doubled hexose uptake without affecting cyclic AMP. Insulin did not modify the cyclic AMP response to MIX; nor did MIX alter the hexose uptake response to insulin. There was no effect of 0.1 mM L-isoproterenol (ISO) or 0.1 mM prostaglandin E1 (PGE1) on cyclic AMP. PGE1 slightly stimulated uptake of 2DG but not 3OMG; ISO did not affect hexose uptake. We conclude that cyclic AMP does not directly regulate hexose uptake in these cells.

1-Methyl-3-isobutylxanthine↗
PubMed1985

The possible cyclic AMP-dependence of an early prereplicative event that determines mitosis in regenerating rat liver.

The beta-adrenergic blocker dl-propranolol prevented a large proportion of regenerating rat liver cells from entering the mitotic phase of their first cell division cycle without affecting their ability to initiate or complete DNA replication. The drug, at a dose of 20 or 50 mg/kg of body weight, was most effective in reducing mitosis when injected between 1 and 2 hours after the proliferatively activating partial hepatectomy, which was 22 to 23 hours before the peak of DNA-synthetic activity. Propranolol also inhibited the early prereplicative surge of total liver cyclic AMP, which occurs shortly after partial hepatectomy, but this effect was not correlated to the mitosis-inhibiting activity. However, cyclic AMP or dibutyryl cyclic AMP completely reversed propranolol's mitosis-inhibiting action when injected between 1.5 and 2 hours (but not sooner or later) after partial hepatectomy, which was just before the total liver cyclic AMP content began to rise. Thus, there appears to be a transient, propranolol-inhibitable, probably cyclic AMP-initiated event in the early prereplicative development of rat hepatocytes that determines entry into mitosis rather than the initiation of DNA replication.

Adenine Nucleotides↗
PubMed1987

In vitro effect of a thymic epithelial culture supernate or thymosin fraction 5 on rabbit platelet aggregation and intracellular cyclic AMP levels.

Supernates of thymic epithelial cell culture (STEC) strongly inhibit aggregation induced by addition of adenosine diphosphate (ADP: 1 microM) or thrombin (0.5 unit per ml) to washed platelet suspensions and accelerated the restoration from ADP-triggered aggregation. At the same time, STEC increased the level of platelet adenosine 3',5'-cyclic monophosphate (cyclic AMP) in a dose-dependent manner. Depending on the concentration used, thymosin fraction 5 increased the level of intracellular cyclic AMP ranging between 5 and 100 micrograms per ml, as well as inhibiting ADP-induced platelet aggregation. The activities of both STEC and thymosin fraction 5 were found to act exclusively on cyclic AMP phosphodiesterase activity in platelets. In contrast the supernates from Chang, HeLa, or HCC-M cells did not affect platelet aggregation induced by ADP, but slightly increased the cyclic AMP level (Chang, HeLa). Within 2 min after the treatment with STEC, more than 50% of the maximum inhibitory activity on platelet aggregation and increases in intracellular cyclic AMP were observed. These activities disappeared following STEC treatment with pronase E. STEC activity was found predominantly in the 1,000-50,000-dalton fractions. These activities were not altered when STEC was treated by adenosine deaminase. The level of prostaglandin E (PGE) derivatives in STEC was about two times that found in the control culture medium. These data suggest that the biological activity of STEC in the platelets might be attributed to thymosinlike polypeptides and PGE1.

Adenosine Deaminase↗
PubMed1990

Dual effects of glucagon and cyclic AMP on DNA synthesis in cultured rat hepatocytes: stimulatory regulation in early G1 and inhibition shortly before the S phase entry.

Although several lines of evidence implicate cyclic AMP in the humoral control of liver growth, its precise role is still not clear. To explore further the role of cyclic AMP in hepatocyte proliferation, we have examined the effects of glucagon and other cyclic AMP-elevating agents on the DNA synthesis in primary cultures of adult rat hepatocytes, with particular focus on the temporal aspects. The cells were cultured in a serum-free, defined medium and treated with epidermal growth factor (EGF), insulin, and dexamethasone. Exposure of the hepatocytes to low concentrations (10 pM-1 nM) of glucagon in the early stages of culturing (usually within 6 h from plating) enhanced the initial rate of S phase entry without affecting the lag time from the plating to the onset of DNA synthesis, whereas higher concentrations inhibited it. In contrast, glucagon addition at later stages (24-45 h after plating) produced only the inhibition. Thus, if glucagon was added at a time when there was a continuous EGF/insulin-induced recruitment of cells to S phase, the rate of G1-S transition was markedly decreased within 1-3 h. This inhibitory effect occurred at low glucagon concentrations (ID50 less than 1 nM) and was mimicked by cholera toxin, forskolin, isobutyl methylxanthine, and 8-bromo cyclic AMP. The results indicate that cyclic AMP has dual effects on hepatocyte proliferation with a stimulatory modulation early in the prereplicative period (G0 or early G1), and a marked inhibition exerted immediately before the transition from G1 to S phase.

Animals↗
PubMed1991

B16 mouse melanoma cells selected for resistance to cyclic AMP-mediated growth inhibition are cross-resistant to retinoic acid-induced growth inhibition.

B16 mouse melanoma cells are grown inhibited by cyclic AMP or by retinoic acid (RA). However, the combination of these two agents results in less growth inhibition than either agent alone. In order to investigate this interaction, cells were selected for resistance to 8-bromo-cyclic AMP-induced growth inhibition. Two clones (3 and 7) which demonstrated significant resistance were isolated. When these two clones were treated with retinoic acid (RA) it was observed that they also exhibited different degrees of resistance to this growth inhibitor. This cross-resistance did not appear to be due to a lack of uptake or retention of the respective inhibitors, since the mutants took up and retained more 3H-cAMP and 3H-RA than wild type cells, suggesting that the dual resistance was not due to an amplification of P-glycoprotein. The mutation confering cAMP-resistance did not appear to involve cyclic AMP-dependent protein kinase, since both catalytic activity and the amount of cAMP protein binding was similar in wild type and mutants. Thus, the mutation must be beyond the interaction of cAMP with cAMP-dependent protein kinase. We have previously reported that RA induces protein kinase C in B16 melanoma cells (Niles and Loewy: Cancer Res. 49:4483-4487, 1989). Therefore, we measured the ability of RA to induce protein kinase C in the cyclic AMP-resistant mutants. We found an inverse correlation between RA-induced protein kinase C activity and growth inhibition in these mutants. The data reported here suggest that cyclic AMP regulates some step in the RA signal transduction pathway.

Animals↗