Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.4.24.3 (collagenase)
 18,340 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Liver cells were obtained from adult rats by a collagenase perfusion technique and cultured as monolayers in serum-free media. Epinephrine and isoproterenol both induced large increases in intracellular adenosine 3':5'-monophosphate (cAMP) within 1-2 min whereas epinephrine (but not isoproterenol) induced 2- to 3-fold increases in the rate of alpha-aminoisobutyric acid transport within 2-4 hr after a 1 hr lag. Propranolol abolished the increase in cAMP elicited by epinephrine and isoproterenol, but did not block the induction of alpha-aminoisobutyric acid transport by epinephrine. In contrast, dihydroergotamine abolished and phentolamine diminished the induction of alpha-aminoisobutyric acid transport by epinephrine but did not decrease the stimulation of cAMP levels by epinephrine. Epinephrine dose response curves for cAMP and alpha-aminoisobutyric acid transport were similar. Once exposed to epinephrine, cells became refractory to further stimulation of cAMP levels by epinephrine.
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PMID:3':5'-cyclic AMP: independent induction of amino acid transport by epinephrine in primary cultures of adult rat liver cells. 1 65

Hepatocytes isolated from the liver of the common goldfish Carassius auratus L. with crude bacterial collagenase maintained ATP levels for at least 2 h. Glycogenolysis was maximally activated by 1 X 10(-6) M epinephrine and 5.8 X 10(-9) M glucagon. In liver cells incubated in calcium-free buffer containing 1 mM ethylene glycol-bis-(beta-aminoethylether)-N,N'-tetraacetic acid, basal glycogenolysis was enhanced by the addition of 1-4 mM calcium but the elevation of cyclic AMP and glycogenolysis due to epinephrine was unaffected by calcium. The divalent cation ionophore A23187 did not alter basal or hormone-stimulated glycogenolysis. Isoproterenol was approximately as potent as epinephrine but phenylephrine was glycogenolytic only at very high concentrations. l-Propranolol competitively inhibited the increased glycogenolysis due to catecholamines but phentolamine was ineffective as a blocking agent. Isoproterenol and epinephrine stimulated glycogenolysis at lower concentrations than those required to elevate cyclic AMP accumulation. Phenylephrine was without effect on cyclic AMP. Propranolol competitively inhibited both epinephrine- and isoproterenol-stimulated cyclic AMP accumulation, but phentolamine did not block either response. Catecholamine-stimulated glycogenolysis in goldfish liver is apparently a beta-adrenergic effect. However, low concentrations of epinephrine enhance glycogenolysis without affecting total cyclic AMP.
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PMID:Hormone-stimulated glycogenolysis in isolated goldfish hepatocytes. 18 9

Hepatocytes from adult male Sprague-Dawley rats were isolated by the two-stage collagenase perfusion technique; 1 x 10(6) cells/plate were incubated in primary cell culture in Leibovitz's L-15 medium for 24 hr with or without various concentrations (12.5 to 400 mumol/L) of cardioactive cationic amphiphilic compounds such as propranolol, verapamil, sotalol, atenolol and procainamide. Propranolol and verapamil caused a significant release of lactate dehydrogenase (used as cytotoxic index in this study) in the culture media in a concentration-dependent manner, with LC50 values of 220 +/- 10 and 224 +/- 7 mumol/L, respectively. Atenolol, sotalol and procainamide had no effect on lactate dehydrogenase release. Electron microscopy of the hepatocytes showed that subtoxic concentrations of propranolol (12.5 to 125 mumol/L) and verapamil (12.5 to 100 mumol/L) induced multilamellar inclusion bodies after 24 hr of incubation. The two higher concentrations of propranolol (50 and 125 mumol/L) and 100 mumol/L of verapamil produced a significant decrease in the percentage of volume density of the mitochondria as quantitated by morphometrical analysis. An unusual feature of the electron microscopical changes with propranolol and verapamil was the presence of mitochondria within the multilamellar inclusion bodies. When these two drugs were used together or with subtoxic concentrations of amiodarone or desethylamiodarone, release of lactate dehydrogenase was significantly enhanced. No correlation was evident between the cytotoxic response and the volume density of cellular inclusions in hepatocytes treated with different concentrations of propranolol, verapamil, amiodarone or desethylamiodarone. Sotalol, atenolol and procainamide in concentrations up to 400 mumol/L did not produce any ultrastructural changes in hepatocytes after 24 hr of incubation. These results show that (a) cationic amphiphilic structure per se is not the only requirement for induction of multilamellar inclusions, (b) propranolol and verapamil can induce the formation of multilamellar inclusion bodies and cause a concentration-dependent release of lactate dehydrogenase from hepatocytes and (c) combination of different cationic amphiphiles in subtoxic concentrations can enhance cytotoxicity and increase the volume density of multilamellar inclusions.
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PMID:Cytotoxic interactions of cardioactive cationic amphiphilic compounds in primary rat hepatocytes in culture. 237 84

This study investigated the direct effect of catecholamines, epinephrine (EPI), and norepinephrine (NE) on basal and gonadotropin-releasing hormone (GnRH)-stimulated secretion of luteinizing hormone (LH) from dispersed pig pituitary cells in vitro. Pig pituitaries were dispersed into cells with collagenase and DNAase and then cultured in McCoy's 5a medium containing horse serum (10%) and fetal calf serum (2.5%) pretreated with dextran-coated charcoal for 3 days. EPI and NE did not affect basal LH secretion after 4 h of incubation. When pituitary cells were incubated with EPI or NE (1 microgram/ml) for longer than 30 min, GnRH-stimulated LH secretion was reduced. The degree of this reduction was dependent on EPI and NE, and a concentration of EPI and NE higher than 1 ng/ml and 100 ng/ml, respectively, was needed. L-isoproterenol, a nonselective beta-agonist, also inhibited the LH response to GnRH. Propranolol, a beta-antagonist, blocked the inhibitory effect of EPI, whereas phentolamine, an alpha-antagonist, had no effect. These results suggest that catecholamines, acting by a beta 2-adrenergic receptor, may play a role in the control of the porcine pituitary gonadotrope's response to GnRH.
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PMID:Catecholamine inhibition of luteinizing hormone secretion in isolated pig pituitary cells. 266 85

Effects of adrenergic and cholinergic drugs and prostaglandin E1 on cyclic nucleotide accumulation and parameters of growth and basement membrane synthesis were examined in corneal epithelial cell cultures. 8-bromo-cGMP significantly (p less than 0.05) enhanced incorporation of labeled thymidine and leucine, as did acetylcholine and carbamylcholine, which elevated cGMP and decreased cAMP/cGMP ratio. Responses to acetylcholine were abolished by atropine and alpha-bungarotoxin. Precursor incorporation was inhibited by dibutyryl cAMP and adenosine 5'-monophosphate and by norepinephrine, epinephrine, prostaglandin E1, and theophylline, which significantly elevated cAMP levels and cAMP/cGMP ratio. Propranolol, but not phenoxybenzamine, blocked responses to effective concentrations of norepinephrine. Norepinephrine, PGE1, and dibutyryl cAMP also significantly elevated uptake of labeled glucosamine and incorporation of labeled proline into collagenase-sensitive protein or the hydroxyproline fraction of protein hydrolysates, while acetylcholine had no effect on parameters of basement membrane synthesis. Propranolol blocked responses to norepinephrine. Results were consistent with a cGMP-mediated stimulatory role of the cholinergic transmitter in corneal epithelial growth regulation, cAMP-mediated beta-adrenergic suppression of regrowth and increased basement membrane production after initial injury to the corneal epithelium, and potentiation of the adrenergic effect by prostaglandins.
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PMID:Cholinergic, adrenergic, and PGE1 effects on cyclic nucleotides and growth in cultured corneal epithelium. 629 65