Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: 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)

Polymorphonuclear (PMN) leukocytes mediate that phase of inflammation at which vascular responses become translated into tissue injury. After phagocytosis, the PMN leukocyte generates derivatives of molecular oxygen (O2-.,OH., and H2O2) that stimulate a metabolic burst and assist in the killing of microorganisms. They also release oxidation products of membrane fatty acids (e.g., arachidonate), which are detected as thromboxanes and protaglandins. After interaction of phagocytic ligands (immune complexes and C3b-opsonized particles), the PMN leukocyte secretes lysosomal enzymes from open phagocytic vacuoles, and, especially when phagocytosis is blocked by cytochalasin B, secretes them directly into the cell's surrounding fluids. Secretion is enhanced by agents that elevate intracellular levels of cyclic GMP, and inhibited by agents that raise cyclic AMP. These reciprocal changes are associated with assembly and disassembly (respectively) of cytoplasmic microtubules. These cytoskeletal structures, together with contractile elements, regulate in part the secretory events of inflammation in which lysosomal constituents (e.g., elastase, collagenase, and cathepsin G) are diverted from their intracellular depots to an inappropriate assault on the tissues of the host.
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PMID:Polymorphonuclear leukocytes as secretory organs of inflammation. 21 Feb 34

Renal gluconeogenesis was studied in suspended tubule fragments isolated by collagenase treatment of rat kidney cortices. Angiotensin II increased glucose formation from pyruvate, lactate, and to a lesser extent from oxoglutarate and glutamine, but not from other substrates such as malate, succinate, dihydroxyacetone or fructose. Stimulation was significant with peptide concentration exceeding 1 . 10(-8) M and was also shown with an 8-Sar derivative. Other peptides such as 4-Ala-8-Ile-angiotensin II, hexapeptide and bradykinin had no effect. The stimulatory action of angiotensin II was additive to that of L-lysine, and 3',5'-adenosine cyclic monophosphate, suggesting a different mechanism of action. In the presence of maximally stimulatory concentrations of oleate, phenylephrine and 3',5'-guanosine cyclic monophosphate, however, the stimulatory effect of angiotensin II was absent. Cyclic GMP levels, however, did not increase in tubules after angiotensin II and phenylephrine addition, making a messenger function of this nucleotide unlikely. Omission of Ca2+ from the medium markedly reduced basal gluconeogenesis but did not result in a complete loss of angiotensin II effect. Reduction of medium potassium to 2 mM, however, increased basal gluconeogenesis and blunted the peptide effect. 1 mM ouabain was also able to inhibit the stimulatory effect of angiotensin II. Therefore changes in intracellular potassium levels are discussed as a possible mechanism of angiontensin action, whereas calcium seems not to be specifically linked to this metabolic action of angiotensin on the proximal tubule.
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PMID:Stimulation of renal gluconeogenesis by angiotensin II. 45 78

The lapine synovial cell line HIG-82 secretes factors that activate cultures of articular chondrocytes. We showed that these "chondrocyte-activating factors" (CAF) also activate quiescent cultures of HIG-82 cells in an autocrine fashion. After exposure to partially purified preparations of CAF, HIG-82 cells increased their synthesis of prostaglandin E2 (PGE2) and the neutral proteinases collagenase, gelatinase, and stromelysin. CAF also induced their own synthesis. Both PGE2 synthesis and endogenous production of CAF started to increase between 1 and 3 h after treatment of cells with exogenous CAF, but the neutral proteolytic activity of the conditioned medium took approximately 12 h to increase. Induction of neutral proteinases by CAF was inversely related to the degree of cell confluency, whereas their induction by phorbol myristate acetate (PMA) was independent of this parameter. Both CAF and PMA provoked morphologic changes in subconfluent cultures of HIG-82 cells. Although the intracellular concentration of free Ca2+ increased rapidly in response to CAF, the results of experiments with calcium channel blockers and ionophores failed to support a role for Ca2+ fluxes in induction of neutral proteinases. In similar types of experiments, no evidence could be found to implicate fluxes in cyclic AMP or cyclic GMP in the induction of collagenase, gelatinase, or stromelysin. Because PMA is such a strong inducer of these enzymes, protein kinase C may be involved in signal transduction, but further work is needed to determine whether this is so.
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PMID:Studies on the autocrine activation of a synovial cell line. 165 86

Enterocytes from the intestinal epithelium of the winter flounder were isolated by collagenase digestion and incubated in flounder Ringer solution. Conventional whole-cell and amphotericin-perforated whole-cell recording techniques were used to characterize the properties of a voltage-activated K current present in dissociated cells. Resting membrane potentials and series resistances were significantly lower (from -23 to -39 mV and 29 to 13 M omega, respectively) when amphotericin was used to achieve the whole-cell configuration. When cells were placed in flounder Ringer solution, held at -80 mV and subsequently stepped to a series of depolarizing voltages (from -70 to 0 mV), an outward current was observed that exhibited inactivation at voltages above -20 mV. This current was sensitive to holding potential and was not activated when the cells were held at -40 mV or above. When cells were bathed in symmetric K Ringer solution and the same voltage protocol was applied to the cell, inward currents were observed in response to the negative intracellular potentials. Reversal potentials at two different extracellular K concentrations were consistent with K as the current-carrying ion. BaCl2 (2 mM) and CsCl (0.5 mM) both produced voltage-dependent blockade of the current when added to the bathing solution. Charybdotoxin (300 nM extracellular concentration) completely blocked the current. The IC50 for charybdotoxin was 50 nM. Cyclic GMP inhibited the voltage-activated current in flounder Ringer and in symmetric K Ringer solution. The cyclic GMP analog, 8-Br cGMP, lowered the threshold for voltage activation and potentiated inactivation of the current at voltages above -40 mV.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Cyclic GMP regulation of a voltage-activated K channel in dissociated enterocytes. 166 85

The present study evaluates suitable in vitro methods for the assessment of the inhibiting properties of four principally different antidepressant drugs. This was done by comparing the acute effects of antidepressants on autonomic receptor binding (homogenates) together with parallel tests evaluating the biological activities of the receptor systems in collagenase-isolated rat parotid acini. The responses were measured as receptor-activated changes in cyclic nucleotide formation and acinar oxygen consumption. Muscarinic acetylcholine receptor binding, carbachol-induced cGMP formation, and oxygen consumption all reflected the various inhibiting effects of the antidepressants tested. Measurements of the carbachol-induced O2 consumption was however, the most sensitive method and may be considered a well-suited and reliable parameter concerning the expected severity of anticholinergic side-effects caused by medication. The disturbing 'dry mouth' symptoms following treatment with amitriptyline or mianserin are however, also attributed to their substantial adrenoceptor-blocking effects, which are best demonstrated by alpha 1-adrenoceptor binding studies in combination with measurements of the adrenaline-induced O2 consumption in the rat parotid gland.
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PMID:In vitro methods for the assessment of the inhibitory effects of antidepressants in rat parotid glands. 166 35

The present study examines the mechanism(s) of action of anethole trithione compared to the sialogogue pilocarpine. This was done by comparing the acute effects of these drugs on autonomic receptor binding (homogenates) together with parallel tests evaluating the biological activities of the receptor systems in collagenase-isolated rat parotid acini. The responses were measured as receptor-activated changes in cyclic nucleotide formation and acinar oxygen consumption. The results revealed that anethole trithione was unable to bind to muscarinic acetylcholine receptors and unable to stimulate the dynamic processes directly. It did, however, inhibit part (about 50%) of the carbachol-induced cyclic guanosine 3',5'-monophosphate (cyclic GMP) formation and O2 uptake. Furthermore, anethole trithione (greater than 1 microM) displaced [3H]prazosin (but not [3H]dihydroalprenolol ([3H]DHA] binding, without any effect upon the adrenaline-induced cyclic adenosine 3',5'-monophosphate (cyclic AMP) formation and O2 uptake. In conclusion, this study has shown that anethole trithione is not to be considered as a simple cholinergic agonist like pilocarpine, and further elucidation of the mechanism(s) of action of this agent would be useful.
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PMID:Acute effects of a possible sialogogue, anethole trithione, in rat parotid glands. 166 56

Cyclic guanosine monophosphate (GMP) productions by alpha rat atrial natriuretic peptide 1-28 (alpha-rANP), carbamylcholine or sodium nitroprusside were assessed in isolated glomeruli microdissected from collagenase-treated kidneys of 2- to 34-day-old and adult rats. In both young and adult animals, alpha-rANP-stimulated cyclic GMP generation was proportional to the number of glomeruli and was enhanced in a dose-dependent and saturable fashion with increasing alpha-rANP concentrations. The apparent activation constant values were 6.4 nM for 5-day-old and 9.7 nM for adult rats. Maximal doses of either alpha-rANP or rANP 5-28 elicited similar responses in young and adult animals. Clear differences appeared between the developmental patterns of cyclic GMP productions stimulated by either alpha-rANP, carbamylcholine or sodium nitroprusside. The response to alpha-rANP was very large in the youngest rats tested, declined sharply during the suckling period and represented about 1.6 times the adult control level in 34-day-old rats. In contrast, the response to carbamylcholine was low after birth and rose progressively with age up to the adult level at the end of the weaning period, and the response to nitroprusside seemed to be independent of the animal's age.
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PMID:Developmental pattern of cyclic guanosine monophosphate production stimulated by atrial natriuretic peptide in glomeruli microdissected from kidneys of young rats. 217 15

A microradioimmunoassay has been developed in order to measure the changes in cGMP cell content induced in vitro by atrial natriuretic peptides (ANP) in either glomeruli or defined portions of tubules microdissected from collagenase treated rat and rabbit kidneys. When tested at 0.1 microM or 1 microM, all ANP analogues used produced in rat glomeruli a 20-25 fold increase in cGMP accumulation compared to basal values. Threshold responses were obtained with about 1 nM ANP and apparent Ka values ranged between 5 and 50 nM. Atriopeptin III led to similar results in glomeruli isolated from rabbit. Under the same experimental conditions, no cGMP could be detected in any ANP-treated nephron segment from the rat kidney (namely, from the proximal convoluted tubule up to the outer medullary collecting tubule) nor in cortical collecting tubules isolated from the rabbit kidney. Moreover, ANP did not alter the forskolin-induced increase in cAMP content in glomeruli or collecting tubules, nor the AVP-induced increase in cAMP content in collecting tubules. Our data confirm the marked effect of ANP on cGMP generation by isolated glomeruli from rat and rabbit; however, they are not compatible with a direct action of ANP stimulating cGMP generation in tubules or inhibiting vasopressin-induced cAMP generation in collecting tubules.
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PMID:Atrial natriuretic peptide effects on cGMP and cAMP contents in microdissected glomeruli and segments of the rat and rabbit nephrons. 243 41

The effect of atrial natriuretic peptide (ANP) on renin release is controversial. Several reports state that ANP inhibits renin secretion, while others have shown no effect. We investigated the effect of synthetic rat ANP with 24 amino acids (atriopeptin III) on renin release in vitro in a dynamic superfusion system of renal cortical slices as well as collagenase-dispersed juxtaglomerular cells. In the superfusion system of kidney slices, isoproterenol (5 x 10(-8) M) clearly stimulated renin release from kidney slices, while angiotensin II (AII; 10(-5) M) suppressed renin release. ANP (10(-10)-10(-6) M) did not inhibit basal renin release or blunt the stimulatory effect of isoproterenol. The suppression of renin secretion by AII was never modified in the presence of ANP. The superfusion system of juxtaglomerular cells demonstrated greater sensitivity of renin release in responses to isoproterenol and AII. In this system, ANP (10(-6) M) did not alter renin release from the cells stimulated by isoproterenol (5 x 10(-8) M) or inhibited by AII (10(-8) M). However, basal renin release was slightly stimulated in the late phase of ANP superfusion and for 20 min after the ANP perfusion was stopped. Similarly, 8 bromo-cGMP (10(-6) M) did not inhibit, but, rather, stimulated basal renin release slightly. These results suggest that ANP does not inhibit renin release by a direct effect on the juxtaglomerular cell in the rat.
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PMID:Effect of atrial natriuretic peptide on renin release in a superfusion system of kidney slices and dispersed juxtaglomerular cells. 283 Oct 30

In the present study we investigated the relation between receptor activation and the acinar formation of cyclic nucleotides as a function of time, including effects of calcium. The experiments were performed using collagenase-isolated rat parotid acini and the cyclic nucleotide content was determined using a specific cAMP binding protein and cGMP antibody. Under physiological conditions, activation of beta-adrenoceptors increased cAMP content 27 fold within 60 sec. This response was not dependent upon the presence of extracellular calcium nor could it be mimicked by the calcium ionophore A23187. The adrenaline-induced activation of the alpha-adrenergic receptors lead to a 19% increase in cGMP content within 15 sec. This response was abolished in the absence of extracellular calcium. Pure activation of the alpha-1-adrenoceptors by phenylephrine resulted in a 62% increase in cGMP content within 15 sec. Finally, carbachol-induced activation of the cholinoceptors lead to a 50% transient increase in cGMP content within 7 sec. In the absence of calcium (EGTA present), the basal cGMP level was increased and in addition, the carbachol-induced cGMP formation was slower in onset and amounted to only 23% within 60 sec. The carbachol-induced cGMP formation could be mimicked by the calcium ionophore A23187 or by addition of calcium to acini preincubated in a calcium free buffer containing A23187. In conclusion, stimulation-induced formation of cyclic nucleotides under various conditions proved to be very rapid, well regulated, and sensitive processes.
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PMID:Stimulation-induced changes in cyclic nucleotide content by isolated rat parotid acini: effects of calcium. 284 42


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