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)

The production of collagenase by human skin explants in culture is prevented by 10(-8) M dexamethasone, 5 . 10(-4) M dibutyryl cyclic AMP, or 2.5 . 10(-3) M theophylline. Decreases in collagenase activity are paralleled by reductions in the degradation of explant collagen during the culture period. Progesterone, which effectively inhibits collagenase production in rat uterine explant cultures, has no effect on human skin explants. The inhibition by cyclic AMP is nucleotide specific. When partially inhibitory concentrations of dexamethasone and dibutyryl cyclic AMP, or dexamethasone and theophylline, are added to culture medium together, the resultant inhibition is that predicted by additivity. Synergistic inhibition, as observed in rat uterus between progesterone and dibutyryl cyclic AMP, fails to occur. Dexamethasone inhibits the production of collagenase by cultured explants of rat uterus, with complete inhibition occurring at 10(-7) M steroid. Synergism between glucocorticoids and dibutyryl cyclic AMP or between dexamethasone and progesterone could not be demonstrated in the uterine culture system. These results suggest the existence of three regulatory systems for the control of collagenase production in mammalian tissues, and that cooperativity between systems may occur on a tissue-specific basis.
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PMID:Hormonal interactions in mammalian collagenase regulation. Comparative studies in human skin and rat uterus. 624 13

The effects of a corticosteroid substitute pregn-4-ene-3,20-dione-11 beta,17 alpha-dihydroxy-21-pivalate (tixocortol, JO 1016, Pivalone), hydrocortisone acetate and beclomethasone dipropionate on collagen metabolism in mouse calvariae were compared by histological and biochemical determination of collagen content, and by radio-assays of collagenase and collagenase inhibitor. Hydroxyproline assay revealed dose-related increases in collagen content/wet wt. tissue. These were greatest in explants treated with beclomethasone dipropionate, tixocortol pivalate being effective only at much higher concentrations than the other 2 drugs. Hydrocortisone acetate and beclomethasone dipropionate stimulated collagenase production at the lowest levels tested whereas tixocortol pivalate was only slightly stimulatory at the highest treatment level. These results suggest that in clinical use tixocortol pivalate would be much less likely than hydrocortisone acetate or beclomethasone dipropionate to cause degenerative changes in connective tissue.
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PMID:A comparison of the effects of tixocortol pivalate (JO 1016), hydrocortisone acetate and beclomethasone dipropionate on collagen synthesis and degradation. 626 73

Corpora lutea from cyclic ewes were dissociated by collagenase digestion and trypsin/EGTA treatment. Enriched fractions of endothelial cells, small luteal cells and large luteal cells were prepared on a stepped gradient of Ficoll 400. Progesterone was measured by radioimmunoassay and the results corrected so that progesterone production by each cell type could be determined. Endothelial cells did not produce significant amounts of progesterone, with or without LH stimulation, and endothelial cell contamination of small and large luteal cell fractions did not influence progesterone production by these fractions. Mean +/- s.e.m. basal progesterone production (n = 10) by large luteal cells was greater (P less than 0.001) on a per cell basis than that by small luteal cells (1.16 +/- 0.16 compared with 0.25 +/- 0.06 pg/h/cell). However LH, which stimulated a maximal 3-4-fold increase in progesterone production by small luteal cells (LH ED50 = 0.14 ng/ml), had no significant effect on production by large luteal cells, when contamination by small luteal cells was taken into account. The response of small luteal cells was specific to LH, other hormones having had no significant effect. Basal progesterone production by small luteal cells (0.12 +/- 0.03 fg/h/micron3) calculated per unit volume of cell was not significantly different from that of large luteal cells (0.17 +/- 0.02 fg/h/micron3). After LH stimulation, small luteal cells produced more progesterone than did large luteal cells (0.40 +/- 0.09 compared with 0.18 +/- 0.03 fg/h/micron3) (P less than 0.05). When the amounts of progesterone produced per cell were multiplied by the absolute numbers of large luteal (1 X 10(7] and small luteal (5 X 10(7] cells in the intact corpus luteum, basal progesterone production by large luteal cells (11.6 +/- 1.6 micrograms/h) was similar to that by small luteal cells (12.3 +/- 3.0 micrograms/h). However, under LH stimulation, progesterone production by the small luteal cell type (39.9 +/- 9.5 micrograms/h) was approximately 3 times greater than that by the large luteal cell type (12.3 +/- 1.6 micrograms/h) (P less than 0.05). We therefore conclude that small luteal cells may be the principal source of luteal progesterone production in the sheep.
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PMID:Progesterone production in vitro by small and large ovine luteal cells. 631 Jan 6

Experiments were conducted to determine if methylation is a part of the mechanism by which luteinizing hormone (LH) and epinephrine stimulate progesterone production by dispersed bovine luteal cells. Corpora lutea (CL) were collected from 24 Holstein heifers on Day 10 of the estrous cycle and dispersed with collagenase. Net progesterone accumulation, representing total progesterone synthesized by 10(6) cells during a 2-h incubation was determined. Cells from 7 CL were treated with 0 and 5 ng LH, in the presence and absence of methylation inhibitor, S-adenosyl-homocysteine (SAH, 1 mM). LH-stimulated progesterone production was inhibited (P less than 0.05) in the presence of SAH(209 +/- 19 vs. 119 +/- 7 ng/10(6) cells). In the absence of LH, progesterone production was unaffected (87 +/- 22 vs. 68 +/- 28) by SAH. Cells from 4 CL were treated with 10 micrograms epinephrine or 10 micrograms isoproterenol with and without SAH. Both epinephrine and isoproterenol-stimulated progesterone production was inhibited (P less than 0.05) by the presence of SAH (204 +/- 24 vs. 125 +/- 18 and 198 +/- 15 vs. 130 +/- 8). Progesterone production by cells from 4 CL was unaffected by the presence of SAH when treated with Medium 199 (M199) (75 +/- 32), 10 micrograms cholera toxin, which directly stimulates adenylate cyclase on the cytoplasmic side of plasma membranes (168 +/- 19), or 3 mM dibutyryl cAMP (210 +/- 40).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Methylation in bovine luteal cells as a regulator of luteinizing hormone action. 631 96

The present investigation was designed to study the effect of synthetic ACTH on the synthesis of progesterone, 20 alpha-OH-progesterone and adenosine-3', 5'-monophosphate (cAMP) in isolated luteal cells. Experiments were conducted on rats from three groups. Group I: PMS primed immature rats. Group II: PMS plus hCG primed immature rats. Group III: pregnant rats. Luteal cells were isolated by the Kumai Method (7) using a sucrose density gradient after digestion with trypsin and collagenase. Luteal cells were divided into three fractions; S-1, S-2 and S-3. Following an 18 hr-incubation of S-1 cells of day 7 after PMS injection, a significant increase in progesterone release by ACTH lasted from 6 to 18 hr, whereas 20 alpha-OH-progesterone decreased significantly by ACTH from 8 to 18 hr. There were no differences in progesterone and 20 alpha-OH-progesterone releases from S-2 cells of day 7 between media with and without ACTH. Progesterone release without ACTH reached the peak on day 7 in Group I and on day 6 in Group II. ACTH stimulated progesterone and inhibited 20 alpha-OH-progesterone releases in Groups I and II. The maximum effect of ACTH in both Groups was noted on days 6 and 7. There were no differences in the Effective Dose (ED50) and the Inhibitory Dose (ID50) of ACTH between Group I and Group II. In Group III, releases of progesterone and 20 alpha-OH-progesterone from S-1 cells to media with or without ACTH decreased remarkably after 11 days of gestation. On days, 3, 5 and 8 of gestation, a significant increase in progesterone release from S-1 cells was noted by the ACTH addition. 20 alpha-OH-progesterone release from S-1 cells to media with or without ACTH decreased as the pregnancy advanced. Total cAMP of intra- and extra-cellular S-1 cells (Group II) on day 5 after PMS injection was assayed. ACTH induced an increase in intracellular cAMP. The present results indicate the following: (1) In Group I and Group II, progesterone release increased with the age of the luteal cells and ACTH dose. In Group III, ACTH stimulated progesterone release in a dose-dependent manner in early gestation. (2) 20 alpha-OH-progesterone release decreased by ACTH dose in Group I and Group II, and decreased in Group III as the gestation advanced. (3) Intracellular cAMP increased by ACTH in Group II.
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PMID:[Effect of adrenocorticotropin on progesterone, 20alpha-OH- progesterone and adenosine 3',5'-monophosphate in isolated luteal cells from rat ovaries]. 631 5

Isolation of progesterone secreting cells from the ovaries of immature rats pretreated with pregnant mare serum gonadotropin (PMS) was conducted by a simple procedure which combined the collagenase digestion with a density gradient method. After digestion of the ovarian tissue slices by the enzyme, the residue was gently pressed and placed on a sucrose density gradient. Three bands appearing in the tube after centrifugation were designated as S-1, S-2 and S-3 from the top to the bottom, respectively. The S-1 cells from the ovaries at 6 days after PMS secreted the greatest amount progesterone, i.e. approximately 430 ng per 10(5) cells during the 18th incubation. Progesterone secretion from the S-2 cells was less than 48% of that from the S-1 cells. A physiological interrelation between the S-1 and S-2 cells remains unexplained by the present experiment. The luteal cells were yellow, spheroidal and 15 to 40 mus in diameter. Many vesicle-like particles were found on the cell surfaces. Progesterone secretion from the prepared cells was stimulated significantly by hCG in vitro. This result indicates that progesterone secreting cells isolated by the collagenase-sucrose density gradient preserve their native function as luteal cells. The procedure for preparation of luteal cells in the present report may provide a suitable model for in vitro studies on the corpus luteum.
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PMID:[Preparation of progesterone secreting cells from rat ovaries by a density gradient]. 683 27

A new hydrolase activity has been identified by its capability of cleaving t-boc-Ala-Ala-Pro-Ala-AMC, the released 7-amino-4-methylcoumarin (AMC) being quantified fluorometrically. The activity in the 28,000 X g supernatant fraction of homogenates of weanling mouse uterus was about one fifth that of the adult mouse. The administration of estradiol to the weanling mouse caused a prompt increase in uterine hydrolase, the response being biphasic with peaks at 2 and 6 h. Stimulation was dose responsive and effectively blocked by cycloheximide and puromycin. Estrogen stimulation of hydrolase activity was also observed in the kidney (one fourth that of in the uterus), but not in the heart or liver. Progesterone and testosterone were poor stimulators, but estriol was as effective as estradiol. According to its elution profile in gel filtration, a molecular weight for the hydrolase of about 60,000 is suggested. Inhibition studies in vitro with crude enzyme preparations indicate a serine protease with a SH group essential for maximal activity. The natural substrate for the hydrolase has not been elucidated. It does not solubilize [3H]elastin, and the properties seem to eliminate plasminogen or latent collagenase as possible substrates.
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PMID:A new hormone-response hydrolase activity in the mouse uterus. 700 May

Epithelial cell-rich fractions of rat mammary gland were prepared using percoll gradients after collagenase dispersion. Their insulin-binding characteristics were similar to those of crude acini but superior to unfractionated isolated cells. Optimal binding was obtained after 60 min at 20 degrees C or 16 h at 4 degree C at pH 7.8 Binding at 37 degrees C was lower due probably to an enhanced rate of insulin degradation. 48 h after ovariectomy of 18-day pregnant rats insulin binding to acini doubled due to an increase in the number of insulin receptors. Progesterone but not bromocriptine (which prevented the rise in serum prolactin which occurred after ovariectomy) prevented this increase in insulin binding. These results illustrate that the change in serum progesterone rather than prolactin increases insulin binding to the mammary cell at parturition whilst insulin binding decreases in adipose tissue at the same time (Flint et al., Mol. Cell Endocrinol, 20, 101-111, 1981) enabling coordinated changes in the metabolism of these 2 tissues to take place during the perinatal period.
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PMID:Insulin binding to rat mammary gland at various stages of cell isolation and purification. 704 14

Isolated luteal cells, prepared from superovulated rat ovaries by digestion with collagenase, were subjected to density-gradient centrifugation on Percoll to give a more highly purified preparation of luteal cells than has been reported previously. The cells formed progesterone when incubated in vitro; lutropin stimulated this steroidogenesis. Progesterone formation was linear for at least 2 h; a minimal lutropin concentration of 1.0 ng/ml was needed for stimulation and concentrations of 3.0 and 100 ng/ml gave half-maximal and maximal responses respectively. The cells were unresponsive towards hormones other than lutropin. Exposure to lutropin raised the cellular cyclic AMP concentration, and dibutyryl cyclic AMP, but not dibutyryl cyclic GMP, was as effective in stimulating steroidogenesis as was lutropin. Aminoglutethimide, an inhibitor of cholesterol side-chain cleavage, completely blocked progesterone formation by the cells, showing cholesterol side-chain cleavage to be an obligatory step in steroidogenesis by these cells. Neither the activity of 3-hydroxy-3-methylglutaryl-CoA reductase nor the incorporation of radioactively labelled acetate or mevalonate into cholesterol by cells incubated in vitro were detectable unless the rats had been treated previously with 4-aminopyrazolo[3,4-d]pyrimidine. In cells from rats so treated, compactin was found to block almost completely the incorporation of radioactively labelled acetate, but not of mevalonate, into cholesterol, indicating that this inhibitor acts in corpus luteum in the same way as it does in other tissues. In cells from rats not treated with 4-aminopyrazolo[3,4-d]pyrimidine compactin had no effect on progesterone formation in vitro, showing cholesterol biosynthesis to be unnecessary for the rapid steroidogenic response by luteal cells to lutropin.
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PMID:The preparation and purification of isolated rat corpus-luteum cells and their use in studying the relationship between cholesterol biosynthesis and the lutropin-stimulated formation of progesterone. 723 25

In this study we examined the stimulatory effects of PGF2 alpha on progesterone secretion by porcine luteal cells on different days of the estrous cycle, and the effects of PGF2 alpha, A23187 and PMA on progesterone secretion by isolated large and small luteal cells, in vitro. Corpora lutea were obtained from cycling pigs (days 6-16), collagenase dispersed and luteal cells incubated in medium 199 in the absence or presence of increasing doses of PGF2 alpha, A23187, and PMA. Progesterone concentrations in spent media were measured by RIA. PGF2 alpha stimulation of progesterone secretion by mixed luteal cells did not vary significantly throughout the estrous cycle. Progesterone secretion by large, but not small, luteal cells was increased (p < 0.05) in a dose-dependent fashion by PGF2 alpha. A23187 also caused a dose-dependent increase in progesterone secretion by large luteal cells but inhibited small luteal cells. Progesterone secretion by both large and small luteal cells was significantly increased by increasing doses of PMA. We conclude that the stimulatory response of luteal cells to PGF2 alpha in vitro did not correlate with PGF2 alpha receptor concentrations (not measured in this study), and we speculate that calcium/protein kinase C may be involved in mediating the stimulatory action of PGF2 alpha on luteal cell progesterone secretion.
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PMID:Prostaglandin F2 alpha stimulates progesterone secretion by porcine luteal cells in vitro throughout the estrous cycle. 799 75


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