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)

Prolactin receptors were monitored by measuring 125I-labeled prolactin binding to collagenase-dissociated mammary epithelial cells of lactating BALB/c mice. Specific receptors for iodine-labeled prolactin with an apparent dissociation constant (Kd) of 0.99 . 10(-9) M were present on the dissociated mammary cells. The binding was inhibited by ovine prolactin, human growth hormone and human placental lactogen but not by follicle stimulating hormone, luteinizing hormone, thyroid stimulating hormone, bovine growth hormone or insulin. Adrenal ablation of nursing mothers caused a reduction of the number of prolactin receptors and this effect was preventable by hydrocortisone therapy. Hydrocortisone injections to mothers 3 days after adrenalectomy also induced a replenishment of the prolactin receptors on the mammary cells. Injections of progesterone failed to sustain the high level of mammary cell prolactin receptors in adrenalectomized animals. Stimultaneous injections of hydrocortisone and progesterone to animals 3 days after adrenalectomy caused a partial suppression of the stimulatory action of hydrocortisone alone. The results suggest that hydrocortisone can exert a modulatory influence on mammary cell prolactin receptors in non-hypophysectomized post-partum mice without altering the dissociation constant (Kd) of the receptors.
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PMID:Glucocorticoid modulation of prolactin receptors on mammary cells of lactating mice. 21 16

The present study determined whether a developmental increase in placental low density lipoprotein (LDL) uptake occurred in baboon pregnancy, which was related to the increasing concentrations of estrogen typical of advancing gestation. LDL uptake was determined on collagenase-dispersed placental trophoblast cells purified via 50% Percoll gradient centrifugation and obtained from baboons between days 55-178 of gestation (i.e. the last two-thirds of gestation; term = 184 days). The majority of cells in the 50% Percoll-isolated fraction used to determine LDL uptake were syncytiotrophoblasts at all stages of gestation examined, as determined by immunohistochemical staining for syncytiotrophoblast-specific placental lactogen and pregnancy-specific-beta 1-glycoprotein. Placental LDL uptake, as determined by Scatchard analysis, increased progressively during the last two-thirds of gestation and was correlated (r = 0.87, P less than 0.001; curvilinear regression) with gestational age. Mean +/- SE LDL uptake early in pregnancy on days 55-58 was 1.9 +/- 0.2 ng/micrograms cell protein (n = 3). Placental LDL uptake (ng/microgram cell protein) at midgestation on days 94-104 (2.8 +/- 0.2; n = 5) increased to a value late in gestation on days 159-178 (14.6 +/- 1.0; n = 13), which was approximately 5-fold greater (P less than 0.001) than at midgestation, whereas uptake on days 128-138 was intermediate in value (8.3; n = 2) between the latter two periods. The apparent dissociation constant for placental LDL uptake was lower (P less than 0.01) at midgestation (0.33 micrograms/ml) than late in gestation (0.81 micrograms/ml). Placental LDL degradation, which depends on uptake, also increased with advancing stages of pregnancy, and was correlated (r = 0.74, P less than 0.01; curvilinear regression) with gestational age. Overall mean peripheral serum LDL cholesterol concentration was 46.5 +/- 1.7 mg/dl between days 50-170 of gestation. However, there was no significant change in serum LDL levels during this period. Maternal peripheral serum estradiol concentrations increased from 0.3 ng/ml on day 55 to an initial peak of approximately 3.5 ng/ml on days 70-80, then declined to approximately 1.0 ng/ml at midgestation. Estradiol then increased progressively throughout the remainder of pregnancy to maximal values of over 6 ng/ml late in gestation. In summary, there was a progressive increase in placental LDL uptake with advancing stages in the last two-thirds of baboon pregnancy, which was associated with a concomitant rise in maternal serum estradiol concentrations.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Developmental increase in placental low density lipoprotein uptake during baboon pregnancy. 153 17

We have previously shown that placental low density lipoprotein (LDL) uptake is decreased in baboons treated with antiestrogen and we have proposed, therefore, that estrogen regulates placental LDL uptake and use during primate pregnancy. In the present study, an alternate in vivo approach was employed to determine whether restoration of estrogen in animals in which the formation of estrogen was decreased would reverse the decline in LDL uptake. Placental estrogen was suppressed by removing the fetus (fetectomy) and thus adrenal androgens on day 100 of baboon gestation (term is 184 days). Placental LDL uptake was determined on day 160 after fetectomy alone, and after fetectomy and sc administration of the estrogen precursor androstenedione (50 to 150 mg every 10 days). Placental cells (10(6] were dispersed with 0.1% collagenase, isolated via 50% Percoll gradient centrifugation, then incubated at 37 C for 12 h in medium 199 with 10-100 micrograms [125I]LDL and LDL uptake (i.e. binding and internalization) determined by Scatchard analysis. In intact baboons and animals that had undergone fetectomy, syncytiotrophoblasts predominated and formed a continuous surface covering of the placental villi. Moreover, placental cells of intact and fetectomized baboons isolated on 50% Percoll consisted primarily of syncytiotrophoblasts, as evidenced by their immunohistochemical reaction with antisera against placental lactogen and pregnancy-specific-beta 1-glycoprotein. Serum estradiol in untreated baboons increased with advancing gestation and mean (+/- SE) concentrations were 1.29 +/- 0.04 ng/ml on days 101-160 of gestation. Placentas remained in situ and viable after fetectomy, but serum estradiol decreased to 0.24 +/- 0.02 ng/ml, or 19% of normal (P less than 0.01). Androstenedione restored serum estradiol after fetectomy to a mean of 0.69 +/- 0.03 ng/ml on days 101-160, or 53% of normal. Specific LDL uptake (nanograms per microgram protein) by placental cells after fetectomy alone (3.2 +/- 0.4) was 22% (P less than 0.001) of controls (14.4 +/- 1.2). Androstenedione increased (P less than 0.005) LDL uptake after fetectomy to a value (8.8 +/- 1.2) that was 61% of normal. LDL degradation, which depends on uptake, was 59 +/- 1% of normal after fetectomy and restored with androstenedione treatment to 94 +/- 2% of normal. Apparent dissociation constants (microgram/ml) for LDL uptake were similar after fetectomy (0.38), and fetectomy and androstenedione treatment (0.41), but lower (P less than 0.01) than in intact animals (0.80).(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Regulation of placental low density lipoprotein uptake in baboons by estrogen. 198 38

High density lipoprotein (HDL3) binds with high affinity to many types of cells, but controversy exists concerning the nature and biological significance of the binding. We have recently demonstrated that HDL and apoproteins (apo)-AI, -AII, and -CI stimulate a specific and dose-dependent increase in placental lactogen (hPL) release from human trophoblast cells. To examine the possible relationship between HDL3 binding and stimulation of hPL release, we have characterized the binding of [125I]HDL3 to an enriched fraction of hPL-producing trophoblast cells. Binding studies were performed on trophoblast cells isolated by isopycnic centrifugation of collagenase/hyaluronidase-dispersed placental tissue and apo-E free-HDL3 (density, 1.125-1.215 g/ml). Scatchard analysis of binding studies performed at 37 C for 2 h revealed two classes of binding sites: 1) high affinity binding sites with a Kd of 9.7 +/- 2.2 micrograms/ml (1.3 x 10(-7) M) and 9.8 +/- 3.2 x 10(5) binding sites/trophoblast cell, and 2) low affinity binding sites with a Kd of 172.8 +/- 64.8 micrograms/ml (2.3 x 10(-6) M) and an estimated 3.2 x 10(6) sites/cell. As has been found in hepatocytes and other cells, the number of HDL3-binding sites per trophoblast cell (but not the binding affinity) decreased at lower incubation temperatures. In addition, HDL3 binding to trophoblasts cells did not require calcium and was not affected by prior treatment of the cells with pronase or trypsin. HDL3-binding sites on trophoblast cells, however, were not specific for HDL3. Low density lipoprotein (density, 1.063-1.055 g/ml), which does not stimulate hPL release, was nearly as potent on a molar basis as HDL3 in binding to the high and low affinity binding sites on trophoblast cells. Furthermore, nitrated HDL3, which does not compete for high affinity binding to trophoblast cells, stimulated hPL release. Although the characteristics of HDL3 binding to trophoblast cells are similar to those of other cells, these results strongly suggest that the binding of HDL3 to high affinity binding sites is not essential for HDL-mediated hPL release.
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PMID:High density lipoprotein3 binding and biological action: high affinity binding is not necessary for stimulation of placental lactogen release from trophoblast cells. 258 47

Hepatocytes were isolated by gentle collagenase digestion of liver fragments from human fetuses of 8-16 weeks gestation obtained following prostaglandin-induced pregnancy terminations. They were maintained on collagen-coated tissue culture dishes in selective arginine-free medium for up to 72 hr, and the action of hormones and growth factors on DNA synthesis was studied by autoradiography following incubation with 3H-thymidine. The labeling index of hepatocytes was consistently enhanced by 25-250 ng/ml human placental lactogen (HPL), 25-250 ng/ml human growth hormone (HGH), 10-50 ng/ml insulin-like growth factor I/somatomedin-C (IGF I/Sm-C), and 10% dialyzed fetal calf serum, reaching a maximum of three- to four-fold greater than in basal medium alone. Under basal conditions, 30% of hepatocytes stained positively for the presence of IGF peptides using a monoclonal antibody raised against purified human IGF I/Sm-C. Although this proportion did not change following treatment with HGH and HPL, IGF I/Sm-C released by cells into culture medium was considerably increased in the presence of both hormones. Incubation with the SmC 1.2 monoclonal antibody abolished the increase in labeling index in response to IGF I/Sm-C and partially blocked the response to both HPL and HGH. These results indicate that both HPL and HGH stimulate DNA synthesis in human fetal hepatocytes and suggest that this effect is at least partly indirect through the release and paracrine action of IGF I/Sm-C.
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PMID:Regulation of DNA synthesis in human fetal hepatocytes by placental lactogen, growth hormone, and insulin-like growth factor I/somatomedin-C. 329 89

The dynamics of the release of human placental lactogen (hPL) under basal conditions and response to various secretogogues has been studied in perifused enriched hPL-producing cells from term placentae prepared by the isopycnic centrifugation of collagenase/hyaluronidase-dispersed placental cells on Percoll gradients. Under basal conditions, the perifused cells released hPL at a relatively constant rate for up to 24 h in culture. The mean rates of hPL release from cells (5 x 10(6) cells) from 18 normal full-term placentae varied from 1.8 to 20.2 ng/5 min (mean 7.7 ng/5 min). The cells from term placentae, however, did not release detectable amounts of chorionic gonadotrophin or the cytosolic enzymes lactic dehydrogenase and alkaline phosphatase. The amounts of hPL released by the perifused cells were inversely related to cell density with mean rates of hPL release by 2, 5, and 10 x 10(6) cells of 15.8, 8.6, and 5.7 ng/10(6) cells/0.5 h. The perifused cells responded to provocative stimuli (high-density lipoproteins (HDL), apolipoproteins AI, AII, and CI, partially purified hPL-releasing factor, phorbol esters, sn-1,2-diacylglycerol, and cAMP) in a manner qualitatively similar to enriched trophoblast cells and placental explants in static culture. Release of hPL in response to HDL, apoproteins AI, AII, and CI, and partially purified hPL-releasing factor was dose-dependent and occurred within 5 min of exposure. Basal and stimulated hPL release by perifused trophoblast cells that had been previously frozen at -70 degrees C for four weeks was identical to that of freshly dispersed cells from the same placenta. These experiments indicate that perifused trophoblast cells may be used as a model system to examine the dynamics of hPL release under basal conditions and in response to provocative stimuli.
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PMID:Characterization of placental lactogen release from perifused human trophoblast cells. 339 89

Fetal placental tissue from 11 days pregnant mice was dissociated in collagenase and DNase solution and then separated on a 40 per cent Percoll gradient. Trophoblast cells banded at a density of 1.05 g/ml. When cultured on rat tail collagen, these cells formed colonies of mono- and binucleate cells varying in size from 40 to 70 microns. At the time of plating, about 13 per cent of the trophoblast cells secreted mouse placental lactogen II (mPL-II) as determined by reverse haemolytic plaque assay. The ratio of mPL-II-producing cells increased significantly in culture and reached 63 per cent after 48 h. The secretion of mPL-II increased continuously during six days of culture, whereas the total protein release was highest after the first day, declined the second day and then remained relatively constant for the last four days of culture. The DNA content of the cells did not change significantly during the six-day period. When the trophoblast cells were incubated with insulin (1 ng/ml to 5 micrograms/ml), a modest but significant reduction in mPL-II secretion was observed. No change in the mPL-II secretion was seen when epidermal growth factor was administered to the culture in concentrations from 1 ng/ml to 10 micrograms/ml. It is concluded that this in vitro culture system is suitable for studying both mPL-II secretion and the differentiation of mPL-II-producing cells.
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PMID:Development of a placental cell culture system for studying the control of mouse placental lactogen II secretion. 343 55

The direct effects of human GH (hGH), ovine pituitary PRL (oPRL), and human chorionic somatomammotropin [placental lactogen (hPL)] on the endocrine pancreas were studied in isolated pancreatic islets maintained in tissue culture. Islets of Langerhans were isolated by collagenase treatment of pancreatic tissue obtained from adult NMRI mice and adult or newborn Wistar rats. The islets were maintained for up to 3 weeks in petri dishes containing tissue culture medium RPMI 1640 supplemented with newborn calf serum or normal human serum. The release of insulin during culture and the islet content of insulin, glucagon, and DNA after culture were determined. The DNA synthesis in the newborn rat islets was evaluated by the incorporation of [methyl-3H]thymidine into islet cell DNA. In mouse islets, 1 micrograms/ml hGH, oPRL, or hPL markedly stimulated insulin release during a 2-week culture period and caused a significant increase in the insulin content in the islets after culture. While hGH did not affect the DNA content in adult mouse islets, an increase was observed in adult rat islets after 2-3 weeks of culture. In islets isolated from 3- to 5-day-old rats cultured for 2 weeks with hGH, there was a 30-40% higher DNA content than that found without hGH. Correspondingly, a significant stimulation of the incorporation of [methyl-3H]thymidine could be demonstrated 24 h after the addition of hGH, oPRL, or hPL. hCG and porcine ACTH had no effect. In conclusion, these results indicate that GH and related hormones have a direct stimulatory effect on both the insulin production and DNA synthesis in isolated islets of Langerhans. Whether the effect is directly on the beta-cell or mediated via locally produced growth factors remains to be determined.
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PMID:Effects of growth hormone, prolactin, and placental lactogen on insulin content and release, and deoxyribonucleic acid synthesis in cultured pancreatic islets. 627 41

An enriched fraction of human placental cells that synthesize and release both placental lactogen (hPL) and hCG was obtained by isopycnic centrifugation of collagenase/hyaluronidase-dispersed cells through a density gradient of 40% Percoll. The enriched cells, which banded at a density of approximately 1.01 g/ml, comprised 10-15% of the total DNA. During the first 24 h after attachment, the cells released 50-250 ng hPL and 4-10 mIU hCG/10(6) cells. Thereafter, the rate of hPL release decreased, while the rate of hCG and [35S]trichloroacetic acid-precipitable protein release remained constant. The enriched cells responded to phospholipase A2, low extracellular calcium, and (Bu)2cAMP in a manner similar to that of placental explants. Phospholipase A2 (0.1 and 1 U/ml) stimulated hPL release by 270% and 568%, respectively, and low extracellular calcium (0-0.18 mM) stimulated hPL release by 48%. (Bu)2 cAMP (1 mM) stimulated hCG release by 42%, but had no effect on hPL. Estradiol (10(-5)-10(-12) M) and progesterone (10(-5)-10(-10) M) had no effect on the synthesis and release of either hPL or hCG over a 6-day period. In addition, insulin (8.3 X 10(-7) M) and changes in medium glucose content (0-5 mg/ml) had no effect on hPL release over a 72-h period. Since the enriched trophoblast cells respond to provocative stimuli in a manner similar to that of explants and placental fragments, this cell population is a useful model system for investigations of the cellular mechanisms of hPL and hCG release.
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PMID:Characterization of the synthesis and release of human placental lactogen and human chorionic gonadotropin by an enriched population of dispersed placental cells. 630 87

To determine whether cAMP regulates mouse placental lactogen-I (mPL-I) and mPL-II secretion at midpregnancy in vitro, mouse placental tissue from day 9 of pregnancy was dispersed with collagenase, cells were fractionated on a Percoll gradient, and the purified trophoblast cells were plated in a serum-free medium. The cells were then incubated with various agents that increased the intracellular cAMP level for 5 days. 8-Bromo-cAMP stimulated mPL-I secretion, but inhibited mPL-II secretion in a time- and dose-dependent manner without changing the amount of newly synthesized trichloroacetic acid-precipitable proteins. Cholera toxin and forskolin, which increase intracellular cAMP accumulation, also regulated mPL-I and mPL-II secretion in the same manner. 8-Bromo-cAMP increased the intracellular mPL-I concentration, decreased the intracellular mPL-II concentration, and increased the immunoprecipitable newly synthesized mPL-I concentration in both the medium and cells. 8-Bromo-cAMP increased the expression of mPL-I messenger RNA and decreased the expression of mPL-II messenger RNA. The sequential reverse hemolytic plaque assay and double immunocytochemistry indicated that 8-bromo-cAMP regulates the subpopulation of giant cells containing and releasing mPL. These findings suggest that an increase in intracellular cAMP stimulates mPL-I secretion, but inhibits mPL-II secretion by changing the subpopulation of giant cells containing and releasing mPL.
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PMID:Cyclic adenosine-3',5'-monophosphate stimulates mouse placental lactogen-I (mPL-I) secretion but inhibits mPL-II secretion at midpregnancy. 789 49


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