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)

Pituitary cells were isolated from adult human pituitary glands obtained at autopsy 4-12 h postmortem by enzyme treatment (collagenase and dispase) and by Percoll density gradients. Cells thus isolated were maintained in culture for more than 6 months. By immunoperoxidase staining methods using rabbit sera monospecific against various pituitary hormones, a large number of cultured cells reacted positively. The hormones identified in these cells were growth hormone, prolactin, adrenocorticotropin, follicle-stimulating hormone, luteinizing hormone and thyrotropin. Electron-microscopic examination of cultured cells revealed the presence of secretory granules in cytoplasm characteristic of in vivo human pituitary cells.
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PMID:Isolation, culture and cell-type identification of adult human pituitary cells. 408 22

The role of prolactin on some ovarian functions was studied in collagenase-dispersed luteal cells obtained from PMSG/hCG-primed rats. The in vitro effect of ovine prolactin (oPrl) on luteal cell function was assayed. This hormone produced a dose-dependent increase of progesterone production and an additive effect on hCG stimulation. oPrl had no effect on cAMP production. Chronic effects of prolactin were studied in sulpiride (S), bromocriptine (Br) and oPrl-treated rats. Serum levels of prolactin were significantly higher in S-treated animals whereas Br administration rendered undetectable values. Serum progesterone was reduced in Br-treated animals and LH levels were similar in all groups studied. In vitro studies demonstrated a marked reduction of hCG stimulation of progesterone and cAMP production by luteal cells from hypoprolactinemic animals, while a significant increase was observed in hyperprolactinemic states. oPrl and S treatment significantly increased ovarian LH binding sites while a reduction was observed in Br-treated rats. These data suggest that luteal cell function is regulated by circulating levels of prolactin and that this hormone has some direct effect on the steroidogenic process.
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PMID:Effect of prolactin on the steroidogenic response of rat luteal cells. 608 23

The pineal indole melatonin suppresses the neonatal rat luteinizing hormone (LH) and follicle-stimulating hormone (FSH) responses to LH-releasing hormone (LHRH), as shown in previous studies from this laboratory. We show in this study that the melatonin inhibition is a selective effect and is not due to general inhibition of pituitary function. The effects of the indole on the responses to thyrotropin-releasing hormone (TRH) and somatostatin (SRIF) and on basal pituitary hormone secretion were examined with cells in culture. Neonatal rat anterior pituitary cells dissociated with collagenase and hyaluronidase were cultured overnight and distributed to 35-mm dishes at the time of use. For examination of melatonin effects on the response to releasing hormones, the cells were incubated for 3 h in control medium or medium containing LHRH (10-9-10-6 M), TRH (10-10-10-6 M), or SRIF (10-9-10-6 M), either alone or in the presence of melatonin (10-8 or 10-6 M). For examination of basal hormone secretion, the cells were incubated for 1.5, 3, 6, 15, or 24 h in either medium alone or medium containing melatonin (10-6 M). Medium and cell lysate concentrations of LH, FSH, thyroid-stimulating hormone (TSh), prolactin (PRL) and growth hormone (GH) were determined by double antibody RIA. As previously, melatonin (10-8 M) significantly suppressed LH and FSH release by all concentrations of LHRH. This concentration of the indole produced maximal suppression of both LH and FSH responses to LHRH. By contrast, melatonin at a 100-fold greater concentration (10-6 M) had no effect on TRH stimulation of TSH or PRL release or on SRIF inhibition of GH release. Similarly, melatonin had no effect on basal release of TSH, PRL, or GH at the times examined. These findings show that melatonin inhibition of the gonadotroph response to LHRH is a selective effect.
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PMID:Selectivity of melatonin pituitary inhibition for luteinizing hormone-releasing hormone. 612 68

Multialveolar mammary epithelial structures have been prepared from rabbit mammary gland by treating the tissue with collagenase plus hyaluronidase. These structures synthesize milk specific fatty acids when cultured with physiological concentrations (0.5 micrograms/ml) of prolactin in the presence of insulin and corticosterone. They have many of the advantages but few of the disadvantages of either mammary explants or primary cells in culture. For example, they are easily prepared in large numbers and respond to prolactin in culture even in the absence of serum or other tissue extracts. Because their level of organization is intermediate between that of explants and single cells, they provide a complementary system for studies on mammary differentiation.
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PMID:Novel multialveolar epithelial structures from rabbit mammary gland that synthesize milk specific fatty acids in response to prolactin. 626 43

Membrane preparations of collagenase-dispersed Langerhans islets of female Wistar rats exhibit specific binding sites for 125I-labelled ovine prolactin (125I-oPrl). Almost negligible binding was detected in islets of male animals. The binding is a saturable and time-temperature dependent process, equilibrium being reached after 16 h incubation at 0 degrees C. The bound oPrl is not displaceable by hFSH, hLH, bGH or hGH. In contrast with other cell fractions, the 12,000 g pellet accounts for more than 80% of the specific binding of 125I-oPrl. Scatchard plots of data obtained in saturation studies indicate a single class of binding sites with Ka = 0.21 x 10(10)M-1. Protein and phospholipid moieties are essential for the receptor activity, since after trypsin or phospholipase C digestions marked loss of binding was verified. In islets of streptozotocin diabetic rats a marked reduction in the number of binding sites was observed. These findings may suggest that some of the actions of prolactin on endocrine pancreas could be explained by its specific interaction with islet cell membranes.
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PMID:Prolactin binding in rat Langerhans islets. 627 57

Multi-alveolar mammary structures (mammary lobules) were prepared from mammary glands of pseudopregnant rabbits by controlled digestion with collagenase and hyaluronidase. The overall rate of fatty acid synthesis and the proportion of milk-specific fatty acids (C8:0 and C10:0) synthesized by these lobules when cultured with insulin, corticosterone and prolactin were measured. Maximum response to physiological concentrations of prolactin (1.1 or 2.2 nmol/l) occurred in the presence of insulin (1.7 mumol/l) and corticosterone (0.58 mumol/l). In general, the results obtained on the effect of progesterone were negative. Though explants showed a ninefold greater response to prolactin per mg DNA than did mammary lobules, the latter have the advantage of being easily prepared for culture in large numbers. Reduction to below 500 microns diameter and culture in conditions which allow cell outgrowth onto plastic limited their response to prolactin. The probable roles of membrane damage by digesting enzymes and of tissue architecture in limiting prolactin response are discussed.
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PMID:Milk-fat synthesis by lobules prepared from rabbit mammary gland: response to insulin, corticosterone, prolactin and progesterone. 634 42

It is well-known that the hypothalamus predominantly exerts an inhibitory control on prolactin secretion and that dopamine (DA) is the main prolactin inhibiting factor (PIF). In addition, the hypothalamus contains prolactin-releasing factors (PRF). Thyrotropin-releasing hormone (TRH), vasoactive intestinal polypeptide (VIP) and peptide-histidine-isoleucine (PHI) are the components of PRF. However, the detailed mechanism by which the peptides release prolactin (PRL) at the pituitary level is still unknown. Therefore, in this paper, an in vitro perifusion system using the cell column of cultured rat pituitary cells attached on Cytodex beads was employed to investigate the mechanism of PRL release. The rat anterior pituitary cells were isolated using collagenase, and the dispersed pituitary cells were cultured with swollen Cytodex beads in Dulbecco's modified Eagle medium (DMEM) containing fetal calf serum at 37 degrees C in 5% CO2 and 95% air for 2--3 days. The cultured anterior pituitary cells attached on Cytodex beads were packed in a column and perifused with DMEM at a constant flow rate of 0.4 ml/min using a peristaltic pump. The following results were obtained. A five minute perifusion with 100 pg/ml to 100 ng/ml TRH caused a significant increase of PRL in a dose-related manner. A continuous perifusion with 2 ng/ml or 10 ng/ml DA inhibited PRL release in a dose-related manner. When TRH at a dose of 1 ng/ml, 10 ng/ml or 100 ng/ml was perifused for 120 min at a rate of 0.4 ml/min, a large amount of PRL was released during the early period of the TRH infusion, and then the PRL release gradually decreased to the basal levels in spite of the continuous TRH infusion. An additional TRH, of which the concentration was ten-fold higher than the TRH level in the continuous infusion, when added at the end of the continuous TRH infusion, had no effect on PRL release. On the other hand, a 5 minute TRH infusion given at 30 min after the end of the continuous TRH infusion caused a significant increase in PRL release. A continuous perifusion with 1 mM 8-bromo-cyclic AMP caused a small but continuous PRL release. An additional continuous 8-bromo-cyclic AMP infusion during the late period of a continuous TRH infusion caused a continuous PRL release similar to that induced by the continuous infusion of cyclic AMP only. A short period perifusion with 1 X 10(-9)M to 1 X 10(-7)M of vasoactive intestinal polypeptide (VIP) enhanced a significant increase of PRL release in a dose-related manner, but the amounts of PRL release induced by VIP were smaller than those induced by TRH.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[A study on the prolactin releasing mechanism using an in vitro perfusion system with a cell column of cultured rat anterior pituitary cells]. 644 Aug 13

The effect of bromocriptine (BR) on pituitary-testicular function has been investigated in vivo and in vitro in adult male rats. Testosterone production in vitro by collagenase- dispersed Leydig cells from 84-day-old rats was evaluated in the presence and absence of hCG and/or different doses of BR. In the presence of 1.5 X 10(-5) M BR, both basal and hCG-stimulated testosterone production were decreased whereas at lower doses BR was ineffective. In vivo 60-day-old rats were injected sc with BR (150 micrograms/rat or 750 micrograms/rat twice daily) or vehicle for 24 days. This treatment reduced the plasma level and pituitary content of prolactin, slightly increased the plasma levels of LH and FSH but did not affect pituitary gonadotrophin content. Irrespective of the dose of BR injected, plasma levels of androgen did not change, but with the large dose of BR a decrease in testicular content of testosterone (P = 0.05) was observed. In the same animals the number of LH/hCG receptors was significantly reduced, and the sensitivity of the isolated Leydig cells to hCG stimulation in vitro was reduced; however, both the basal secretion and the maximum testosterone response to hCG were unaffected. These results show impairment of pituitary-testicular function in BR-treated rats, either as a result of BR-induced hypoprolactinaemia or as a consequence of direct effects of BR on the Leydig cells.
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PMID:Effects of bromocriptine on pituitary-testicular function in the rat: possible inhibition of in vitro production of androgen by Leydig cells. 666 83

The stimulatory effect of metoclopramide upon aldosterone secretion is independent of the known aldosterone-regulating mechanisms (renin, potassium, adrenocorticotropic hormone), is unrelated to its effect on prolactin and is absent when metoclopramide is directly added to isolated adrenal zona glomerulosa cells. To examine the possibility of a "humoral" mediation of aldosterone stimulation by metoclopramide, we evaluated the effect of serum of 10 normal subjects injected with metoclopramide (10 mg i.v.) on aldosterone production by collagenase-dispersed calf adrenal zona glomerulosa cells. Whereas no effect was observed with serum collected before the injection, serum collected from 5 to 30 min after the injection stimulated aldosterone production. The effect was seen 2.5 min after the injection, was significant at 5 min (P 0.05), 10, 15, 20 and 30 min (P 0.01). The effect disappeared 40 min after the injection, when plasma aldosterone in subjects was still elevated (P 0.01). The biological half-life of the factor (t1/2) is about 12.5 min. A significant correlation was found between the maximal aldosterone response to metoclopramide in vivo and the maximal effect of serum in vitro (r2=0.69;P 0.01). We suggest that metoclopramide stimulates aldosterone production in vivo by the increase in serum of a factor which, in turn, stimulates aldosterone and whose physiological significance remains to be evaluated.
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PMID:Evidence for a role of a serum factor stimulated by metoclopramide in regulating aldosterone secretion. 670 35

Mammary epithelial cells were prepared by collagenase digestion of tissue from mid-pregnant rabbits and cultured for up to 6 days on either collagen gels or an extracellular matrix prepared from the same tissue. The behaviour of the cells in serum-supplemented medium containing combinations of insulin, prolactin, hydrocortisone, estradiol and progesterone were monitored by measuring rates of casein synthesis, lactose synthesis, DNA synthesis and protein degradation. After 6 days, epithelial cells on floating collagen gels showed substantial increases in casein synthesis and DNA synthesis over freshly-prepared cells, following a decline during the first 3 days when the collagen gels are contracting. The optimum hormone combination for casein synthesis was insulin + prolactin + hydrocortisone, whereas for optimum DNA synthesis the additional presence of estradiol and progesterone was required. Cells on extracellular matrix showed increased rates of both casein synthesis and DNA synthesis by day 6 in the presence of insulin + prolactin + hydrocortisone, with additional estradiol + progesterone having an inhibitory effect. Whereas on day 2 rates of intracellular protein degradation were generally lower in cells on extracellular matrix, by day 6 rates of protein degradation were lowest in cells cultured on collagen gels with insulin + prolactin + hydrocortisone. In all cases, rates of lactose synthesis fell to low levels as the culture proceeded. Pulse-chase labelling of freshly-prepared cells with [32P]orthophosphate in medium containing serum and insulin + prolactin + hydrocortisone demonstrated that newly-synthesized casein was degraded during its passage through the epithelial cell. The influences of the collagen gels and extracellular matrix and of the hormone combinations on epithelial cell differentiation and secretory activity are discussed.
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PMID:Comparison of collagen gels and mammary extracellular matrix as substrata for study of terminal differentiation in rabbit mammary epithelial cells. 670 39


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