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:3.4.21.4 (trypsin)
42,187 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We reviewed the pathology records from January 1965 through July 1975 for aphakic eyes. After exclusion of unsuitable cases, ten eyes (nine patients) with cystoid macular edema and 142 eyes without cystoid macular edema were studied. Clinical ophthalmic records were available for five of the ten eyes with the Irvine-Gass syndrome. Histologic sections were examined, revealing a significant correlation between the Irvine-Gass syndrome and retinal phlebitis, which has not been reported previously, as well as cyclitis and vitritis. Anterior segment operative complications tended to be more prevalent in eyes with the Irvine-Gass syndrome than in those without the Irvine-Gass syndrome, although the assocation was not statistically significant (P less than .1). Retinal trypsin digestion showed the phlebitis to be distributed posteriorly within primary and secondary retinal veins, frequently occurring near points of bifurcation. The changes in permeability seen in the Irvine-Gass syndrome may be due to this retinal phlebitis and to a generalized inflammation-induced increase in capillary permeability. The case of the phlebitis is not known.
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PMID:Retinal phlebitis in the Irvine-Gass syndrome. 84 44

There is extensive evidence that the posterior pituitary (PP) participates in the regulation of PRL secretion. We recently reported that a putative PRL-releasing factor is localized, and possibly produced, in the intermediate lobe of the PP. The aim of the present investigation was to determine whether cultured PP cells affect anterior pituitary (AP) function in terms of cell content and cumulative release of PRL. Anterior and posterior pituitaries from adult male rats were dispersed with trypsin and cultured either alone or together for 4 and 8 days in serum-free medium. The concentrations of PRL, GH, and LH in cell extracts and culture media were measured by RIA. Coculturing of AP and PP cells at different plating densities resulted in a 2-fold rise in PRL cell content after 4 days. The cumulative release of PRL in the cocultures was significantly increased only after 8 days. LH and GH were affected slightly, or not at all. Medium conditioned by PP cells mimicked the effects of coculture on the cumulative release of PRL, but not on the cell content. Short-term incubation with TRH induced a much larger release of PRL from AP + PP cocultures than from AP cells cultured alone. In conclusion, these data suggest that 1) PP cells stimulate the production and release of PRL in a hormone-specific manner, and 2) coculturing of AP + PP cells augments the responsiveness of lactotrophs to secretagogues such as TRH. We propose that at least two factors, one of which might be PRL-releasing factor, are involved in these effects.
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PMID:Coculture of anterior and posterior pituitary cells: selective stimulation of lactotrophs. 190 68

The extent to which pituitary explants secrete GH requires clarification. In the present study GH release from ectopic pituitary tissue was assessed using the reverse hemolytic plaque assay. In addition, the effects of this tissue on eutopic GH and PRL release were simultaneously investigated. Anterior pituitary glands from adult female donor rats were grafted beneath the kidney capsule of adult male hosts. Four weeks later, this ectopic pituitary tissue and the eutopic pituitary glands of the host animals were removed, dispersed with trypsin, and subsequently assayed for GH and PRL release. Contrary to expectations, we found that 37% of the ectopic pituitary cells were GH secretors. Furthermore, these GH cells remained highly responsive to GRF (10(-7) M), which evoked a 7-fold increase (P less than 0.05) in mean GH plaque area. By comparison, only 28% of these ectopic cells secreted PRL, and this release was not consistently augmented by exposure to TRH (10(-7) M). In the second half of this study we found that the presence of ectopic pituitary tissue severely compromised the secretory capacity of the eutopic pituitary cells. More specifically, GH-releasing factor induced a 3-fold increase in GH secretion from the eutopic pituitary cells of sham-operated control animals, but it enhanced the release from cells of host animals by only 2-fold. Moreover, the response to TRH by the eutopic PRL cells from explant-bearing animals was curtailed to such an extent that it was not significantly greater (P greater than 0.05) than basal release in that group. We conclude that the potential of pituitary explant cells to release GH is far greater than previously believed and that this ectopic hormone production may inhibit hormone release from the eutopic pituitary cells.
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PMID:Pituitaries transplanted under the renal capsule contain functional growth hormone (GH) secretors and suppress GH and prolactin release from individual eutopic pituitary cells. 251 Sep 89

Glandular kallikrein (a trypsin-like serine protease) is a major estrogen-induced and dopamine-repressed protein in the rat anterior pituitary which appears to be associated with lactotrophs. In the pituitary the enzyme predominantly exists as a latent zymogen (pro-glandular kallikrein) which can be activated by trypsin. This study reports experiments employing biochemical techniques to investigate the subcellular localization of glandular kallikrein. Anterior pituitaries from estrogen-treated rats were fractionated on a discontinuous sucrose density gradient and the distribution of various organelles in the gradient was determined by conventional enzyme or protein marker assays. Each of the 8 organelle markers exhibited a unique distribution profile within the gradient. The distribution of glandular kallikrein was closely correlated (r = 0.91) with that of nucleoside diphosphatase (a marker for trans cisterna of the Golgi apparatus). For both glandular kallikrein and nucleoside diphosphatase, 35-45% of the total activity was found in Golgi zones of the gradient, and 18-22% was in the secretory vesicle fraction. In all of the subcellular fractions, 91-97% of the glandular kallikrein existed in the zymogen form (pro-glandular kallikrein). In Golgi fractions, 38% of the glandular kallikrein remained membrane-bound following freeze-thawing and two washes in hypotonic media; 94% of the nucleoside disphosphatase remained membrane-bound following such treatment. The results indicate that glandular kallikrein is most highly concentrated in trans cisternae of the Golgi apparatus with substantial activity also present in secretory vesicles. This localization is consistent with a role for glandular kallikrein as a prohormone processing enzyme in lactotrophs.
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PMID:Biochemical investigation of the subcellular localization of the estrogen-induced pro-glandular kallikrein in the rat anterior pituitary. 272 45

Immunocytochemistry (ICC) and a reverse hemolytic plaque assay for GH were used to investigate the temporal relationships between the initiation of hormone storage and release by developing somatotropes and the onset of responsiveness of these cells to stimulatory and inhibitory secretagogues. Anterior pituitaries obtained from rats on days 18-21 of fetal development (pups were generally delivered on fetal day 22, which is equivalent to day 0 of neonatal life) were monodispersed with trypsin, cultured for 24 h, and then subjected to reverse hemolytic plaque assay and/or ICC for GH. GH-containing cells (determined by ICC) were extremely rare (less than 1%) in cultures derived from day 18 fetuses, but accounted for 22.4%, 25.2%, and 24.5% of all cells in cultures from day 19-21 fetuses, respectively. The proportion of GH-releasing cells, as determined in a long term (120-min incubation with antibody) plaque assay, was less than 1%, 22.4%, and 22.9% for days 18, 20, and 21, respectively, but only 13.6% for day 19 cells. Thus, many pituitary cells from day 19 fetuses contained, but did not release, GH. While GH-releasing factor (1-44) (1 X 10(-7) M) had no effect on the percentage of GH plaque-forming cells in long term incubations, it enhanced (by approximately the same degree in day 19-21 groups) the percentage of cells that formed plaques and the size of the plaques in short term (45-min) incubations with antibody. Somatostatin (1 X 10(-7) M) exerted inhibitory effects on these variables when tested in long term incubations, and age of the donor rats did not influence pituitary responsiveness to this secretagogue. These results suggest that the capacities of fetal somatotropes to store GH and release it under basal and regulated conditions are attained, in large part, within an extremely narrow time frame between days 18 and 19 of fetal development.
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PMID:Functional maturation of somatotropes in fetal rat pituitaries: analysis by reverse hemolytic plaque assay. 285 84

To determine whether dihydrotestosterone (DHT) or estradiol (E2) exerts negative or positive feedback effects on rat pituitary gland, Testosterone (T) metabolite (T, DHT, 5 alpha-androstane-3 alpha, 17 beta-diol:3 alpha-diol or E2) was added to the cultured pituitary cells. Anterior pituitary glands were obtained from 6-week-old male rats. Pituitary cells were prepared by trypsin digestion and incubated with various concentrations of steroid hormones for 72 h to determine the effects of steroid hormones on basal secretion of luteinizing hormone (LH) and follicle stimulating hormone (FSH) after 48 h preculture without steroids. Then 10 nM luteinizing hormone-releasing hormone (LH-RH) with appropriate concentrations of these steroid hormones was added to the pituitary cells in culture and incubated for another 6h to determine the effects of steroid hormones on LH-RH induced gonadotropin release. After the incubation, pituitary cells were lysed with 0.1% Triton X100 to measure the intracellular gonadotropin content. The concentration of LH and FSH was determined by radioimmunoassay. T, DHT and 3 alpha-diol stimulated basal FSH but not basal LH secretion, and inhibited both the release of FSH and LH from cultured pituitary cells during incubations with LH-RH in a dose-dependent fashion. Intracellular content of both FSH and LH were increased, and total FSH and not LH was also increased by the addition of DHT in a dose-dependent manner. E2 did not exert any of such effects on pituitary cells in culture. These studies suggest that 5 alpha-reduced metabolites but not aromatized metabolite of T play an important role on feedback regulation of gonadotropin secretion at pituitary level. DHT directly acts on pituitary gland not only to stimulate the production of FSH but also to suppress FSH and LH secretion induced by LH-RH.
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PMID:[Studies on the feedback regulation of gonadotropin concentrations in male rats. (III). The effects of testosterone and its metabolites on gonadotropin secretion from rat pituitary cells in culture]. 312 50

The observation that suckling evokes a modest rise in serum TSH when compared with that of prolactin is inconsistent with the hypothesis that TRH serves as a hypophysiotropic mediator of this response. In the present study we attempted to provide an explanation for this discrepancy by determining whether any of a growing number of putative prolactin releasing factors could alter pituitary responsiveness to TRH. Anterior pituitaries from lactating (day 14) rats were monodispersed with trypsin, cultured for 2 days, and then incubated in the presence of medium alone or medium containing TRH, dopamine, or a combination of these secretagogues. Companion sets of cultures were incubated concurrently with either beta-endorphin, neurotensin, oxytocin, serotonin, vasoactive intestinal polypeptide, or lysine vasopressin. As expected, TRH stimulated and dopamine suppressed prolactin release. None of the substances tested except oxytocin had a significant effect on pituitary cell responsiveness to TRH or dopamine. Oxytocin had no effect on prolactin secretion when tested alone or in combination with TRH and dopamine. TRH alone stimulated TSH release by these cultures, while oxytocin and dopamine were ineffective by themselves. However, TSH secretion by cultures treated simultaneously with TRH and oxytocin could be suppressed to approximately half of that released by cells incubated with TRH alone. These results demonstrate that oxytocin attenuates TRH-induced TSH release by a direct action on pituitary cells without affecting the prolactin response. This selectivity of responsiveness imparted by oxytocin might contribute to the blunted release of TSH after suckling.
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PMID:Oxytocin attenuates TRH-induced TSH release from rat pituitary cells. 315 75

Anterior uveitis or iritis occurs in a variety of systemic diseases including sarcoid, Behcet's, and spondyloarthritis. Iritis is, therefore, presumed to result from a variety of pathogenetic mechanisms. We hypothesized that unique chemotactic factors should be associated with different etiologies for inflammation. We have tested this hypothesis using rabbit models of anterior uveitis. We have found that aqueous humor generally contained chemotactic activity for monocytes 24 h after an intravitreal injection of endotoxin, killed mycobacteria, or human serum albumin (in a rabbit previously immunized against human serum albumin). Anterior chamber paracentesis resulted in aqueous humor with a high protein content. However, in contrast to the other models of inflammation, paracentesis did not result in a cellular infiltrate in the anterior chamber, and aqueous humor after paracentesis was not chemotactic. For either immunologically mediated inflammation or for inflammation resulting from injection of a killed bacterial product, chemotactic activity could be digested by papain or trypsin and tended to coelute with albumin on either gel filtration or ion-exchange chromatography. These observations suggest that a similar chemotactic factor for monocytes appears to be associated with ocular inflammation that follows either an immune response or injection of a killed bacterial product.
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PMID:Similar chemotactic factor for monocytes predominates in different animal models of uveitis. 341 43

Anterior pituitaries of adrenalectomized and sham operated adult rats were dispersed by trypsin and cultured for 4 and 8 days. Adrenalectomy caused a moderate increase in number of corticotrophs in both zero-time cell suspensions and cultures. There was a pronounced elevation of immunoreactive ACTH content in both cells and media and an enhanced secretory response to stimulation of cultures with stalk-median eminence extract containing cortiocotropin releasing (CRF) activity. Some cells identified as corticotrophs by a specific immunostaining incorporated tritiated thymidine into their nuclei suggesting their ability to enter the cell cycle. The relatively smaller increase in number of ACTH cells and the considerably higher ACTH producing capacity of the corticotrophs after adrenalectomy seem to be inconsistent with the quantal response model of hormone secretion recently introduced by Rodbard.
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PMID:A quantitative approach to trace the corticotrophs in culture after adrenalectomy. 627 27

We have used fractionation on density gradients of Percoll to separate the cell types in the rat anterior pituitary gland and to produce a purified preparation of somatotrophs. The method differs from those described previously which used, for example, albumin or Ficoll gradients, in being more rapid and avoiding low temperatures, and therefore gives cells with improved viability. Anterior pituitary glands from male rats were dispersed with trypsin to produce 1.5 x 10 (6) -2.0 x 10 (6) cells/gland. These were fractionated on hyperbolic density gradients of Percoll. Two bands of cells containing somatotrophs were detected, one of which (band A; density 1.075-1.082 g/cm3) contained approximately 90% somatotrophs, whereas the other (band B; density 1.055-1.068 g/cm3) contained about 70% somatotrophs mixed with other cells, especially lactotrophs. Cells in band A appeared more responsive to secretagogues than those in band B; growth hormone secretion was stimulated markedly by cyclic AMP derivatives and prostaglandin E2, and inhibited by somatostatin. Such purified somatotrophs are well suited to biochemical studies on the mechanism of the control of growth hormone secretion.
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PMID:A procedure for the purification of somatotrophs isolated from rat anterior pituitary glands using Percoll density gradients. 628 34


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