Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01189 (beta-endorphin)
 21,003 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A mouse anterior pituitary tumor cell line (AtT-20) that secretes adrenocorticotropin and beta endorphin sorts the proteins it transports to the surface into two exocytotic pathways. AtT-20 cells also synthesize a secretory granule-specific sulfated molecule and secrete it on stimulation (Moore, H.-P., B. Gumbiner, and R. B. Kelly, 1983, J. Cell Biol., 97:810-817). We show here that this molecule is sensitive to proteolysis and that the residual sulfated material co-migrates with a chondroitin sulfate standard on thin-layer electrophoresis. Furthermore, this sulfated molecule is completely sensitive to chondroitinase ABC digestion. Thus the secretory granule-specific sulfated molecule is a proteoglycan with chondroitin sulfate side chains. We examined the role of proteoglycans in the sorting and secretion of adrenocorticotropin in AtT-20 cells by severely decreasing the amount of this vesicle-specific proteoglycan in two ways. First, a xyloside was used to inhibit proteoglycan biosynthesis; second, a variant of the AtT-20 cell line was isolated that synthesized little of the sulfated proteoglycan. In neither case was the sorting or secretion of adrenocorticotropin detectably altered, suggesting that the proteoglycan is not required for these processes.
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PMID:Sorting and secretion of adrenocorticotropin in a pituitary tumor cell line after perturbation of the level of a secretory granule-specific proteoglycan. 609 92

This study investigated the direct effects of hydrocortisone (HS), corticotropin-releasing factor (CRF), and adrenocorticotropin (ACTH) on basal and gonadotropin-releasing hormone (GnRH)-stimulated secretion of follicle-stimulating hormone (FSH) from dispersed pig pituitary cells in vitro. Pig pituitaries were dispersed into cells with collagenase, DNAase, and hyaluronidase and then cultured in McCoy's 5a medium containing horse serum (10%) and fetal calf serum (2.5%) pretreated with dextran-coated charcoal for 3 days. Cells were preincubated with steroids, CRF, or ACTH before GnRH was added. HS did not affect basal FSH secretion after 72 h of incubation. Treatment of pituitary cells with increasing concentrations (0.001-800 micrograms/ml) of HS for 72 h resulted in a dose-dependent decrease in GnRH-stimulated FSH release. HS pretreatment did not cause a change in cellular FSH content. Increasing duration (6-72 h) of treatment with HS (200 micrograms/ml) led to a time-dependent decrease in GnRH-stimulated FSH release, achieving statistical significance by 12 h. Porcine ACTH had no influence on basal and GnRH-stimulated FSH secretion. CRF decreased GnRH-stimulated FSH secretion in a dose-dependent manner, and the inhibitory effect required preincubation (6-18 h) with CRF. HS inhibited the FSH secretory responses to phospholipase C, melittin, and 8-bromo-cAMP but did not affect the response to 1,2-dioctanoyl-sn-glycerol and ionophore A23187. These results indicate that both cortisol and CRF can act directly on pig pituitary to inhibit FSH responsiveness to GnRH.
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PMID:Actions of corticotropin-releasing factor or cortisol on follicle-stimulating hormone secretion by isolated pig pituitary cells. 839 May 96

Opioid peptides have been localized in a variety of peripheral tissues like placenta, thyroid, pancreas, gastrointestinal tract, in the reproductive tract of male and female and in the testes of rats. Immunoassayable material was detected in extracts of gonads, reproductive tract and accessory reproductive organs. Studies with naloxone have suggested that beta-endorphin may have an important role in steroidogenesis and may have a role in regulating transport of luminal material. In our studies met-enkephalin, beta-endorphin, naloxone or N-acetyl beta-endorphin antiserum were microinjected intra testicularly once on alternate days for one week and autopsied 24 h after the last injection. Intratesticular administration of 25, 50 and 100 micrograms doses of naloxone induced significant decrease in in vitro secretion of testosterone per se, which was significantly greater with 50 micrograms dose than with those of the other two doses. A 25 micrograms dose had no effect on hyaluronidase or acid phosphatase activity while 50 micrograms dose significantly decreased the enzyme activity. One hundred micrograms dose also significantly decreased hyaluronidase activity. Intratesticular injection of 10 micrograms met-enkephalin or 1 microgram beta-endorphin significantly decreased hyaluronidase activity whereas 20 microliters N-acetyl beta-endorphin antiserum increased the specific activity of hyaluronidase. There was no change in the weight of the testes on treatment with the above agents.
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PMID:Studies on the effect of intratesticular administration of opioid peptides, naloxone or N-acetyl beta-endorphin antiserum on some testicular parameters in rats. 951 1

Systemic administration of opioid peptides, methionine-enkephalin and beta-endorphin, chronically, lowered gonadotropin levels in plasma and had an inhibitory effect mainly on the testicular enzymes hyaluronidase, acid phosphatase and on incorporation of 3[H] thymidine in the tissue. When rats were similarly treated with opioid peptide antagonist naloxone and N-acetyl beta-endorphin antiserum, induced an opposite effect. This is either the direct effect of opioid peptides/antagonist on the gonads or it may be via the circulating levels of gonadotropin.
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PMID:Effects of chronic systemic administration of opioid peptides, naloxone and N-acetyl beta-endorphin antiserum on gonadotropins and testicular functions in the rat. 971 45

Opioid receptors are expressed in cells of the immune system, and potent immunomodulatory effects of their natural and synthetic ligands have been reported. In some studies, the opiate receptor antagonist naloxone itself displayed immunomodulatory actions. We investigated effects of naloxone on leukocyte chemotaxis. Cell migration was tested in micropore filter assays using modified Boyden chambers, and receptor expression was investigated using radiolabel binding assays. Naloxone induced peripheral blood nonadherent mononuclear cell and neutrophil chemotaxis at nanomolar concentrations and deactivated their migration toward beta-endorphin, angiotensin II, somatostatin, or interleukin-8 but not toward RANTES, vasoactive intestinal peptide, or substance P. Ligand binding studies showed no alteration in the binding of interleukin-8 to neutrophils by naloxone. Cleavage of heparan sulfate from proteoglycans on the cells' surface completely inhibited chemotactic and deactivating properties of naloxone but not other attractants. Chemotactic properties were abolished by pretreating cells with heparinase, chondroitinase, sodium chlorate, and anti-syndecan-4 antibodies, indicating the involvement of syndecan-4. The extent of migration toward naloxone was diminished by pretreatment with dimethylsphingosine, a specific sphingosine kinase inhibitor. As syndecan-4 signaling in leukocyte chemotaxis involves activation of sphingosine kinase, results indicate that naloxone interacts with syndecan-4 function in cell migration and suggest a role for heparan sulfate proteoglycans as coreceptors to members of the delta-opiate receptor family.
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PMID:Heparan sulfate proteoglycans are involved in opiate receptor-mediated cell migration. 1470 51