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)

This study evaluates the presence of proopiomelanocortin (POMC)-related peptides in four embryos and eight fetal pituitaries starting from 5 to 25 weeks of pregnancy. Moreover, fetal membranes (amnion and chorion) were also investigated. Freshly collected samples were boiled in acetic acid to destroy enzymes, homogenized and submitted to high performance liquid chromatography (linear gradient from 25 to 40% acetonitrile in 0.01 M HCI, in 15', 1.5 ml/min). The collected fractions were tested for the presence of beta-lipotrophin (beta-LPH), beta-endorphin(beta-EP), gamma-endorphin(gamma-EP) through RIAs. beta-EP and beta-LPH were detected from 7 weeks of pregnancy while gamma-EP appeared later. Only the cephalic portion of the embryos contained the peptides where beta-LPH predominates while no immunoreactivity was detected in the rostral one. In the fetal pituitary there is a progressive increase of gamma-EP according to the gestational age and both beta-EP and beta-LPH showed a trend toward constancy in the 15-25 week range. Amnion and chorion contain a significant amount of the three peptides. Their ontogenesis starts earlier than in the embryo; beta-LPH or beta-EP were detected at 5 weeks of pregnancy. In both tissues beta-EP was higher in the first than in the second trimester. These data demonstrate a different pattern of POMC ontogeny and processing between the conceptus and his environment. This suggests that the POMC-related opiod system of the fetus and of fetal adnexes are independent of each other, possibly subserving to different functions.
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PMID:Proopiomelanocortin-related peptides in feto-placental structures throughout pregnancy. 243 58

The effect of intraperitoneal administration of cocaine on the concentrations of hypothalamic corticotropin releasing factor like-immunoreactivity (CRF-LI), plasma ACTH, beta-endorphin, and corticosterone was investigated. Groups of rats were injected with 20 mg/kg cocaine HCI or 0.9% NaCl and then killed 0, 10, 20, 30 or 60 minutes later. Hypothalamic CRF-LI, plasma ACTH, beta-endorphin, and corticosterone concentrations were determined by radioimmunoassay. A significant increase in plasma ACTH, beta-endorphin, and corticosterone concentrations was observed after cocaine administration. In contrast, cocaine had no significant effect on hypothalamic CRF-LI concentrations. Intravenous administration of 0.5 and 2.0 mg/kg cocaine to rats in which the endogenous release of CRF was blocked by chlorpromazine, morphine, and pentobarbital elicited a significant increase in plasma corticosterone concentrations. These results demonstrate that cocaine induces the release of ACTH, beta-endorphin, and corticosterone and suggest that this response is mediated at the pituitary level.
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PMID:Cocaine induced secretion of ACTH, beta-endorphin, and corticosterone. 282 43

Urotensin I (UI), a 41-residue mammalian hypotensive and fish or mammalian corticotropin-releasing peptide, isolated from 0.1 N HCI extracts of urophyses of the carp (Cyprinus carpio) was purified and the amino acid sequence was determined to be: H-Asn-Asp-Asp-Pro-Pro-Ile-Ser-Ile-Asp-Leu-Thr-Phe-His-Leu-Leu- Arg-Asn-Met-Ile-Glu-Met-Ala-Arg-Asn-Glu-Asn-Gln-Arg-Glu-Gln-Ala-Gly-Leu-Asn-Arg-Lys-Tyr-Leu-Asp-Glu-Val-NH2. When the extraction procedure included heating at 100 degrees C for 15 min, UI was cleaved at a highly acid labile Asp-Pro bond to give the fully active UI (4-41). Urotensin I shows close structural and biological homology with the recently isolated ovine hypothalamic corticotropin-releasing factor (CRF) and the frog skin peptide sauvagine and thus may be considered an evolutionary prototype of unique mammalian-hypotensive and vertebrate corticotropin-releasing factors.
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PMID:Isolation and amino acid sequence of urotensin I, a vasoactive and ACTH-releasing neuropeptide, from the carp (Cyprinus carpio) urophysis. 675 95

6-[6-(4-Hydroxypiperidinyl)hexyloxy]-3-methylflavone HCI (NPC 16377), a structurally novel compound, was found to be a highly potent and selective ligand for sigma-sites. Although 5-fold less potent than haloperidol and 2-fold less potent than ifenprodil to inhibit 1,3-di-o-tolylguanidine binding, NPC 16377 (IC50 = 36 nM) was more potent than alpha-(4-fluorophenyl)-4-(5-fluoro-2-pyrimidinyl)-1-piperazinyl butanol (BMY 14802), rimcazole and the atypical antipsychotic, clozapine. A similar rank order of potency was observed when [3H](+)-3-(3-hydroxyphenyl)-N-(1-propyl)piperdine was used as the radioligand. Like BMY, rimcazole and clozapine, NPC 16377 (IC50 = 2671 nM) had low affinity for dopamine type 2 receptors. Additionally, the compound was only weakly active in 35 additional receptor binding assays including those for serotonin2 and serotonin1C receptors. In vivo, NPC 16377 potently inhibited the binding of [3H]-(+)-N-allylnormetazocine to sigma sites after both intraperitoneal and oral administration. At doses 30-fold in excess of the ID50 to inhibit [3H](+)N-allylnormetazocine, NPC 16377 failed to displace [3H]raclopride from dopamine type 2 binding sites. Unlike haloperidol, BMY 14802, ifenprodil and clozapine, behaviorally effective doses of NPC 16377 did not increase dopamine turnover in the frontal cortex, nucleus accumbens or corpus striatum of rats. In contrast, each of these agents increased circulating levels of both adrenocorticotropin and corticosterone, but only NPC 16377 decreased circulating plasma levels of prolactin. The results of the current study are consistent with the notion that NPC 16377 is a potent, selective and orally active sigma site ligand. At behaviorally relevant doses the compound produces neuroendocrine effects both similar to, and different from, neuroleptics, other sigma-ligands and atypical antipsychotics, while having no effect on dopamine turnover. Given these data, NPC 16377 should prove to be a useful compound to explore further the physiological and functional significance of sigma-sites in brain.
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PMID:NPC 16377, a potent and selective sigma-ligand. I. Receptor binding, neurochemical and neuroendocrine profile. 838 61

Besides its acute and chronic effects on corticosteroid synthesis, the pituitary adrenocorticotropic hormone (ACTH) regulates diverse adrenocortical biological functions including the synthesis of a number of mitochondrial, cytoplasmic, and secreted proteins. ACTH-induced secreted proteins are candidates to act as local extracellular relays of the hormone in either an autocrine or a paracrine manner. In the present study, we report that stimulation of primary cultures of bovine adrenocortical (BAC) fasciculata cells with 10 nM ACTH for 24 h results in a mean 8 +/- 4-fold induction of the synthesis of a secreted protein presenting an apparent Mr of 21 kDa. Peptide microsequencing and Western blotting allowed us to identify this 21-kDa ACTH-induced protein as the tissue inhibitor of metalloproteinase-2 (TIMP-2). The induction of TIMP-2 by ACTH required transcription, was mimicked by 8-bromo cyclic 3'-5' adenosine monophosphate, but was not observed in response to angiotensin II, IGF-1, fibroblast growth factor-2, transforming growth factor-beta1, or cortisol treatments. ACTH stimulated TIMP-2 mRNA levels by a factor 4, whereas TIMP-1 mRNA levels were not affected and TIMP-3 mRNA remained undetectable. The biological activity of TIMP-2 varied accordingly, as we observed that the conditioned medium of ACTH-treated BAC cells was four times more potent at inhibiting gelatinolytic activity than was the conditioned medium of control cells. Because the proteolytic activity of both progelatinase-B and progelatinase-A secreted by BAC cells remained latent, whether in the presence or in the absence of ACTH, a paracrine rather than autocrine role is proposed for TIMP-2 in the adrenal cortex.
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PMID:Tissue inhibitor of metalloproteinase-2 (TIMP-2) expression is strongly induced by ACTH in adrenocortical cells. 1043 Jan 77

The purpose of the present study was to examine the effect of a selective serotonin (5-HT) reuptake inhibitor (SSRI) on exercise performance during a 90 min time trial. Eight well trained male cyclists (VO2max 68.1 +/- 9.5 ml/kg/min) performed three 90 min time trials at 65% Wattmax. Blood samples were collected via an indwelling venous catheter for adrenocorticotropin hormone (ACTH), prolactin (PRL), cortisol, catecholamines, growth hormone (GH) and beta-endorphins. The evening before and the morning of the time trials, the subjects ingested a capsule containing either placebo (lactose) or 20 mg Fluoxetine-HCI (Prozac, Ely Lilly Belgium). A double blind, randomized, placebo controlled, cross-over design was performed. Performance was not influenced by the SSRI. As expected, all blood parameters increased significantly during exercise (p < 0.05). During the SSRI trial most parameters were slightly lower but only significantly for endorphins and PRL (p < 0.05). The results demonstrate that performance is not influenced by an SSRI, although some plasma hormones indicate a central effect of the drug. Surprisingly, the increases in PRL and endorphins were lower during the SSRI trial, meaning that the hormonal modulation during exercise might be regulated by the interaction between neurotransmitters rather than by serotonin alone.
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PMID:Exercise performance is not influenced by a 5-HT reuptake inhibitor. 1151 Aug 68

Alpha-melanocyte stimulating hormone (alpha-MSH) is a proopiomelanocortin derivative and a multi-function neuropeptide, well know for its pigment-inducing capacity, inhibitory action on proinflammatory cytokines and chemoattractant cytokines, and suppressive action on collagen synthesis. Human Tenon's capsule fibroblasts (HTF) are the main effector cells in the initiation and mediation of wound healing and fibrotic scar formation after trabeculectomy. In this study the effects of alpha-MSH on proliferation of HTF stimulated by transforming growth factor beta1 (TGF-beta1), have been investigated and discussed. Fibroblasts were cultured in Dulbecco's modified Eagle's medium (DMEM) in the control group, and in DMEM with TGF-beta1 at concentration of 10(-12) M in the TGF-beta1 group, and DMEM with 10(-12) M TGF-beta1 and alpha-MSH ranging from 0, 10(-8) to 10(-4) M in the TGF-beta1/alpha-MSH groups. Cell proliferation was assessed 48 h later by the CellTiter 96 Aqueous One Solution Cell Proliferation Assay. After administration of TGF-beta1 at a concentration of 10(-12) M, or TGF-beta1 at 10(-12) M plus alpha-MSH at 10(-6) M, the mRNA level of type I (alpha1) collagen, fibronectin, TNF-alpha, intercellular cell adhesion molecule-1 (ICAM-1), vascular cell adhesion molecule-1 (VCAM-1), MMP-1, MMP-2, TIMP-1, and TIMP-2 in HTF were analyzed using the real time reverse transcription polymerase chain reaction. Alpha-MSH demonstrated an inhibitory effect on the proliferation of HTF induced by TGF-beta1 in a dose-dependent manner, when the concentration was lower than 10(-5) M, and a suppressive effect on the mRNA expression of type I (alpha1) collagen, TNF-alpha, ICAM-1 and VCAM-1, which were up-regulated by TGF-beta1. Our results showed a reverse effect of alpha-MSH on the imbalance between MMPs and TIMPs compared with TGF-beta1. Based on all these results, we conclude that alpha-MSH could effectively suppress HTF proliferation and modulate correlative genes in collagen synthesis stimulated by TGF-beta1, which implies that alpha-MSH could be exploited in the treatment of conjunctival fibrotic scar disorder.
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PMID:Alpha-melanocyte stimulating hormone suppresses the proliferation of human tenon's capsule fibroblast proliferation induced by transforming growth factor beta 1. 2311 52