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)

The major cystosolic aminopeptidase (alanylaminopeptidase) was purified to homogeneity from human cerebral cortex and the specificity of its actions on a series of Leu-enkephalin-related peptides of increasing chain length was determined. In each case, only the N-terminal Tyr-Gly bond was hydrolysed. Kinetic analysis of the data revealed that the specificity constant (kcat/Km;s-1M-1) falls with increasing chain length from a maximum of 13.6 x 10(4) for Leu-enkephalin (5 residues) to 5.8 x 10(2) for dynorphin (1-13). Dynorphin 1-17, while not being degraded itself acted as a competitive inhibitor (Ki = 2.7 microM) of the degradation of smaller peptides. Beta-endorphin was not hydrolysed by analylaminopeptidase, nor did it act as an inhibitor of the enzyme.
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PMID:Specificity of action of human brain alanyl aminopeptidase on Leu-enkephalin and dynorphin-related peptides. 256 98

The three major classes of neurons in the paraventricular nucleus (PVH) provide a rich model for studying hormonal and neural influences on multiple neuropeptides expressed in individual cells. A great deal of previous work has examined this problem at the immunohistochemical level, where hormonal and neural influences on peptide levels have been established. In situ hybridization methods were used here to determine whether these effects are accompanied by measurable changes in neuropeptide mRNA levels. In the first series of experiments, the time-course of corticosterone replacement effects on corticotropin-releasing hormone (CRH) mRNA levels in parvicellular neuroendocrine cells of adrenalectomized animals were determined, and a dose-response curve was established. CRH mRNA hybridization remains maximal with plasma levels of steroid up to about 50 ng/ml, then declines sharply between about 60-130 ng/ml, and is just detectable at higher levels. We confirmed that corticosterone decreases vasopressin mRNA levels in this cell group and showed that levels of preproenkephalin mRNA are also decreased, whereas no significant changes in cholecystokinin, beta-preprotachykinin, and angiotensinogen mRNA levels could be detected. Thus, corticosterone decreases some neuropeptide mRNA levels and has no influence on others in this cell group. Tyrosine hydroxylase mRNA hybridization is also unaffected in this part of the nucleus. In a second group of experiments, the cell-type specificity of corticosterone influences was examined. It was found that while the hormone depresses CRH mRNA levels in parvicellular neurons, it increases such levels in PVH neurons with descending projections, in certain magnocellular neurosecretory neurons, and in a part of the central nucleus of the amygdala, whereas no influence was detected in the rostral lateral hypothalamic area. Furthermore, the stimulatory effects of corticosterone have different threshold levels in different cell groups. Thus, in different types of neurons, corticosterone may increase, decrease, or have no influence on CRH mRNA levels. In contrast, while corticosterone depresses vasopressin mRNA levels in parvicellular CRH neurons, it has no obvious effects on vasopressin mRNA levels in magnocellular or descending neurons; as with CRH, the effects of corticosterone on vasopressin mRNA levels are cell-type specific. In a third series of experiments it was shown that glucocorticoid receptor and mineralocorticoid receptor mRNAs are found in all three cell types in the PVH and that corticosterone tends to produce modest increases in mRNA levels for both receptors. Finally, it was shown that unilateral catecholamine-depleting knife cuts do not change mRNA levels for any of the neuropeptides (or steroid hormone receptors) examined here, although dramatic changes in neuropeptide levels themselves have been shown.4+
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PMID:Differential steroid hormone and neural influences on peptide mRNA levels in CRH cells of the paraventricular nucleus: a hybridization histochemical study in the rat. 256 87

Recent evidence has suggested that stress may suppress the immune system and increase the frequency and severity of viral and neoplastic disease. The mechanisms for stress-induced modulation of immune function are unclear, but several neuropeptides are thought to be involved. Because macrophages play an important role in the host defense against infection and neoplasia, several stress-related neuropeptides were screened in efforts to determine whether these substances affect macrophage-mediated tumoricidal activity. Adrenocorticotropin and noradrenaline each completely blocked the capacity of mouse recombinant interferon-gamma (INF-gamma) to activate murine peritoneal macrophages to a tumoricidal state as measured by the lysis of 125I-UdR-labeled melanoma target cells. Vasoactive intestinal peptide significantly potentiated the suppressive effects of noradrenaline. In contrast, neurotensin markedly enhanced the cytolytic capability of peritoneal macrophages activated with INF-gamma. Several other neuropeptides, including substance P, alpha-endorphin, beta-endorphin, Leu-enkephalin, and Met-enkephalin, had no effect on macrophage activation. These findings demonstrate that selected stress-related neuropeptides and neurohormones significantly modulate the capacity of macrophages to attain a tumoricidal state and suggest that alteration of macrophage function by neuropeptides may be a prominent feature of stress-induced enhancement of neoplastic disease.
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PMID:Modulation of macrophage-mediated tumoricidal activity by neuropeptides and neurohormones. 258 37

The regional distribution of peptidergic nerves in the juvenile and adult human prostate has been studied immunohistochemically using highly specific polyclonal antibodies. Nerves displaying immunoreactivity of Met-enkephalin, Leu-enkephalin, heptapeptide and octapeptide were detected in the dorsolateral stroma closely related to smooth muscle predominantly of juvenile glands. A less strong immunoreactivity was present around stromal vessels and periurethral. Subepithelial peri-acinar nerves showing Leu-enkephalin, Met-enkephalin, octa- and heptapeptide immunoreactivity were found in a few instances. The most prominent immunoreaction was achieved with octapeptide antiserum, followed in decreasing order by Met-enkephalin, Leu-enkephalin and heptapeptide. Their density decreased with age. Antisera against beta-endorphin, alpha-neoendorphin, beta-neoendorphin and dynorphin A gave to positive immunoreaction with prostatic nerves. The regional distribution pattern described is in favor of a postsynaptic peptidergic sympathetic innervation of prostatic stroma acting with classical neurotransmitters.
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PMID:Age-dependency and regional distribution of enkephalinergic nerves in human prostate. 262 85

It is theorized that intermediate filaments are important in the modulation of membrane activity and cell motility; however, their functions are unknown. The assembly and organization of these filaments are under hormonal regulation. We investigated in human monocytes the in vitro effects of Met-enkephalin, Leu-enkephalin, and beta-endorphin on the expression of immunoreactive cytoskeletal vimentin filaments. We simultaneously examined their effect on the phagocytosis of Candida albicans and on the membrane display of surface molecules. The three opioid peptides markedly reduced the expression of vimentin filaments, the phagocytic activity, and the display of HLA-DR molecules at concentrations of 10(-6), 10(-8), and 10(-10) M. On the other hand, the intravenous administration of fentanyl, a synthetic opiate agonist, to patients undergoing surgery induced similar changes in monocytes. In other experiments, 10(-8) M beta-endorphin also decreased the expression of CR3 but did not influence the display of CD13, a surface protein of unknown function. Expression of vimentin filaments correlated directly with the display of HLA-DR antigens and CR3 and with the phagocytic activity. The results of this paper indicate that opiates and opioids, neuropeptides known to be released during stress, can directly depress several monocyte functions. Furthermore, from these data it may be speculated that intermediate filaments may regulate the membrane expression of some surface molecules and the phagocytic process.
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PMID:Opioid peptides modulate the organization of vimentin filaments, phagocytic activity, and expression of surface molecules in monocytes. 271 83

An enkephalin-binding protein was found in human plasma and serum. The protein was partially purified by DEAE-cellulose column chromatography. The binding of [3H]leucine-enkephalin to this protein was competitively inhibited by unlabeled leucine- and methionine-enkephalin and various peptide hormones such as beta-endorphin and glucagon, but not by Leu-enkephalin-amide. The fact that amide derivatives of leucine-enkephalin and methionine-enkephalin did not inhibit the binding suggests that c-terminuses of enkephalins might have an important part in binding the protein. From these results, physiological roles of the enkephalin-binding protein are discussed.
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PMID:Enkephalin-binding protein in human blood. 281 10

Double-staining in either vibratome or paraffin sections using contrasting chromogens revealed an alpha-melanocyte-stimulating hormone (alpha-MSH)-containing cell group in the arcuate nucleus, a metorphamide-containing cell group in the paraventricular hypothalamus, and an extensive group of magnocellular perikarya in the zona incerta (ZI) and the lateral hypothalamus (LH) that appeared to contain both antigens. Staining of adjacent paraffin sections also suggested that most (and perhaps all) of the magnocellular perikarya in the ZI and LH that contained metorphamide-like immunoreactivity also contained alpha-MSH-like immunoreactivity. Metorphamide-like immunoreactivity in the ZI and the LH was abolished by absorption of the antiserum with metorphamide but was unaffected by absorption with alpha-MSH. alpha-MSH-like immunoreactivity in the ZI and LH was abolished by absorption of the antiserum with alpha-MSH but was unaffected by absorption with metorphamide. Antisera directed against [Met5]-enkephalin (Met-ENK), [Met5]-enkephalin-Arg6,Gly7,Leu8 (ENK-8), [Met5]-enkephalin-Arg6,Phe7 (ENK-7), neuropeptide Y, and FMRF-amide did not stain magnocellular perikarya in the ZI and LH. Pretreatment of paraffin sections with trypsin resulted in the appearance of [Met5]-enkephalin-Arg6-like immunoreactivity in the ZI and LH. Pretreatment of paraffin sections with trypsin did not reveal any occult Met-ENK-, ENK-7- or ENK-8-like immunoreactivity in either the ZI or the LH. These observations indicate that magnocellular neurons in the ZI and LH contain both a metorphamide-like and an alpha-MSH-like peptide but do not express either the preproenkephalin or the prepro-opiomelanocortin48 gene.
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PMID:Characterization of metorphamide-like immunoreactivity in the zona incerta and lateral hypothalamus: co-localization with alpha-melanocyte-stimulating hormone-like immunoreactivity. 284 Oct 10

Leu-enkephalin, leu-enkephalinamide, ala-leu-enkephalin, met-enkephalin and dynorphin-A[1-13] were administered in microinjection into one of the self-stimulation sites of SN-VTA or MFB-LH and the electrical self-stimulation (SS) of the injected site and of the second site was recorded. The study revealed that the leu-enkephalin and the leu-enkephalinamide inhibited the SS of SN-VTA and produced no effect on the SS of MFB-LH, when administered into these sites. The MFB-LH injection, however, facilitated the SS of SN-VTA. The effect of ala-leu-enkephalin injection in MFB-LH was similar to the above, but the effect of the injection in SN-VTA was different in that it caused the facilitation of its SS and not the depression as seen with leu-enkephalin. Met-enkephalin injections in the two regions caused no direct or indirect changes of the SS of the regions. Dynorphin injection in SN-VTA facilitated its SS, like the injection of ala-leu-enk, but dynorphin injections in MFB-LH produced no effects. The results essentially demonstrate the differences in the effects of the different opioids in the reward system of the SN-VTA, and it is discussed that these differences are probably due to the preferences in the types of the receptors upon which these opioids act in the SN-VTA neuronal organisation. The results also demonstrate the major difference in the organisation of the reward substrate of the MFB-LH from that of the SN-VTA, as the effects of the opioids in the MFB-LH are markedly different or none compared to the effects in the SN-VTA.
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PMID:Differential effects of opioid peptides administered intracerebrally in loci of self-stimulation reward of lateral hypothalamus and ventral tegmental area--substantia nigra. 285 95

Effect of beta-endorphin and morphine injected intraventricularly on the release of immunoreactive Met-enkephalin, Leu-enkephalin and dynorphin1-13 from the spinal cord was studied in anesthetized rats. Intraventricular beta-endorphin, 16 micrograms, caused a marked spinal release of immunoreactive Met-enkephalin and to a much lesser extent, of immunoreactive Leu-enkephalin while intraventricular morphine, 40 micrograms, did not cause any significant release of immunoreactive enkephalins. The release of immunoreactive Met-enkephalin was not blocked by the pretreatment with 5 mg/kg naloxone, i.p. Immunoreactive dynorphin1-13 was not released by either beta-endorphin or morphine. High performance liquid chromatographic analysis indicated that immunoreactive Met-enkephalin released by beta-endorphin had a retention time identical to [3H]Met-enkephalin. These findings in conjunction with previous pharmacological studies suggest different modes of pharmacological action for beta-endorphin and morphine.
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PMID:Release of immunoreactive Met-enkephalin from the spinal cord by intraventricular beta-endorphin but not morphine in anesthetized rats. 286 5

Proenkephalin B-derived opioid peptides, such as dynorphin1-17, dynorphin1-8, dynorphin B, alpha-neo-endorphin and beta-neo-endorphin in the human hypothalamo-neurohypophyseal tract were quantitated and characterized by the combined use of various radioimmunoassays, gel filtration, high performance liquid chromatography and enzymatic cleavage. Chromatographic analysis of immuno-reactive peptide levels determined that, in each case, these were comprised almost exclusively of the authentic peptides both in the neurohypophysis and hypothalamus. Concentrations of authentic proenkephalin B-peptides were 100-5000-fold lower in the human as compared to the rat neurohypophysis. However, in the paraventricular nucleus (PVN), supraoptic nucleus (SON) and certain other nuclei of the human hypothalamus concentrations of authentic peptides were found to be in the same range as those in the rat hypothalamus. The ratio of proenkephalin B-peptides in PVN and SON to those of the neurohypophysis in the rat was ca. 1:50. Conversely, in man these ratios were shown to be 80:1 for dynorphin B, 6:1 for alpha-neo-endorphin and 1:1 for all other peptides evaluated. Examination of postmortem degradation of peptides indicated that these lower levels in the neurohypophysis are not due to a higher rate of postmortem breakdown. Since levels of both vasopressin and beta-endorphin were very high, these deficits in proenkephalin B-peptides were selective and do not represent a generalized property of the human pituitary. Experiments involving enzymatic cleavage demonstrated the occurrence of higher molecular weight forms containing the Leu-enkephalin sequence which were not recognized by the antisera employed.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Characterization of proenkephalin B-derived opioid peptides in the human hypothalamo-neurohypophyseal axis. 286 12


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