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 factor(s) controlling the secretion of ACTH in peripheral plasma are not well known. The effects of non-extracted and extracted plasma on ACTH secretion were investigated using rat anterior pituitary cell cultures. Medium ACTH was assayed by radioimmunoassay, and the corticotropin releasing activity (CRA) was expressed as ACTH released. One hundred ul of non-extracted plasma showed significant CRA, whereas greater volumes of plasma showed reduced activity. Non-extracted plasma (250 approximately 500 microliter) rather reduced the secretion of ACTH evoked by hypothalamic extract (HE). When plasma was extracted with 0.2 N-acetic acid-acetone and divided into an acid phase and an acetone-ether phase by adding ether, the CRA was recovered in the acid phase while no significant activity was observed in the acetone-ether phase. The acid phase extract of plasma showed a positive dose-response relationship between the amount of plasma extract (50 approximately 800 microliter plasma equivalent) and ACTH release in pituitary cell cultures. The organic phase of plasma extract inhibited HE-induced release of ACTH, and this ACTH-release inhibiting activity was presumed to be corticosterone. When the acid phase extract of 20 ml plasma was applied to a Sephadex G-25 (fine) and eluted with 0.2 N acetic acid, two peaks of CRA were observed. One eluted in the region of void volume and another eluted in the retarded region where no activity was found in chromatography of HE. HE increased both ACTH and cyclic AMP release, but the plasma extract reduced cyclic AMP release. These results suggest that plasma contains both CRA and ACTH release inhibiting activity which can be extracted separately, and that plasma CRA is different from the hypothalamic corticotropin releasing factor.
Nihon Naibunpi Gakkai Zasshi 1979 Dec 20
PMID:[Factor(s) controlling the secretion of adrenocorticotropin (ACTH) in peripheral plasma (author's transl)]. 23 44

The DMS-79 continuous line of human small cell lung carcinoma cells, which produces immunoreactive (IR)-corticotropin (ACTH), -lipotropin (LPH), and -beta-endorphin (beta END), was found to produce IR-calcitonin (CT). Two major high molecular weight (HMW) forms of IR-CT were observed after gel exclusion chromatography under denaturing conditions (mol wt. approximately 7,000 and approximately 14,000), as well as a minor HMW IR-CT component (mol. wt. approximately 70,000). None of these IR-CT materials was extracted from DMS-79 medium by affinity chromatography using an ACTH antibody covalently bound to agarose. These results demonstrate ectopic production of HMW forms of CT and ACTH/LPH/beta END by human lung tumor cells in tissue culture, but do not support the existence of a common CT/ACTH/LPH/beta END precursor molecule.
J Clin Endocrinol Metab 1978 Dec
PMID:Ectopic production of high molecular weight calcitonin and corticotropin by human small cell carcinoma cells in tissue culture: evidence for separate precursors. 23 96

Factors controlling proliferation of adrenocortical cells have been studied in monolayer cultures of bovine adrenocortical cells. Angiotensin II stimulated cell proliferation and [3H]thymidine incorporation into DNA with a half-maximal effective concentration of 0.96 +/- 0.27 nM. Similar sensitivity to angiotensin III with reduced sensitivity to angiotensin I and tetradecapeptide renin substrate was observed. Although sensitivity to angiotensin II was equivalent to that for fibroblast growth factor (1.5 nM half-maximal effective concentration), maximal effects of angiotensin were less than for fibroblast growth factor and serum. High concentrations of insulin (1-10 micrometer) also stimulated [3H]thymidine incorporation into DNA and cell proliferation. [Sar1,Ile5,Ile8]Angiotensin II, a competitive antagonist of angiotensin II, blocked angiotensin II stimulation of DNA synthesis but did not affect fibroblast growth factor and insulin stimulation of DNA synthesis. Corticotropin (ACTH) blocked the stimulatory effects of both angiotensin II and fibroblast growth factor. The dose-response curves for angiotensin II stimulation of steroidogenesis were similar to those for stimulation of [3H]thymidine incorporation into DNA. Among the seven cell types examined, only adrenocortical cells responded to angiotension II with stimulation of DNA synthesis.
Proc Natl Acad Sci U S A 1977 Dec
PMID:Angiotensin stimulation of bovine adrenocortical cell growth. 27 83

Highly purified calf brain cathepsin D (EC 3.4.23.5) selectively splits the Leu77-Phe78 and Ala36-Ala37 peptide bonds of human beta-lipotropin. It is suggested that the formation of human "beta-melanotropin" from gamma-lipotropin, and that of gamma-endorphin from beta-endorphin, is due to the action of cathepsin D during isolation procedures.
Proc Natl Acad Sci U S A 1979 Dec
PMID:Action of cathepsin D on human beta-lipotropin: a possible source of human "beta-melanotropin". 29 8

The pituitary glands of two urodelan species (Mertensiella caucasica, Triturus cristatus) and one one caecilian species (Chthonerpeton indistinctum) were examined with histological (Alcian blue, Brookes' trichrome stain), enzyme histochemical (acid phosphatase, alpha-naphthylacetate-esterase, acetylcholinesterase) and immunofluorescence techniques (anti-carp GTH, anti-ovine prolactin, anti-synthetic alpha-MSH). In the pituitary gland of Mertensiella and Triturus six chromophilic cell types could be distinguished. A strong fluorescence was observed in the MSH-, GTH- and TSH-cells. In the pituitary gland of Chthonerpeton only five chromophilic cell types could be distinguished: in the rostral part of the pituitary gland the B3-cell; in the basal region of the central area the B2-cell; dorsocaudally the B1-cell. The acidophilic cells were found in the central and caudal part of the pars distalis. The basophils of the pars intermedia could be observed in the dorsocaudal part of the pituitary gland surrounding the neurohypophysis. All acidophilic cells showed a strong immunofluorescence with anti-ovine prolactin (LTH).
Cell Tissue Res 1977 Dec 19
PMID:Histological, immuno- and enzyme-histochemical investigations on the adenohypophysis of the urodeles, Mertensiella caucasica and Triturus cristatus and the caecilian, Chthonerpeton indistinctum. 34 44

Serial sections from epoxy resin-embedded rat anterior pituitaries were sequentially immunostained for endorphin, [Met]enkephalin, and growth hormone, respectively. We found that [Met]enkephalin immunoreactivity was confined to the growth hormone producing cells. Corticotropin/endorphin cells in the anterior pituitary from both normal and adrenalectomized rats did not contain any [Met]enkephalin immunoreactivity. When anterior pituitary cells were maintained in monolayer culture for 10 days, [Met]enkephalin immunoreactivity was still located in the growth hormone-producing cells although the staining was weaker than in the somatotrophs in pituitary tissue fixed immediately after death of the animals. This suggested that somatotrophs synthesize [Met]enkephalin. However, this cannot be proved conclusively until biosynthesis experiments have been performed. The following conclusions were drawn from these findings. (i) Anterior pituitary [Met]enkephalin is not an extraction artifact derived from beta-endorphin with which it shares the NH2-terminal pentapeptide sequence. (ii) In the anterior pituitary, beta-endorphin is not the precursor to [Met]enkephalin. [Met]Enkephalin in somatotrophs may be of brain origin and in the somatotrophs may be bound to intracellllar receptors as has been shown for luteotropin releasing hormone in gonadotropic cells.
Proc Natl Acad Sci U S A 1978 Dec
PMID:Pituitary somatotrophs contain [Met]enkephalin-like immunoreactivity. 36 11

Using a highly specific antibody we found Met-enkephalin-like immunoreactivity in large granules of numerous distinct cells that are embedded in a layer of secretory terminals inside the octopus vena cava. Application of antibodies against fragments of the mammalian pro-opiocortin precursor -- alpha-MSH, ACTH, beta-endorphin and 16k-fragment -- and against growth hormone did not produce immunostaining in the octopus enkephalin cells. The vena cava neuropil may represent a favourable system for the examination of the physiological role of the opioid peptide enkephalin.
Neurosci Lett 1979 Dec
PMID:Met-enkephaline-like immunoreactivity in a cephalopod neurohemal organ. 39 32

The distribution and concentration of alpha-MSH in the rodent brain has been determined by radioimmunoassay. The limbic system contained substantial quantities of alpha-MSH. Forty per cent of the alpha-MSH present in the brain was localized in the hypothalamus, with the highest concentration of alpha-MSH in the arcuate nucleus. More than 40% of the extrahypothalamic alpha-MSH in the brain was found in the following areas: midbrain (16%), preoptic area (13%), septum (7%), and thalamus (7%). To determine the source of the hypothalamic and extrahypothalamic alpha-MSH, the anterior hypothalamic preoptic area of the brain was surgically separated from more caudal diencephalic structures, and the arcuate region of the hypothalamus was surgically isolated from the remainder of the brain. Following these deafferentations, no significant reduction in hypothalamic alpha-MSH levels was observed; however, a significant reduction in extrahypothalamic alpha-MSH level was demonstrated. This dramatic decrease of alpha-MSH in extrahypothalamic areas of the rodent brain strongly suggests that the bulk of the extrahypothalamic alpha-MSH arises from neuronal perikarya in the arcuate region. These findings are consistent with the hypothesis that a population of neuronal cell bodies producing alpha-MSH originate in the arcuate region of the hypothalamus and that they send axonal projections to many areas of the limbic system and brain stem.
Brain Res 1979 Dec 07
PMID:Distribution of alpha-melanocyte-stimulating hormone in the rat brain: evidence that alpha-MSH-containing cells in the arcuate region send projections to extrahypothalamic areas. 49 64

In chicks with cannulae chronically implanted into the III cerebral ventricle, the effects of a single dose (10 micrograms) of beta-endorphin on GABA and free glutamic acid content, GAD and GABA-T activities in the diencephalon, brain-stem and brain hemispheres were studied at the time of maximal behavioural stuporous state and analgesia. A significant decrease in GABA concentration both in the diencephalon and brain-stem, accompanied by a significant increase in GABA-T activity in the same areas, was shown to occur. No changes were observed in GAD activity and in glutamic acid content in the studied areas of the brain. In conclusion, present experiments suggest that some central effects of a beta-endorphin may be due to an interference with GABA-ergic transmission.
Res Commun Chem Pathol Pharmacol 1979 Dec
PMID:Effects of intraventricular beta-endorphin on GABA system in some areas of chick brain. 52 83

To identify the site of action of opiate-induced prolactin elevation, in vitro rat hemipituitary incubations were performed in the presence of morphine, met-enkephalin, ala2-met5-enkephalinamide and dopamine (DA) and combinations of opiate with the catecholamine. No opiate stimulated prolactin release directly nor did any opiate block the inhibitory effect of DA. We conclude that this opiate endocrine action is not mediated at a pituitary level but may involve interference with hypothalamic DA release.
Eur J Pharmacol 1979 Dec 07
PMID:Failure of opiates to reverse dopamine inhibition of prolactin secretion in vitro. 52 60


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