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)

There are two regions of steroidogenic tissue in the bird adrenal gland: a subcapsular zone (SCZ) 40-60 cells thick consisting of cells with irregularly shaped nuclei, relatively little smooth endoplasmic reticulum, and mitochondria with shelflike cristae that surrounds an inner zone (IZ) of tissue comprised of smaller cells with rounded nuclei, a more abundant endoplasmic reticulum, and mitochondria with tubular cristae. The cristae in the mitochondria of IZ cells, but not the SCZ cells, seem to be quite labile and only assume the tubular configuration when subjected to corticotropic stimulation. The properties of the steroidogenic cells in the two zones are quantitatively distinct, the cells of the SCZ producing relatively more aldosterone and relatively less corticosterone than the cells of the IZ. The corticotropic responsiveness of the IZ cells is dependent on the synthesis of protein in the cytoplasm and a normal pattern of microfilament assembly. The dose responsiveness of both the IZ and the SCZ cells in vitro is a complex quadratic function of the corticotropin concentration to which they are exposed; the semilogarithmic linear response to corticotropin is restricted to a narrow midrange of concentrations, and at high concentrations cells from both zones of the gland respond submaximally. Throughout the dose-response range, however, the steroidogenic cells of the IZ are more sensitive and more responsive to corticotropic stimulation than are the cells of the SCZ.
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PMID:Adrenal gland: some evidence for the structural and functional zonation of the steroidogenic tissues. 609 33

The present study examined the effects of cytochalasin B on various steps in the luteinizing hormone (LH)-stimulated increase in testosterone synthesis by collagenase-dispersed interstitial cells of adult rat testis. Cytochalasin B at a concentration range of 0.1--50 microM inhibited the LH-stimulated increase in testosterone synthesis in a dose-dependent manner. Both intracellular and medium (released) testosterone levels were reduced, thus indicating that the decrease was not due to the accumulation of testosterone inside the cell as a result of cytochalasin B treatment. Cytochalasin B also inhibited the 8-bromocyclic AMP and pregnenolone-stimulated testosterone synthesis in a similar dose-dependent manner. Cytochalasin B at the two higher doses (10 and 50 microM) also inhibited the LH-stimulated generation of cyclic AMP by interstitial cells. However, this drug had no effect on basal testosterone synthesis except at the highest concentration added. Previous studies on adrenocorticotropic hormone (ACTH)- and LH-stimulated increase in glucocorticoid and testosterone synthesis in adrenal and Leydig cells, respectively, demonstrated that cytochalasin B or anti-actin inhibited the transport of cholesterol into mitochondria. The present studies suggest that cytochalasin B inhibits at least two additional steps in the LH-stimulated increase in testosterone synthesis: (1) the generation of cyclic AMP at the level of the plasma membrane, and (2) the conversion of pregnenolone to testosterone at the level of the smooth endoplasmic reticulum. It remains to be established whether these are direct effects of cytochalasin B, or whether they are mediated by disruption of microfilaments by cytochalasin B.
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PMID:The effects of cytochalasin B on testosterone synthesis by interstitial cells of rat testis. 625 9

The subcellular localization of the post-translational processing steps which occur in the conversion of pro-adrenocorticotropic hormone (ACTH)/endorphin into beta-endorphin-sized molecules in rat intermediate pituitary has been studied. Primary cell cultures were incubated in radioactively labeled amino acids, and a subcellular fraction containing secretory granules was separated from a subcellular fraction containing rough endoplasmic reticulum and Golgi apparatus by centrifugation of homogenates on gradients on Percoll (Pharmacia Fine Chemicals). The radiolabeled beta-endorphin-related material in the granule and rough endoplasmic reticulum/Golgi apparatus fractions was quantitated by immunoprecipitation and sodium dodecyl sulfate polyacrylamide gel electrophoresis. A pulse-chase labeling experiment demonstrated that newly synthesized beta-endorphin-related material first appeared in the rough endoplasmic reticulum/Golgi apparatus fraction and after longer incubations (chase) appeared in the secretory granule fraction. After 2 h of chase incubation, about 85% of the beta-endorphin-related material synthesized during the 30-min pulse incubation had been transferred from the rough endoplasmic reticulum/Golgi apparatus to the secretory granule fraction. The conversion of most of the newly synthesized pro-ACTH/endorphin into beta-lipotropin occurred in the rough endoplasmic reticulum/Golgi apparatus fraction, whereas the conversion of most of the beta-lipotropin into beta-endorphin-sized molecules occurred in the secretory granule fraction.
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PMID:Subcellular fractionation studies on the post-translational processing of pro-adrenocorticotropic hormone/endorphin in rat intermediate pituitary. 626 49

Rat adrenals in different states of stimulation were examined by transmission electron microscopy following perfusion fixation using an in situ isolated-circulation technique. In unstimulated glands, intracortical capillaries were constricted and the cells of the cortex were pressed closely together with little development of filopodia or intercellular spaces. Glands fixed during the period of operative stress, or following a 1 hr perfusion with Adrenocorticotropic hormone (ACTH) showed that the radially orientated capillaries of the cortex were massively expanded, and the cells of both the glomerulosa and fasciculata exhibited an extensive development of filopodia on their surfaces. These filopodia extended into large intercellular spaces, where they often entered into complex relationships with filopodia from neighboring cells. The development of filopodia by cells of the adrenal cortex was also observed using scanning electron microscope techniques. In cells either incubated with ACTH in vitro or isolated from adrenals of rats treated with ACTH in vivo, the filopodia were numerous, often branched, and could reach as much as 1 micro m in length. In contrast, adrenal cells obtained from animals pretreated with cortisol were smooth surfaced. Other cell characteristics, including mitochondria, smooth endoplasmic reticulum, dense granules, and coated vesicles did not show such dramatic correlations with the state of stimulation. It is considered that the development of filopodia and intercellular space is related to secretory mechanisms in the rat adrenal cortex.
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PMID:Morphological correlates of hormone secretion in the rat adrenal cortex and the role of filopodia. 627 16

A significant proportion of the steroidogenic response of isolated rat adrenocortical cells to dibutyryl cyclic AMP does not require extracellular calcium, and this component is profoundly depressed by low concentrations of the putative calcium antagonist, TMB-8. The inhibition is reversed by either the readdition of calcium or the calcium ionophore A23187. The steroidogenic response to pregnenolone, whose mode of action does not require calcium, was not depressed by TMB-8. Corticotropin (ACTH)-induced steroidogenesis, which requires extracellular calcium, was markedly depressed by TMB-8, although enhanced cyclic AMP formation is only slightly depressed by this drug. Adrenal cortical microsomes possess an ATP-dependent 45calcium (45Ca2+) uptake system which responded to EGTA with a rapid efflux of 45Ca2+; EGTA-induced calcium efflux from this microsomal fraction was markedly reduced by a concentration of TMB-8 that blocked dibutyryl cyclic AMP-evoked steroidogenesis. TMB-8 produced a smaller but significant reduction of EGTA-facilitated 45Ca2+ efflux from a mitochondrial-enriched fraction. We interpret these results to mean that TMB-8 blocks the steroidogenic effect of dibutyryl cyclic AMP by interfering with the mobilization of a cellular pool of calcium that is probably localized to the endoplasmic reticulum. The physiological implications of these findings in relation to the complex interactions between calcium and cyclic AMP in adrenal steroidogenesis are discussed.
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PMID:Inhibition of dibutyryl cyclic AMP induced steroidogenesis in rat adrenocortical cells by the putative calcium antagonist TMB-8. 628 80

The subcellular site of the further processing (NH2-terminal acetylation and COOH-terminal proteolysis) of beta-endorphin-sized molecules in the rat intermediate pituitary has been studied. Rat intermediate pituitary primary cultures that had been incubated in radioactively labeled amino acids were homogenized and the secretory granule fraction was separated from the rough endoplasmic reticulum/Golgi apparatus fraction. The labeled beta-endorphin-sized molecules in each subcellular fraction were analyzed by immunoprecipitation, gel filtration chromatography, and ion exchange chromatography. A large percentage of the labeled beta-endorphin-sized molecules became NH2 terminally acetylated after becoming associated with the secretory granule fraction; most of the further COOH-terminal proteolytic processing of alpha-N-acetyl-beta-endorphin(1-31) to form alpha-N-acetyl-beta-endorphin(1-27) and alpha-N-acetyl-beta-endorphin(1-26) also occurred when the labeled beta-endorphin-sized molecules were associated with the secretory granule fraction. The acetylation of alpha-melanocyte-stimulating hormone (alpha MSH)-sized molecules was also investigated in rat intermediate pituitary primary cell cultures by immunoprecipitation, gel filtration chromatography, and reverse-phase high pressure liquid chromatography. Pulse-chase labeling experiments showed that newly synthesized molecules co-migrating with adrenocorticotropic hormone ((ACTH)(1-13)NH2) were converted first to molecules similar to alpha MSH (alpha-N-acetyl-ACTH(1-13)NH2) and then to molecules similar to alpha-N,O-diacetyl-alpha MSH. These results demonstrate that the enzyme activity(s) responsible for the NH2-terminal acetylation of beta-endorphin alpha MSH-sized molecules is located in the secretory granules of the rat intermediate pituitary.
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PMID:Acetylation of alpha-melanotropin and beta-endorphin in the rat intermediate pituitary. Subcellular localization. 628 56

Neurointermediate lobes from amphibians (Rana pipiens) were incubated in Medium 199 containing dopamine, beta-endorphin or dopamine plus beta-endorphin. Dopamine inhibited melanocyte-stimulating hormone (MSH) secretion as measured by bioassay in hypophysectomized frogs, an effect which was transiently reversed by beta-endorphin. The effects of endorphin were in turn partially suppressed by the opiate antagonist, naloxone hydrochloride. Cells treated with all three agents exhibited expanded rough endoplasmic reticulum and decreased secretory granule content, indicative of peptide release and new synthesis. Beta-Endorphin alone did not stimulate MSH secretion above control levels, and at one time period was seen to reduce MSH secretion. The findings indicate a complex interaction between beta-endorphin and dopamine directly upon MSH secretion at the level of the neurointermediate lobe.
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PMID:Interaction of beta-endorphin, naloxone and dopamine: effects on melanocyte-stimulating hormone secretion of amphibian pituitaries in vitro. 628 39

The effects of acute injections of synthetic opiate peptides into the lateral cerebral ventricle of young adult male rats on cells of the intermediate lobe of the pituitary were studied. Met-enkephalin (100/micrograms) injected into anesthetized rats, or 20 micrograms beta-endorphin administered via a previously implanted cannula to unanesthetized animals, will lead to cell degranulation and often to expanded Golgi zones and prominent regions of rough endoplasmic reticulum in secretory cells when tissue is fixed 45--60 min after peptide administration. Treatment of animals with the opiate antagonist naloxone hydrochloride prior to enkephalin injection appeared to prevent the cellular changes elicited with peptide alone. Observations suggest that opiate peptides administered to the cerebrospinal fluid may stimulate release of pro-opiomelanocortin-peptide from pituitary cells.
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PMID:Effects of acute opiate-peptide administration on pro-opiomelanocortin cells of the intermediate lobe of the rat pituitary. 628 49

Detailed studies on the effects of the ionophore monensin upon synthesis, maturation, and intracellular transport of pro-opiomelanocortin in cultures of rat pituitary intermediate lobe cells have been carried out. When added at concentrations larger than 5 X 10(-8) M monensin significantly inhibited protein synthesis by cultured intermediate lobe cells. Pro-opiomelanocortin synthesis was also reduced proportionally to the overall rate of protein synthesis. During pulse-chase experiments, monensin when added at a concentration of 10(-5) M at the beginning of the chase incubation completely inhibited the proteolytic processing of pro-opiomelanocortin. Using a subcellular fractionation procedure of intermediate lobe cell extracts on Percoll gradients, we were able to show that after the addition of monensin (10(-5) M), labeled pro-opiomelanocortin molecules synthesized during a 15-min pulse-incubation were recovered intact after a 2-h chase, in the fractions of the density gradient corresponding to the rough endoplasmic reticulum and Golgi elements. No maturation products or precursor molecules entered the granule fractions as observed in nontreated cells. Taken together these results strongly suggest that monensin blocks the intracellular transport of newly synthesized pro-opiomelanocortin molecules at the Golgi level and that inhibition of proteolytic processing is due to the failure of the prohormone to enter the cell compartment (probably the secretion granules) where maturation proteases are located.
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PMID:Effects of the monovalent ionophore monensin on the intracellular transport and processing of pro-opiomelanocortin in cultured intermediate lobe cells of the rat pituitary. 632 21

Using two immunocytochemical methods, we have shown in light microscopy that the met-enkephalin-like immunoreactivity within striatum and spinal cord of the rat is differentially distributed in either perikarya or nerve terminals according to the technical conditions used [1]. The present electron microscopic study has been undertaken in order to elucidate the subcellular localization of immunoprecipitates according to the same technical conditions. In the neostriatum, numerous met-enkephalin-containing perikarya were stained (principally at the level of rough endoplasmic reticulum) when tissue sections were treated with hydrogen peroxide (H2O2) only, prior to the immunocytochemical procedure. However, injections of colchicine were required to demonstrate perikarya in the dorsal horn of the spinal cord. At variance with previous results, numerous dendritic profiles and nerve terminals were also reactive in this condition. Neurotubules, mitochondria, large granular vesicles (LGVs) and small synaptic vesicles were stained within these structures. The addition of a low concentration of Triton-X-100 (0.02%) in the first incubation medium often resulted in the disappearance of most perikarya and in the staining of only LGVs in nerve terminals. The addition of a higher concentration of Triton-X-100 (0.1%) produced diffusion of immunoprecipitates at the level of nerve terminals, which was probably responsible for the increased intensity of staining and, subsequently, for the better demonstration of fibre varicosities in light microscopy. On the contrary, the disappearance of reactive perikarya seemed to result from the diffusion of the non-protected peptide out of the cytoplasm. The diverse ultrastructural localizations of met-enkephalin-like immunoreactivity in striatum and spinal cord are finally discussed in light of intrinsic connections or afferents described in the literature.
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PMID:Met-enkephalin-like immunoreactivity in rat forebrain and spinal cord using hydrogen peroxide and Triton X-100. Ultrastructural study. 636 52


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