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)

We have used a monoclonal antibody, A2, to study the structure and function on the lipid droplet capsule in steroidogenic adrenal cells. This antibody reacts with a 160-kD protein found in the rat adrenal cortex. Immunofluorescence microscopy shows a dominant rim pattern, which surrounds individual lipid droplets and is distinct from the filamentous vimentin staining. The boundary of lipid droplets in steroidgenic Leydig cells and 3T3 adipocytes is also immunostained by this antibody. The strong association of the 160-kD protein with the lipid droplet is demonstrated by its resistance to Triton X-100 extraction. Stimulation of steroid secretion by adrenocorticotropin results in the detachment of this protein from the lipid droplet and its movement to the cytosol. These findings suggest that the translocation of this 160-kD protein from lipid droplet surface to cytosol on stimulation might be important in facilitating the binding of cholesterol ester hydrolase to the surface of lipid droplets, as proposed for adipocytes, during lipolytic stimulation.
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PMID:A lipid droplet-specific capsule is present in rat adrenal cells: evidence from a monoclonal antibody. 852 43

The cellular nature of the giant eosinophilic cells of tuber and of the cells comprising subependymal giant cell astrocytoma (SEGA) in tuberous sclerosis (TS) remains unclear. To assess the characteristics of these lesions, 13 tubers and 6 SEGA were immunohistochemically studied with glial and neuron-associated antigens. In addition to conventional ultrastructure, 6 tubers and 8 SEGA were subjected to immunoelectron microscopic study for glial fibrillary acidic protein (GFAP) and somatostatin. Eosinophilic giant cells of tubers were positive for vimentin (100%), GFAP (77%) and S-100 protein (92%); such cells were also found to a various extent to be reactive for neuron-associated antigens, including neurofilament (NF) proteins (38%) or class III beta-tubulin (77%). SEGA also showed variable immunoreactivity for GFAP (50%) or for S-100 protein (100%); NF epitopes, class III beta-tubulin, and calbindin 28-kD were expressed in 2 (33%), 5 (83%) and 4 (67%) cases, respectively. Cytoplasmic staining for somatostatin (50%), met-enkephalin (50%), 5-hydroxytryptamine (33%), beta-endorphin (33%) and neuropeptide Y (17%) was noted in SEGA, but not in tubers. Ultrastructurally, the giant cells of tubers and the cells of SEGA contained numerous intermediate filaments, frequent lysosomes and occasional rectangular or rhomboid membrane-bound crystalloids exhibiting lamellar periodicity and structural transition to lysosomes. Some SEGA cells showed features suggestive of neuronal differentiation, including stacks of rough endoplasmic reticulum, occasional microtubules and a few dense-core granules. Furthermore, in one case of tuber, a process of a single large cell was seen to be engaged in synapse formation. Intermediate filaments within a few cells of both lesions were decorated by gold particle-labeled GFAP antiserum. Within the tumor cells of SEGA, irregular, non-membrane-bound, electron-lucent areas often contained somatostatin-immunoreactive particles, whereas the latter could not be detected in tuber. The present study provides further evidence of divergent glioneuronal differentiation, both in the giant cells of tubers and the cells of SEGA. The findings of similar cells at different sites, including the subependymal zone, white matter ("heterotopias"), and cortex indirectly supports the idea that these lesions of TS result from a migration abnormality.
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PMID:Tuber and subependymal giant cell astrocytoma associated with tuberous sclerosis: an immunohistochemical, ultrastructural, and immunoelectron and microscopic study. 854 29

This study demonstrated morphological changes in glial-like cells of the rat pituitary intermediate lobe during early postnatal development, and a subsequent shift in protein expression from vimentin to GFAP. Vimentin immunoreactivity was detected in the lobe at embryo day 14 and was localized in radially-oriented, bipolar cells whose processes spanned the thickness of the intermediate lobe. At electron microscopical resolution, processes contained intermediate filaments, cell nuclei were indented while secretory vesicles characteristic of the endocrine cells were not found. Vimentin immunoreactive intensity began to decrease at postnatal day 5. By postnatal day 7, vimentin-positive, stellate cells were observed, with few radial processes found by day 10. The intensity of vimentin immunoreactivity decreased through day 25. Within the lobe parenchyma, vimentin was localized in glial-like cells since double-label immunohistochemistry revealed no colocalization of beta-endorphin and vimentin, or fibronectin and vimentin. Dopamine-containing axons were in close apposition to vimentin-positive processes. GFAP immunoreactivity first appeared on postnatal day 20 and, by day 25, stellate cell bodies with three to six extended processes were evident. Cells were primarily distributed in the caudal third of the lobe. The characteristic adult pattern of cell clusters in latero-dorsal and ventral portions of the lobe was fully established by postnatal day 55. The transition from vimentin to GFAP expression and concurrent morphological changes resemble those described for radial glial during cerebral cortical development.
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PMID:Glial-like cells of the rat pituitary intermediate lobe change morphology and shift from vimentin to GFAP expression during development. 855 90

S-100, an acidic calcium-binding protein, is co-localized with vimentin in glial-like cells in the adult rat pituitary intermediate lobe. S-100 and melanotrope markers were not co-localized in the adult. During development, S-100 and vimentin were not co-localized but appeared in cells with different morphological characteristics. S-100 was co-localized with POMC mRNA and beta-endorphin during prenatal time and the first three postnatal weeks. This was demonstrated by double-label immunohistochemistry, using combinations of antisera against S-100, vimentin and beta-endorphin, and in situ hybridization histochemistry for POMC mRNA combined with immunohistochemistry for S-100. In the second and third weeks of postnatal development, S-100 was observed in fewer melanotropes and more frequently in stellate cells, which also expressed vimentin. Thus, S-100 appeared to be transiently expressed in melanotropes during prenatal and early postnatal development. S-100 serves as a neurotrophic and glial maturation factor in the CNS. Since S-100 expression in melanotropes coincides with the onset of dopaminergic innervation and morphological changes in glial-like cells of the lobe, it could have similar functions in the rat pituitary intermediate lobe.
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PMID:Transient expression of S-100 by melanotropes of the rat pituitary intermediate lobe during development. 855 91

A 75-year-old female presented with a suprasellar granular cell tumor. Computed tomography (CT) revealed a high dense suprasellar mass with strong postcontrast enhancement. Magnetic resonance imaging showed a round suprasellar mass, which was hyperintense on the T1-weighted images with nonhomogeneous enhancement after the administration of gadolinium-diethylenetriaminepenta- acetic acid, and hypointense on the T2-weighted images. Cerebral angiography demonstrated no abnormal findings. The tumor was partially removed via a right frontotemporal craniotomy. The histological diagnosis was suprasellar granular cell tumor. Her postoperative course was uneventful other than mild and transient diabetes insipidus. She has remained asymptomatic without CT evidence of tumor regrowth for 20 months after the surgery. Immunohistochemical studies showed positive reaction for S-100 protein in the tumor cell nuclei, but no reaction for glial fibrillary acidic protein, neurofilament protein, Leu-7, oxytocin, beta-endorphin, adrenocorticotropic hormone, and vimentin. This case provides additional evidence for the astrocytic origin of suprasellar granular cell tumor.
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PMID:Suprasellar granular cell tumor. 874 Dec 54

The hypothesis proposed here presents a mechanism of melatonin action, which may explain the role of this neurohormone in the genesis of various human pathologies, including fetal abnormalities. It assumes that monomeric or dimeric forms of indoloderived compounds such as melatonin and precursors of melanin have the ability to selectively stimulate the synthesis of prohormone 1 convertase (PC1) or prohormone 2 convertase (PC2), in proportion to their concentrations in the body. Thus, the mean circadian level of melatonin, by determining the manner and rapidity of proopiomelanocortin (POMC) cleavage, would also determine the mean proopiomelanocortin (POMC) level, maintained in dynamic equilibrium as a result of the simultaneous influence of testosterone, estradiol and cortisol on the intensity of POMC mRNA synthesis. The correlative proportions between the activity of PC1 and PC2 would therefore shape the character of hormonal balance in the organism, and in particular the mean ACTH concentration that determines the level of cyclic adenosine monophosphate (cAMP) concentration in its cells. The hypothesis also suggests that melatonin, by influencing the concentration of ACTH and beta-endorphin and their relative proportion could determine the stimulation or suppression of the immune system, thereby confirming its role as an immunomodulator. A disturbance in the above model of immunohormonal equilibrium, resulting from, for example, decreased pineal efficiency, would lead to stimulation of an alternative mode of achieving homeostasis, i.e. increase in concentration of melanin monomers and dimers, with concomitant high activity of tyrosine kinase and high cyclic guanosine monophosphate (cGMP) concentration in the cells. According to the proposed hypothesis, the risk of bearing a developmentally handicapped child would be highest in a woman with a high circadian secretion of melatonin, i.e. with domination of melatonin dimers and high PC1 activity, a condition which may be additionally aggravated by the exposure of the mother to adverse environmental factors or by immunohormonal disturbances. The hypothetical break-up of maternal melatonin dimers when crossing placenta would be the cause of excessive concentration of melatonin monomers and high PC2 activity in the fetus, and thus it should be the reason for very low levels of vimentin filaments and cAMP concentration in embryonal cells, the latter being directly responsible for inducing fetal pathologies.
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PMID:Can high maternal melatonin concentrations be responsible for inducing fetal pathologies, and can melatonin participate in immunohormonal homeostasis by determining prohormone convertase activity?--Hypothesis and facts. 982 29

Adrenal cortical carcinoma (ACC) is a rare neoplasm that affects all age groups, with a bimodal peak of incidence, in young individuals in the first decade or two of life and in older subjects in the fifth to seventh decades. It may be clinically "functional" with Cushing's syndrome, virilization, or feminization, or it may be "nonfunctional." We report on the case of a 42-yr-old woman who complained of abdominal pain and a large adrenal tumor measuring 20 cm in size. No endocrine symptoms were observed. Laboratory tests showed increased levels of adrenocorticotropic hormone (ACTH), serum cortisol, and urinary free cortisol. Cytohistologic features were typical of ACC. A striking presence of hyaline cytoplasmatic globules was seen in cytologic smears and histologically, being immunoreactive for vimentin, consistent with an intracellular store of intermediate filaments. The tumor showed high proliferative activity (40%) with Ki-67 and negativity for p53, cerbB2, and bcl-2. Although hyaline globules are more frequent in pheochromocytomas and other neoplasms, they may also be present in ACC. These globules may be observed in cytologic smears. Also, the identification and immunohistochemical characterization of these hyaline globules in metastases may be useful in determining the origin of primary occult tumors. Diagn. Cytopathol. 1999;21:394-397.
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PMID:Giant adrenal cortical carcinoma, clinically "nonfunctional": report of a case containing cytoplasmic hyaline globules of vimentin. 1057 70

In the last few years it has become apparent that the skin is a locoregional source for several proopiomelanocortin-derived peptides including alpha-melanocyte-stimulating hormone, adrenocorticotropin, and beta-endorphin. The enzymes that regulate expression of these neuropeptides are the prohormone convertases 1 and 2. In this study we demonstrate, by reverse transcriptase polymerase chain reaction and Western immunoblotting, that cultured human dermal fibroblasts express prohormone convertases 1 and 2 as well as 7B2, which is an essential cofactor for enzymatic activity of prohormone convertase 2. Immunofluorescence studies revealed prohormone convertase 1 to be mainly expressed in the perinuclear region in vesicular structures resembling the trans-Golgi network, whereas prohormone convertase 2 was found in the trans-Golgi network as well as in vesicular structures diffusely distributed in the peripheral cytoplasm. Expression of both enzymes was also confirmed in fibroblasts of normal adult human skin by immunohistochemistry using antibodies against prohormone convertases 1 and 2 and vimentin. To assess the relevance of prohormone convertase 1 and 2 expression in human dermal fibroblasts, we studied the expression of proopiomelanocortin and proopiomelanocortin-derived peptides. Proopiomelanocortin expression was detected by reverse transcriptase polymerase chain reaction and Western immunoblotting. Alpha-melanocyte-stimulating hormone, adrenocorticotropin, and beta-endorphin were mainly located in vesicular structures as demonstrated by immunofluorescence. Production of these peptides was confirmed by radioimmunoassay, immunoradiometric assay, or enzyme immunoassay. Among several stimuli tested, interleukin-1 was found to upregulate production of alpha-melanocyte-stimulating hormone in human dermal fibroblasts. In summary, we have shown that human dermal fibroblasts express the enzymatic machinery for proopiomelanocortin processing and make proopiomelanocortin, alpha-melanocyte-stimulating hormone, adrenocorticotropin, and beta-endorphin. Production of proopiomelanocortin peptides by human dermal fibroblasts may be relevant for fibroblast functions such as collagen degradation and/or regulation of dermal immune responses.
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PMID:Human dermal fibroblasts express prohormone convertases 1 and 2 and produce proopiomelanocortin-derived peptides. 1151 Dec 98

Suppression of collagen synthesis is a major therapeutic goal in the treatment of fibrotic disorders. We show here that alpha-melanocyte-stimulating hormone (alpha-MSH), a neuropeptide well known for its pigment-inducing capacity, modulates collagen synthesis and deposition. Alpha-MSH in vitro suppresses the synthesis of collagen types I, III, and V and down-regulates the secretion of procollagen type I C-terminal peptide (PICP) in human dermal fibroblasts treated with the fibrogenic cytokine transforming growth factor-beta1 (TGF-beta1). Alpha-MSH did not interfere with TGF-beta1 signaling, because TGF-beta1-induced expression of collagen mRNA was not affected, implying a posttranscriptional mechanism. Human dermal fibroblasts in vitro express a high affinity binding site for MSH, which was identified by reverse transcription PCR and immunofluorescence analysis as the melanocortin-1 receptor (MC-1R). Immunohistochemical studies on normal adult human skin confirmed MC-1R expression in distinct dermal fibroblastic cells. The MC-1R on fibroblasts appears to be functionally relevant because alpha-MSH increased the amount of intracellular cAMP, and coincubation with a synthetic peptide corresponding to the human Agouti signaling protein abrogated the inhibition of TGF-beta1-induced PICP secretion by alpha-MSH. To assess the in vivo relevance of these findings, a mouse model was used in which dermal fibrosis was induced by repetitive intracutaneous injections with TGF-beta1. The inductive activity of TGF-beta1 on collagen deposition and the number of dermal cells immunoreactive for vimentin and alpha-smooth muscle actin was significantly suppressed by injection of alpha-MSH. Melanocortins such as alpha-MSH may therefore represent a novel class of modulators with potential usefulness for the treatment of fibrotic disorders.
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PMID:Collagen metabolism is a novel target of the neuropeptide alpha-melanocyte-stimulating hormone. 1464 73

Following systemic injection, several different dyes and markers are found to accumulate rapidly in cells in the arcuate nucleus and median eminence, and the capillaries in this region appear specialised for exchange of molecules. The present study used hydroxystilbamidine (FluoroGold equivalent) to identify cells that take up molecules from the circulation in these regions; 2-6 h following injection, uptake was seen in the external and intermediate zones of the median eminence and the adjacent ventral part of the arcuate nucleus, but not in other regions of the hypothalamus. The labelled cells were small; double-labelling experiments revealed that they expressed glial fibrillary acid protein (GFAP), but not NeuN, Agouti-related protein (AgRP) or beta-endorphin. They had the morphology of astrocytes and were readily distinguished from tanycytes by staining for vimentin. Many of these labelled astrocytes also expressed leptin receptors and neuropeptide Y Y1 receptors. The surrounding neurons that expressed these receptors did not take up this dye. This demonstrates that astrocytes take up molecules from the circulation in the median eminence and adjacent arcuate nucleus, and may have a significant signalling role in regulation of food intake.
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PMID:Astrocytes in the arcuate nucleus and median eminence that take up a fluorescent dye from the circulation express leptin receptors and neuropeptide Y Y1 receptors. 1596 34


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