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)

Six atopic subjects with grass pollen allergy and six nonallergic healthy volunteers were enrolled into this study. Substance P-like immunoreactivity (SP-LIR) and beta-endorphin-like immunoreactivity (beta E-LIR) were determined in bronchoalveolar lavage (BAL) and nasal lavage (NAL) fluids before and after allergen (grass pollen) provocation. A significant increase in the baseline concentration of SP-LIR and beta E-LIR was seen in BAL of allergic subjects. In NAL of allergic subjects an increased baseline concentration of SP-LIR was found (beta E-LIR not detectable). After allergen provocation there was a rise of SP-LIR and beta E-LIR in BAL fluids of allergic subjects immediately after provocation. In NAL fluids of allergic subjects allergen challenge resulted in a rise of SP-LIR within 10 minutes. Allergen provocation did not influence SP-LIR and beta E-LIR concentration in BAL and NAL in nonallergic controls. The demonstrated higher baseline levels of SP-LIR and beta E-LIR as well as the increase after provocation in the BAL and NAL of allergic subjects but not in nonallergic controls support the hypothesis that these neuropeptides contribute to allergic reactions in airways of humans.
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PMID:Substance P and beta-endorphin-like immunoreactivity in lavage fluids of subjects with and without allergic asthma. 138 7

Evidence has accumulated that human peripheral blood mononuclear cells (PBMC) may release adrenocorticotropic hormone (ACTH) and endorphin-like peptides into the culture medium when stimulated with different substances such as Newcastle disease virus and the lipopolysaccharide of Escherichia coli. However, to our knowledge, no quantitative assessment of ACTH-LIR (like-immunoreactivity) in human PBMC has been reported. We thus utilized a radioimmunoassay for ACTH to find a median of 30 pg of ACTH-LIR in 10(7) PBMC of 11 normal subjects. ACTH-LIR was also detected in 7 different cell lines derived from patients with lymphoid and myeloid malignancies, two of them, JM and U937, showed values of 135 and 108 pg/10(7) cells respectively. Stimulation with IL-1 beta at the concentration of 1000 U/mL induced, after 48 h, a significant increase of intralymphocytic ACTH levels when compared to basal and 24 h values. The chromatographic characterization of this ACTH-LIR showed, at least, three molecular forms of immunoreactive ACTH; molecular weights were 31 kD POMC, 22 kD ACTH and 4.5 kD ACTH. We used northern blotting with human genomic DNA probe for POMC gene to evidence specific mRNA in PBMC; mRNA was also observed in a T lymphocyte cell line derived from a patient with lymphoma. We conclude that PBMC produce ACTH-LIR which may act as a paracrine immunomodulator similar to lymphokine and/or may signal the adrenal gland to secrete glucocorticoids.
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PMID:[ACTH of lymphocytic origin under normal and pathological conditions]. 166 15

Using Northern blotting with a human genomic DNA probe for the pro-opiomelanocortin (POMC) gene, we have shown specific mRNA in normal human peripheral mononuclear cells (PBMC); the presence of specific mRNA was also observed in a T lymphocyte cell line derived from a patient with lymphoma. We then demonstrated that PBMC translate the message into protein. Thus, using a radioimmunoassay with an antibody for ACTH, a median of 29 pg of ACTH-like immunoreactivity (ACTH-LIR) was found in 10(7) PBMC. ACTH-LIR was also detected in seven different cell lines derived from patients with lymphoid and myeloid malignancies, two of them JM and U937 showing the highest values 135 and 108 pg/10(7) cells, respectively. The chromatographic characterization of this ACTH-LIR showed, at least, three molecular forms of immunoreactive ACTH with molecular weights of the order of 31,000 POMC, 22,000 ACTH, and 4,500 ACTH, in addition to high-molecular-weight material (greater than 43,000). We conclude that PBMC produce ACTH-LIR which may act as a paracrine immunomodulator in a similar way to lymphokines and/or may signal the adrenal gland to secrete glucocorticoids.
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PMID:Expression of pro-opiomelanocortin gene and quantification of adrenocorticotropic hormone-like immunoreactivity in human normal peripheral mononuclear cells and lymphoid and myeloid malignancies. 253 7

Dispersed corticotrophic cells of 3 patients with Nelson's syndrome were studied in tissue culture for up to 25 days. During this culture period a parallel decrease with time was seen in ACTH and beta-endorphin-like immunoreactivity ( LIR ) release. A concomitant decline was observed for intracellular hormones. The time course of hormone release showed a parallel secretion of ACTH and beta-endorphin- LIR up to 8 h. Both the release of ACTH and beta-endorphin LIR were stimulated by 0.1 microM lysine vasopressin (LVP) in all three adenoma cell cultures. Dexamethasone (0.1 and 1 microM) suppressed basal hormone secretion for 4 h. Synthetic ovine corticotrophin-releasing factor (CRF) at 10 and 100 nM stimulated the secretion of ACTH and beta-endorphin LIR maximally. This stimulation was higher than observed with maximal stimulative concentration of LVP (0.3 microM). The CRF-mediated hormone secretion was calcium-dependent. Dexamethasone (0.1 microM) blocked the stimulating effect of 10 nM CRF completely. Gel-filtration chromatography demonstrated the cells to secrete both beta-lipotrophin (beta-LPH) and beta-endorphin. The ratio of beta-LPH to beta-endorphin released remained constant upon stimulation by LVP and CRF. HPLC studies demonstrate the possibility that several beta-endorphin fragments, including alpha-endorphin and gamma-endorphin, were secreted by cells from a Nelson tumour. CRF caused a simultaneous parallel stimulation of the release of these peptides.
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PMID:ACTH and beta-endorphin secretion by three corticotrophic adenomas in culture. Effects of culture time, dexamethasone, vasopressin and synthetic corticotrophin releasing factor. 632 19

The release of immunoreactive beta-endorphin from rat anterior pituitary cells in culture was studied by radioimmunoassay and gel-filtration chromatography. Two forms of immunoreactivity were detected corresponding to beta-lipotrophin (beta-LPH) and beta-endorphin. Cells were found to release beta-endorphin-like immunoreactivity (beta-endorphin LIR) into the culture medium for up to 10 days with a trough in release occurring between days 2-4. The ratio of beta-LPH to beta-endorphin released remained constant during the course of culture. After 4 days in culture beta-endorphin LIR release was constant and responsive to modulation. Incubation with lysine-vasopressin (0.1 units/ml) produced a two- to threefold increase in release and dexamethasone (10 (-6) mol/l) suppressed release to 33% of controls. Neither stimulation nor suppression resulted in a change in the ratio of beta-LPH to beta-endorphin released. Dexamethasone suppression was not overcome by removal of dexamethasone or addition of vasopressin.
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PMID:Regulation of immunoreactive beta-endorphin release from rat pituitary cell culture. 717 16

The present study examines prolactin PRL-like immunoreactivity (PRL-LIR) in the rat central nervous system and describes the distribution of labeled perikarya and fibers using a specific antiserum to ovine PRL. This antiserum does not cross-react with molecules of the pro-opiomelanocortin (POMC) family and recognizes rat PRL. PRL-LIR cell bodies are found exclusively in the lateral hypothalamic area surrounding the fornix, especially dorsolateral to it. No labeled cells are detectable in any other part of the brain, including the arcuate nucleus. Labeled fibers are dispersed in almost all parts of the brain. Dense plexuses are observed in the hypothalamus, midline thalamus nuclei, bed nucleus of stria terminalis, raphe dorsalis, and locus coeruleus. There is no apparent decrease in the number of PRL-LIR cell bodies and fibers in hypoprolactinemic mutant rats or after hypophysectomy, suggesting that central PRL is synthesized in such hypothalamic neurons. Comparison of PRL and alpha-melanocyte-stimulating hormone immunostainings provides evidence that the PRL network is independent of those of POMC and melanin-concentrating hormone. The present results support the hypothesis of two independent PRL systems: one peripheral (pituitary gland) and the other cerebral. Concerning the functional role of brain PRL, its widespread projections suggest that PRL is involved in multiple regulations. The presence of PRL-LIR in brain areas involved in sleep-wake control is a strong argument for its role in such a regulation.
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PMID:Anatomical distribution of prolactin-like immunoreactivity in the rat brain. 812 95