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 effect of Met-enkephalin (MENK) on several immune functions, corticosterone (CS) and adrenocorticotropin (ACTH) levels in the plasma was studied in adrenalectomized (ADX) and sham-adrenalectomized (SADX) mice. Multiple Met-enkephalin injections (10 mg/kg per day in two injections 12 h apart, for 4 days) increased the plaque-forming cell response to sheep erythrocytes in the spleen and enhanced the proliferation of spleen cells in vitro. These effects were comparable in sham-adrenalectomized and adrenalectomized mice. However, spleen cells of mice immunized with sheep red blood cells and injected with Met-enkephalin, showed suppressed blastogeneic transformation with Con A. The effect was equal in adrenalectomized and sham-adrenalectomized mice. In the absence of Con A in spleen cell cultures, MENK treatment of donor mice resulted in a significant mitogenic effect. NK activity of the spleen cells was suppressed in MENK-treated adrenalectomized mice. Injection of MENK decreased corticosterone levels and increased ACTH levels in the plasma of sham-adrenalectomized mice. In adrenalectomized mice plasma levels of ACTH were decreased by MENK. It seems that corticosteroid secretion, although changed by adrenalectomy and influenced by treatment with MENK, does not influence the modulatory effect of MENK on the PFC response and blastogeneic transformation of mouse spleen cells. However, NK activity of the spleen cells treated with MENK seems to the reflect joint action of MENK and corticosteroids.
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PMID:Interaction of Met-enkephalin and corticosteroids in immunomodulation. 132 54

There is strong evidence that the hypophyseal neurointermediate lobe (NIL) mediates 17 beta-estradiol (E2)-induced PRL secretion in rats. Our laboratory has previously demonstrated that E2 stimulates NIL cells to release an activity that acutely increases the relative abundance of PRL-releasing cells in anterior pituitary (AP) cell cultures. We later found that secretory products of the NIL melanotropes, specifically the acetylated forms of alpha MSH and beta-endorphin (beta END), can account for this activity. Given that blood from the NIL initially perfuses the region of the AP proximal to the NIL, we tested the hypothesis that this specific area was preferentially responsive to the lactotrope recruitment activities. AP glands from ovariectomized rats were dissected into an inner zone, proximal to the NIL, and the remaining outer zone of the gland, then dispersed with trypsin. The resulting cells were cultured for 16 h, either alone or in coculture with NIL cells, and subsequently treated with medium alone (control) or with alpha MSH, beta END, or E2 (all at 1 x 10(-7) M) for 3 h and then subjected to reverse hemolytic plaque assays for PRL release. Under control conditions, the proportion of PRL-secreting cells was significantly greater in cultures from the outer zone of the AP than in those from the corresponding inner zone of the gland. Treatment of AP cells from the inner zone with alpha MSH, beta END, or the E2-induced NIL activity significantly increased the percentage of PRL secretors by about 8% of all AP cells. In contrast, the fraction of PRL-secreting cells in cultures from the outer zone was not affected by these treatments. We conclude that the recruitment of PRL-secreting cells in response to products of the NIL occurs only in that region of the AP proximal to the NIL.
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PMID:Neurointermediate lobe peptides recruit prolactin-secreting cells exclusively within the central region of the adenohypophysis. 133 43

Mounting evidence indicates that dopamine (DA) can stimulate as well as inhibit PRL release when given in appropriately low doses. In the present study, we investigated whether the suckling stimulus could influence this response. Pituitary cultures from suckled or nonsuckled rats were exposed to DA (10(-16) - 10(-6) M) during a reverse hemolytic plaque assay for PRL. Pituitary cells from nonsuckled rats exhibited only the inhibitory response to DA; exposure to high-dose DA (10(-6) M) reduced plaque area to 42.3 +/- 7.2% (mean +/- SEM) of control. A low dose of DA (10(-12) M) had no effect on PRL secretion (79.3 +/- 13.3% of control). In striking contrast, a brief suckling stimulus (10 min) rendered the mammotropes responsive to stimulation by low-dose DA (to 152.7 +/- 12.5% of control). Thus, suckling appears to be a requirement for expression of the stimulatory effect of DA in lactators. In a subsequent series of experiments we explored the possibility that a hypophysial factor, released during nursing, might mimic the effects of suckling on mammotrope responsiveness. Accordingly, we tested the effects of alpha-melanocyte-stimulating hormone (10(-7) M) and low-dose DA, alone or in combination, on pituitary cells from nonsuckled rats. Although neither agent alone had a dramatic effect on PRL secretion, concurrent administration of both of these significantly stimulated PRL release to 130.0 +/- 4.2% of control. Taken together, these results demonstrate that suckling renders mammotropes responsive to the stimulatory effects of DA. Moreover, our data indicate that alpha-melanocyte-stimulating hormone could function as a responsiveness factor in this phenomenon.
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PMID:Suckling unmasks the stimulatory effect of dopamine on prolactin release: possible role for alpha-melanocyte-stimulating hormone as a mammotrope responsiveness factor. 164 48

ACTH release from the anterior pituitary gland is principally driven by the two hypothalamic hormones, corticotropin-releasing hormone (CRH) and arginine vasopressin (AVP). Using the reverse hemolytic plaque assay, we have compared the effects of CRH and AVP on ACTH release from individual, dispersed pituitary cells. A small percent (0.36 +/- 0.06%) of pituitary cells formed plaques when exposed to medium alone. AVP caused 3.44 +/- 0.10% of cells to form plaques (P less than 0.01 compared with medium alone), CRH produced 4.85 +/- 0.20% plaque-forming cells (P less than 0.01 compared with AVP), and the combination of CRH and AVP produced a still greater percent of plaque-forming cells (5.80 +/- 0.20%, P less than 0.01 compared with CRH alone). A double reverse hemolytic plaque assay was then employed to examine whether some cells formed plaques only in the presence of one or other secretagogue. Using this technique we found clear evidence of cells that formed plaques in response to CRH but not AVP (P less than 0.005); CRH or AVP (P less than 0.0001), and CRH and AVP (P less than 0.05). There was no evidence of a corticotrope forming a plaque with AVP but not CRH (P = 0.52). Thus there appears to be functionally distinct classes of corticotropes. These findings have important implications for our understanding of the relative responsiveness of the pituitary to hypothalamic secretagogues and provide a new physiological perspective on recent reports of stress-specific hypothalamic responses regulating ACTH release.
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PMID:Distinct classes of corticotropes mediate corticotropin-releasing hormone- and arginine vasopressin-stimulated adrenocorticotropin release. 184 97

A 100 plaque forming unit (pfu) dose of a temperature-sensitive (ts) mutant of vesicular stomatitis virus (VSV), tsG31 KS5, engendered a slowly progressive paralytic central nervous system (CNS) disease that killed all BALB/c nude mice within 28 days. Reconstitution of nude mice with 10(7) syngeneic splenocytes 24 h before intracerebral inoculation with tsG31 KS5 VSV, however, protected 92% of the animals from death. When these reconstituted animals were injected intracerebroventricularly with 14 pmol of beta-endorphin 24 h after reconstitution with splenocytes and 24 h before inoculation with tsG31 KS5 VSV, only 72% of the animals survived. Furthermore, whereas 40% of the afflicted reconstituted nude mice given intracerebroventricular injections of sterile water were able to recover from the symptoms of disease, those surviving animals which received beta-endorphin were unable to do so. A single intravenous injection of 14 pmol beta-endorphin, or repeated postinfection administration of 28 pmol of beta-endorphin intravenously into nude mice reconstituted with syngeneic splenocytes, which were pretreated with beta-endorphin, did not alter the course of CNS disease induced by tsG31 KS5 VSV. The effect induced by intracerebroventricular injection of beta-endorphin was antagonized by naloxone, but not by the neuropeptide fragment beta-endorphin-(1-27). A simultaneous intracerebroventricular injection of reconstituted nude mice with 1220 pmol of naloxone and 14 pmol of beta-endorphin resulted in a 89% survival rate, and 33% of the afflicted animals were able to overcome the symptoms of the disease induced by tsG31 KS5 VSV. Intracerebroventricular injection of reconstituted nude mice with 330 pmol of beta-endorphin-(1-27) and 14 pmol of beta-endorphin resulted in a 72% survival rate and the surviving animals were unable to improve appreciably the clinical status of their disease. Injection of reconstituted nude mice with either 1220 pmol of naloxone or 330 pmol of beta-endorphin-(1-27) alone did not alter the course of the CNS disease in any way. A single intracerebroventricular injection of 29 pmol of another psychoactive peptide, [Des-Tyr]-endorphin, 24 h after reconstitution of nude mice with splenocytes and 24 h prior to infection with virus, resulted in 74% survival; and 39% of the afflicted animals were able to recover from the clinical symptoms.
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PMID:Beta-endorphin alters the course of central nervous system disease induced by a temperature-sensitive vesicular stomatitis virus in reconstituted nude mice. 216 Apr 76

Dissociated neurointermediate lobe cells (75%) bound [biotinyl-Ser1]corticotropin releasing hormone (bio-CRH) and secreted adrenocorticotropin [ACTH(25-39)] in a reverse hemolytic plaque assay (RHPA). The bio-CRH was rapidly internalized (less than 1 min) in vesicles and scattered vacuoles. Plaque percentages increased from 26 +/- 4% to 53 +/- 8% after CRH stimulation. Areas increased from 1688 +/- 791 microns 2 to 3773 +/- 788 microns 2. After AVP treatment for 1 hr, plaque percentages and areas were augmented further. The heterogeneity in secretion may indicate the presence of quiescent IL cells or cells secreting an opiocortin peptide not detected in the plaque assay.
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PMID:Subsets of pituitary intermediate lobe cells bind CRH and secrete ACTH/CLIP in a reverse hemolytic plaque assay. 217 40

Viable pituitary target cells were identified with biotin-labeled corticotropin-releasing factor (1-Bio-CRF) or arginine vasopressin (Bio-AVP) and avidin-fluorescein (cell sorter grade). Stain was reduced from 8-10% of pituitary cells to less than 3% if nonbiotinylated ligands were added to compete with their respective biotinylated ligand for specific binding sites. However, AVP did not decrease the stain for 1-Bio-CRF nor did CRF decrease the Bio-AVP stain. Media adrenocorticotropin (ACTH) levels increased 4-18 times when 1-Bio-CRF or Bio-AVP were added during the staining process. One hour after staining, the cells secreted ACTH at levels identical to prestain basal levels. When challenged with CRF or AVP after this hour, the cells responded again with increases not different from those seen during staining. Tests of stained cell populations also showed that the cells were fully responsive 24 h after staining. The reverse hemolytic plaque assay for ACTH, which was used to study secretion from individual stained cells, showed that approximately 80% of plaques contained a stained cell and that plaque numbers and areas were like those of unstained populations. These data show that corticotropes are not chronically desensitized during exposure to low doses of biotinylated ligands (50-500 pM).
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PMID:Secretion from corticotropes after avidin-fluorescein stains for biotinylated ligands (CRF or AVP). 243 66

CRF, a hypothalamic peptide, is a potent stimulator of POMC synthesis and secretion in the pituitary. POMC biosynthesis has been documented in the testis, specifically in Leydig cells, and recent studies suggest that CRF is synthesized locally in the testis. A reverse hemolytic plaque assay and immunocytochemistry with Leydig cell-specific antibodies were used to study the effect of CRF on secretion of the POMC peptide beta-endorphin (beta EP) from normal rat primary Leydig cell cultures. In enriched Leydig cell preparations incubated with beta EP antiserum (diluted 1:50) then with complement (diluted 1:25), approximately 15% of immunocytochemically identified Leydig cells formed plaques. Preabsorption of the antiserum with beta EP (2 micrograms/microliters antiserum) overnight at 4 C abolished the formation of plaques. Increasing concentrations of CRF (from 10(-1) to 10(-7) M) resulted in an approximately 80% increase in both the percentage of plaque-forming cells and the mean plaque size. When the CRF antagonist CRF-(9-41) (10(-6) M) was added in the presence of CRF, the increases in plaque number and average size did not occur. These results demonstrate that Leydig cells have functional CRF receptors and that beta EP secretion from these cells is stimulated by CRF.
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PMID:Stimulation of beta-endorphin secretion by corticotropin-releasing factor in primary rat Leydig cell cultures. 252 78

Anterior pituitary corticotropes represent only 9-10% of the mixed pituitary cell population. However, their small size precludes their enrichment because they cannot be separated from the more abundant PRL and GH cells. They can be induced to enlarge by adrenalectomy, and this report describes the separation of larger CRH-responsive corticotropes from a subpopulation of small pituitary cells. The separation was done by counterflow centrifugation in an elutriator containing the Sanderson chamber which was designed to separate small cells under 15 micron in diameter. The corticotropes were initially eluted at flow rates under 30 ml/min along with other cells less than 12.5 micron in diameter. They were then stimulated for 2-4 h with 0.5 nM CRH and reeluted with the use of higher flow rates to separate the enlarged corticotropes from the unstimulated cells. Reelutriation of the entire pool of small cells produced an enrichment to 60% corticotropes in five separate experiments. However, when the pool was divided into smaller cells (eluted at 20 ml/min) and medium-sized cells (eluted at 30 ml/min), and the two pools were reeluted separately, the enrichment increased to over 90% corticotropes in eight separate experiments. These corticotrope populations remained enriched for up to 14 days in culture. They also secreted in a reverse hemolytic plaque assay that recognizes ACTH-(25-39). The dual labels for ACTH and beta-endorphin showed that 60% of the corticotropes stored both peptides, whereas 30% stored only ACTH, and 10% stored only beta-endorphin. No differences in storage patterns were seen when small and medium-sized corticotropes were compared. Thus, these studies present the first report of the production of an enriched fraction of CRH-responsive corticotropes by counterflow centrifugation and the first report of heterogeneous storage of ACTH and beta-endorphin. The use of enriched fractions facilitated the analysis of these heterogeneous storage patterns in over 8000 corticotropes.
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PMID:Enrichment of corticotropes by counterflow centrifugation. 284 89

Lymphocytes isolated from morphine addicted mice show a number of impaired immunological functions. They include Con A stimulated mitogenesis, NK cell activity, plaque forming cell activity and delayed-type of hypersensitivity. In addition, the met-enkephalin and beta-endorphin level in the lymph nodes of addicted mice were also depressed.
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PMID:Suppression of immunological functions in morphine addicted mice. 296 24


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