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)

In human Y-79 retinoblastoma cells corticotropin-releasing hormone (CRH) produces a marked and rapid increase of adenylate cyclase activity. The concentration of the peptide producing half-maximal stimulation is 60 nM. The effect of CRH is significantly antagonized by the specific CRH receptor antagonist alpha-helical CHR 9-41 and is mimicked by sauvagine and urotensin I, two peptides displaying sequence homology with CRH. These results demonstrate the presence of functional CRH receptors in human Y-79 retinoblastoma cells and suggest that this cell line may be a suitable model in which to study the action of CRH on human retinal cell function.
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PMID:Human Y-79 retinoblastoma cells express functional corticotropin-releasing hormone receptors. 133 48

Intravenous angiotensin II and ether stress were found to produce a rapid, transient increase in the corticotropin-releasing hormone (CRH) content of the median eminence as measured by a radioimmunoassay employing an antibody against rat CRH(1-41). This confirms previous reports of transient increases in CRH measured by bioassay. The increase did not occur in the paraventricular region or in other parts of the brain. It occurred along with an increase in plasma adrenocorticotropic hormone (ACTH) when a second ether stress was administered 1 h after the first, and it also occurred when rats that had been adrenalectomized for 5 days were exposed to ether. The increases in CHR and the ACTH responses to ether were reduced or abolished by dexamethasone and pentobarbital. Four days after semicircular knife cuts in the posterior hypothalamus, resting CRH in the median eminence was increased but there was no further rise after ether stress. Plasma ACTH was normal at rest after the cuts, but the increase produced by ether was reduced. The ACTH responses to angiotensin II and immobilization were also reduced. Because the posterior knife cuts reduced hypothalamic catecholamine content, the effects of reducing hypothalamic norepinephrine and epinephrine by administration of the dopamine-beta-hydroxylase inhibitor diethyldithiocarbamate (DDC) were tested. Five hours after DDC, plasma ACTH was elevated but there was no further increase with ether stress. The median eminence CRH content was normal but failed to increase after exposure to ether.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Correlation between the stress-induced transient increase in corticotropin-releasing hormone content of the median eminence of the hypothalamus and adrenocorticotropic hormone secretion. 254 56

The aim of the present study was to determine the effect of alpha-MSH on serum LH in order to obtain some clues about the possible, mechanism by which the peptide modifies gonadotropin secretion. Intact female rats treated with alpha-MSH on diestrus 2 afternoon exhibited an increase in serum LH levels at 18 hr on proestrus and an elevated number of ova per rat the day of estrus when compared with saline-treated controls. Moreover, the peptide administered in chronically ovariectomized (CHR-OVX) rats treated with estradiol benzoate (EB) plus low doses of progesterone (P), increased LH in serum as well as P serum levels when compared with levels in CHR-OVX animals treated with EB plus P and saline solution instead of alpha-MSH. It has been shown that LH release is blocked by OVX and adrenalectomy (ADX) on the afternoon of proestrus; this blockade was reversed by an injection of alpha-MSH at the time of the operation. Measurements of P in ADX-OVX animals treated with alpha-MSH showed that P serum levels were maintained for longer periods of time when compared with the P serum levels of ADX-OVX animals treated with saline. On the other hand, alpha-MSH infused into CHR-OVX rats treated with low doses of EB, which can lower serum LH levels, lowered the serum LH even more, although the serum P levels were increased. Finally alpha-MSH did not affect the serum LH levels in diestrous rats. The present results demonstrated that alpha-MSH influences the release of LH by modifying the release and/or the degradation of P. This P, in turn, modifies LH serum concentrations, having either a stimulatory or inhibiting effect on the release of LH, apparently depending on the time period it remains high in serum.
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PMID:Release of LH in response to alpha-MSH administration. 293 12

The effects of the ovarian steroids, oestradiol benzoate (EB), and progesterone (P) on the cells of pars intermedia (PI) from chronically ovariectomized rats (CHR-OVX) were analyzed by qualitative and quantitative electron microscopy (EM) at different intervals after steroid injection. The PI cells of CHR-OVX are rich in secretory granules but poor in organelles related to hormonal synthesis. Twenty-four h after EB administration the cells exhibited cytological features indicative of an increased synthetic activity. These included hypertrophy of rough endoplasmic reticulum, cisternae, a moderately developed Golgi complex, and newly formed granules. These features were also observed in PI cells 48 h after EB administration. Thirty-two and 56 h after the treatment, the PI cells showed signs of both increased synthetic and secretory activity. Thus, it was possible to observe a well-developed rough endoplasmic reticulum, and Golgi apparatus, numerous electron-lucent vesicles, and secretory granules in contact with the cell membrane. However, no exocytotic figures were observed. Progesterone administration resulted in considerable modifications of the ultrastructural features of PI cells also indicative of increased synthetic and secretory activity. The greatest modifications were observed in the mornings with changes that were 12 h out of phase with respect to those observed with EB. Quantitative estimations of the variation in the content of secretory granules of PI cells fully confirmed the qualitative observations described above. The serum alpha-MSH concentrations in ovariectomized rats was found to be increased 24 h after administration of a single dose of EB and thereafter serum MSH exhibited high levels in the afternoon, whereas the values in the morning were lower.
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PMID:Modifications of pars intermedia cells of ovariectomized rats by oestrogen and progesterone. 394 2

We have previously found that proopiomelanocortin (POMC) mRNA and levels of adrenocorticotropin (ACTH) and beta-endorphin peptides are increased in the spleen and thymus of rats with adjuvant-induced arthritis (AA), and immunologically mediated inflammatory disease. To determine whether alterations in immune tissue POMC during AA are also accompanied by changes in immune tissue corticotropin-releasing hormone immunoreactivity (ir-CHR) and arginine vasopressin (AVP), we measured ir-CRH and AVP by radioimmunoassays in spleen and thymic extracts 14 days following injection of adjuvant. Ir-CRH was detectable in all extracts of spleen and thymus. Total contents of ir-CRH in the spleen and thymus were not altered following arthritis, although a significant decrease was observed in splenic extracts from arthritis rats (40.0 +/- 4.2 fmol/g tissue) compared to controls (69.5 +/- 8.4 fmol/g tissue) when contents were expressed as amount per weight of tissue. Low levels of AVP were also detected in immune tissues, with contents significantly increased in spleens from arthritis animals (17.4 +/- 1.6 fmol/g tissue) compared to controls (10.6 +/- 1.9 fmol/g) but thymic contents of AVP were not altered by arthritis (10.6 +/- 1.3 fmol/g) compared to controls (9.2 +/- 0.7 fmol/g). Control levels of AVP were significantly higher in spleens and thymuses from female rats (53 +/- 5 and 25 +/- 4 fmol/g tissue, respectively) compared to males. G-50 chromatography revealed that the principal form of splenic ir-CRH is CRH(1-41), although in non-arthritic animals some ir-CHR eluted in a position indicating a slightly larger form.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Contents of corticotropin-releasing hormone and arginine vasopressin immunoreactivity in the spleen and thymus during a chronic inflammatory stress. 805 Dec 95