UNIPROT:P01189 - FACTA Search

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Query: UNIPROT:P01189 (beta-endorphin)
21,003 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Recent in vitro studies have shown that the release of hypothalamic beta-endorphin (beta-END), like that of adenohypophysial origin, is enhanced by both corticotropin-releasing hormone (CRH) and arginine vasopressin (AVP). However, whereas AVP merely synergizes with CRH in the pituitary, it seems to be essential for the release of hypothalamic beta-END by CRH. The present paper reports on the effects of long-term adrenalectomy (ADX) and subsequent replacement with supraphysiological doses of corticosterone (compound B, CB) upon the in vitro basal and CRH- and AVP-stimulated release of beta-END from the rat hypothalamus. Basal release of beta-END was significantly elevated by ADX, and returned to control levels following CB overdosage. Both ADX and CB replacement significantly reduced the stimulatory effect of CRH (10(-8) M) upon beta-END release. ADX caused no significant change in the AVP (10(-6) M)-induced release of beta-END. However, the AVP-stimulated release of beta-END was completely abolished in ADX rats treated with a high dose of CB. The hypothalamic content of beta-END was also measured following ADX and subsequent CB treatment. Compared with control tissues, those from ADX animals had significantly greater contents of beta-END; the hypothalami from rats with experimentally induced hypercorticalism had markedly reduced concentrations of the opioid peptide. Measurements of basal release and content of AVP in the hypothalamus following long-term ADX and CB treatment revealed that AVP neuronal activity is also subject to manipulations of the glucocorticoid hormone environment.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Adrenalectomy and experimental hypercorticalism modulate the basal, corticotropin-releasing-hormone- and arginine-vasopressin-stimulated release of hypothalamic beta-endorphin. 176 48

Bilateral adrenalectomy (ADX) leads to increased ACTH synthesis and secretion. It is thought that endogenous glucocorticoids exert a feedback mechanism at both pituitary and brain levels. The present study has been performed in order to determine the effect of ADX on the release of hypothalamic neuropeptides with corticotropin-releasing activity (CRA) and if there exists a median eminence site of glucocorticoid action to regulate hypothalamic-pituitary-adrenal (HPA) function. Adrenalectomized and sham-operated male rats were killed at different periods after surgery (2, 5, 7 and 14 days) and trunk blood was collected for ACTH and corticosterone (B) concentrations measurement. Brain (median eminence, ME; and medial basal hypothalamus, MBH) and pituitary (anterior lobe, AP; and neurointermediate lobe, NIL) tissues were dissected in order to evaluate either peptide content or in vitro hormone release. The results indicate that ADX blunted plasma B levels and increased AP ACTH content and secretion in a time-related fashion up to the 14th day. ADX significantly decreased both CRF and CRA contents in the ME at all periods studied; ME arginine-vasopressin (AVP) increased 7 and 14 days after ADX. MBH CRF decreased after ADX, but returned to sham value 2 weeks later; similarly, MBH AVP decreased at all periods after ADX. Removal of endogenous glucocorticoids did not vary neither oxytocin (OXY) content in the ME and MBH nor AVP and OXY contents in the NIL. In our superfusion experiments, we found that ADX increased basal AVP release and did not change spontaneous CRF secretion from ME terminals. Dexamethasone (Dxm, 10 nM) diminished AVP but not CRF output by ME tissues from adrenalectomized rats. A direct relationship was found between ME CRF and 28 mM KCl (hK+)-induced CRF release by MEs from adrenalectomized rats. ME fragments from adrenalectomized rats were hyperresponsive to kH+ stimulation of AVP release. Dxm (10 nM) decreased the hK(+)-evoked CRF and AVP release by MEs from adrenalectomized rats. ADX and dexamethasone treatment did not influence basal and hK(+)-elicited ME OXY release. Additionally, a rapid glucocorticoid inhibitory effect on ACTH secretion by isolated AP cells from both sham and adrenalectomized rats was found, and an in vitro corticotrope hyporesponse to 0.63 nM CRF and 9.25 nM AVP stimulation during several days after ADX.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Changes in the hypothalamo-corticotrope axis after bilateral adrenalectomy: evidence for a median eminence site of glucocorticoid action. 184 20

Effects of the glucocorticoid milieu on the basal and ether stress-induced prolactin (PRL) release and on the immunostaining for hypothalamic vasoactive intestinal peptide (VIP), beta-endorphin (beta-EP), dynorphin-A (DYN-A) and methionine-enkephalin (Met-ENK), were examined in separate groups of male rats. After colchicine treatment in intact rats, VIP-containing cell bodies were observed only in the suprachiasmatic nucleus (SCN). Adrenalectomy (ADX), performed 7 days previously, resulted in the additional appearance of VIP-immunoreactive neurons in the parvocellular subdivision of the paraventricular nucleus (PVN), as well as in significantly higher basal and stressed PRL levels than intact values. Treatment of intact rats with a high dose (500 micrograms/kg body weight (s.c.) daily for 7 days) of dexamethasone (DEX), but not with a low dose (50 micrograms/kg) of DEX, significantly reduced both the basal and stressed PRL release. Administration of either the low or high dose of DEX to ADX rats prevented the appearance of the PVN-VIP neurons. In addition, the ADX-induced high basal and stressed PRL levels were restored to intact values by the low dose of DEX, and completely suppressed by the high dose of DEX. The staining of SCN-VIP-, beta-EP-, DYN-A or Met-ENK neurons was not affected by any treatment employed in this study. These results suggest that the appearance of PVN-VIP immunostaining in ADX rats may, at least in part, be responsible for the enhanced PRL secretion observed in this group. However, SCN-VIP-, beta-EP-, DYN-A- or Met-ENK neurons do not seem to play a pivotal role in the glucocorticoid regulation of PRL secretion.
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PMID:The immunostaining for the hypothalamic vasoactive intestinal peptide, but not for beta-endorphin, dynorphin-A or methionine-enkephalin, is affected by the glucocorticoid milieu in the rat: correlation with the prolactin secretion. 197 81

This study demonstrates that a chronic osmotic stimulus can influence the hypothalamo-pituitary axis by inhibiting the secretion of basal and adrenalectomy-elevated adrenocorticotropin (ACTH) from the anterior pituitary. In rats given 340 mM NaCl instead of tap water to drink for 12 days, plasma concentrations of ACTH decreased to 105 +/- 27 pM (mean +/- S.E.M., n = 6) compared with control animals (182 +/- 13 pM). In adrenalectomised (ADX) rats given 150 mM NaCl to drink for 12 days, plasma ACTH concentrations were greatly increased (783 +/- 141 pM) but in ADX rats treated with 340 mM NaCl for the same period, plasma ACTH was similar to controls (237 +/- 59 pM). The corticotropin-releasing factor (CRF-41) content of the median eminence (ME) was reduced in ADX rats on 150 mM NaCl (854 +/- 78 fmol) and further reduced in ADX rats given 340 mM NaCl (510 +/- 56 fmol) compared with control animals (1239 +/- 114 fmol), suggesting that the decrease in plasma ACTH concentrations in saline-treated animals is secondary to a decrease in the secretion of CRF-41 from the ME. These data are the first evidence for a central mechanism, independent of glucocorticoid feedback, through which a chronic osmotic stimulus can inhibit the activity of CRF-41 neurons.
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PMID:Inhibition of rat corticotropin-releasing factor and adrenocorticotropin secretion by an osmotic stimulus. 216 61

We studied the kinetics of corticotropin (ACTH) induction of mitochondrial cytochromes P450scc and P450c11 and their electron transport proteins, adrenodoxin and adrenodoxin reductase, in bovine adrenal cortex cells in primary culture. The mRNA levels of these enzymes increase and reach a peak within 3-12 h after ACTH addition. The protein levels of adrenodoxin reductase and P450scc show an increase only nearly 24 h after ACTH addition. After ACTH addition, the intracellular level of cAMP reaches maximal levels within 5 min, and then decreases gradually over 60 min. Hence, we examined the effect of a pulse of ACTH or cAMP analogs on enzyme and mRNA levels. Exposure of the cells to ACTH for 1-2 h was sufficient for maximal induction of the enzymes and P450scc mRNA. In contrast, the induction of the enzymes and the mRNA by cAMP analogs or forskolin required the continuous presence of these agents for over 12 h. But, these agents stimulated cortisol secretion to the medium quickly, indicating that they can activate some intracellular processes while not showing any effect on enzyme induction. The absence of any effect of prolonged cAMP pulses on enzyme and mRNA levels weakens the previous hypothesis that cAMP is the sole second messenger for the ACTH induction of steroidogenic enzymes in adrenal cortex cells. The inductive ability of a brief pulse of ACTH indicates that ACTH can rapidly initiate a series of reactions that result in enzyme induction many hours later.
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PMID:Mechanism of corticotropin and cAMP induction of mitochondrial cytochrome P450 system enzymes in adrenal cortex cells. 217 15

Effects of adrenalectomy (ADX) or dexamethasone (DEX) treatment on the immunostaining of hypothalamic peptide histidine isoleucine (PHI) were examined in male rats. After colchicine treatment, PHI-containing cell bodies were observed in the suprachiasmatic nucleus (SCN) and the parvocellular division of the paraventricular nucleus (PVN). ADX increased and DEX dose-dependently decreased the number of PHI-immunopositive neurons in the PVN. The number of SCN-PHI neurons was not affected by any treatment employed in this study. These results suggest that PVN-PHI neurons are under the effects of the glucocorticoid milieu, and that the neurons may be involved in the glucocorticoid regulation of adrenocorticotropin and prolactin secretion.
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PMID:Effect of the glucocorticoid milieu on the immunostaining of peptide histidine isoleucine (PHI) in the rat hypothalamus. 230 37

Bovine adrenodoxin mRNA is found to consist of several distinct mRNA species which can be divided into two sets. Each set utilizes at least three of four separate poly(A)+ addition sites providing an explanation of the three sizes of adrenodoxin mRNA (1.75, 1.4, and 0.95 kilobases) previously observed in bovine adrenocortical RNA by this laboratory (Okamura, T., John, M.E., Zuber, M.X., Simpson, E.R., and Waterman, M.R. (1985) Proc. Natl. Acad. Sci. U.S.A. 82, 5705-5709). The two sets are distinguished from one another by a unique 5' sequence leading to two different amino acid sequences (approximately 10% homology) for the precursor portion of this nuclear encoded, mitochondrial protein. A common mature adrenodoxin sequence is encoded by both sets of mRNA. One set of RNAs is 10-fold more abundant than the other, but the levels of both sets can be induced by treatment of primary bovine adrenocortical cell cultures with adrenocorticotropin. The biological significance of these two types of adrenodoxin precursor sequences remains obscure.
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PMID:Multiple species of bovine adrenodoxin mRNA. Occurrence of two different mitochondrial precursor sequences associated with the same mature sequence. 244 Aug 63

Single and dual immunohistochemical staining techniques were used to assay the effects of disruption of brain stem catecholaminergic inputs on corticotropin-releasing factor (CRF) and arginine vasopressin (AVP) immunoreactivity in parvocellular neurosecretory neurons of the paraventricular nucleus of the hypothalamus (PVH) in normal and in adrenalectomized (ADX) rats treated with dexamethasone or vehicle. The results may be summarized as follows: (1) In adrenally intact rats, confirmed unilateral transection of ascending catecholaminergic pathways near their origins in the medulla produced a decrement in the number of CRF-immunoreactive cells that could be detected on the side of the brain ipsilateral to the cut. No effect on AVP immunoreactivity in the parvocellular division of the PVH was evident. Staining for both peptides in terminals in the external lamina of the median eminence tended to show modest decreases on the lesioned side of the brain. Compatible results were obtained in comparing the effects of bilateral transections with controls. (2) Unilaterally lesioned ADX rats treated with vehicle showed the expected enhancement in CRF immunostaining in the parvocellular division of the PVH, though the response on the side ipsilateral to the lesion was blunted relative to that seen contralaterally; the effect of ADX on AVP immunoreactivity on the ipsilateral side was more markedly reduced, but still showed evidence of enhancement (i.e., could be colocalized in some CRF immunoreactive perikarya). (3) Unilaterally lesioned ADX rats treated with dexamethasone showed no evidence of enhanced CRF or AVP immunoreactivity in perikarya or terminals on either side of the brain. The generally lower levels of staining for both peptides seen on the lesioned side across conditions suggest that the effect of interruption of ascending catecholaminergic pathways on peptide dynamics in the PVH is dissimilar to that of ADX, is manifested via different mechanisms, and that at least some types of feedback inhibition of corticotropin-releasing peptides by adrenal steroids do not require intact catecholaminergic inputs to be exhibited.
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PMID:Effects of catecholamine-depleting medullary knife cuts on corticotropin-releasing factor and vasopressin immunoreactivity in the hypothalamus of normal and steroid-manipulated rats. 246 27

Expression of the CRF gene in the hypothalamus and that of the POMC gene in the anterior pituitary are reduced during the first week of life in the rat. During this so-called stress nonresponsive period (SNRP), stimuli such as ether vapors, electroshocks, and hypoxia do not elicit ACTH secretion from the pituitary, as occurs later in development. The current hypothesis to explain the SNRP is an increased negative glucocorticoid feedback on POMC and CRF synthesis and/or release during this time. To test this hypothesis we studied the effects of adrenalectomy (ADX) on anterior pituitary POMC mRNA expression. In 7-day-old rats POMC mRNA levels were increased only 3-fold 48 h post-ADX, compared to a 7-fold increase in 14-day-old animals. This blunted effect of endogenous glucocorticoid removal on pituitary POMC mRNA could be due to decreased up-regulation of CRF after removal of glucocorticoids or normal up-regulation of CRF but decreased pituitary responsiveness to CRF relative to those in 14-day-old animals. Therefore, we studied in vitro beta-endorphin release from pituitaries obtained from 7- and 14-day-old rats. CRF stimulated basal beta-endorphin release to the same extent in pituitaries from both groups. The inhibition by corticosterone of CRF-stimulated beta-endorphin secretion was also indistinguishable in pituitaries obtained from 7- or 14-day-old rats. Since the responsiveness of the 7-day-old pituitary was normal, the blunted enhancement of POMC biosynthesis after ADX must be mediated at the level of the hypothalamus. Indeed, in situ hybridization showed that while in 14-day-old rats ADX induced a significant increase [190 +/- 10% (+/- SE) of control; n = 5; P less than 0.0005] in hypothalamic mRNA levels, ADX did not change the expression of the CRF gene in the paraventricular nucleus of 7-day-old rats, indicating a lack of glucocorticoid modulation of hypothalamic CRF synthesis. Finally, we studied the effects of 48 h CRF treatment on the post-ADX increase in POMC mRNA levels in 7-day-old rats. Daily injections of 200 ng CRF/rat induced an increase in anterior pituitary POMC mRNA concentrations [669 +/- 139% (+/- SE) of control; n = 6; P less than 0.02 vs. adrenalectomized vehicle-treated rats] comparable to that in adrenalectomized untreated 14-day-old rats. In conclusion, our data indicate that the glucocorticoid regulation of hypothalamic CRF gene expression is not mature during the first week of life, i.e. within the so-called SNRP.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Onset of glucocorticoid responsiveness of anterior pituitary corticotrophs during development is scheduled by corticotropin-releasing factor. 252 76

While the transcriptional effects of glucocorticoid hormone manipulation on the pituitary pro-opiomelanocortin (POMC) gene have been documented, it is not yet clear whether glucocorticoids activate additional post-transcriptional mechanisms to regulate POMC gene expression. We have used RNA probes that span exon/intron junctions in sensitive nuclease protection assays in order to examine changes in POMC precursor RNA as well as mature mRNA in nucleus and cytoplasm following both adrenalectomy (ADX) and administration of exogenous glucocorticoids. ADX led to a rapid and sustained 8- to 10-fold increase in the level of POMC primary transcript in the anterior lobe (AL), from 1 to 14 days after ADX. Stimulation of mature POMC mRNA in the nucleus was also rapid, with 7- to 8-fold increases evident by 1 day after ADX. In sharp contrast, the time-dependent accumulation of POMC mRNA in the cytoplasm was slow in comparison, reaching levels approximately 2-fold higher than sham-operated animals by 1 day post-ADX and 12-fold higher by 14 days after ADX. Despite the constant elevated level of nuclear POMC precursor RNA, the rate of accumulation of POMC mRNA in the corticotroph cytoplasm after ADX was not linear, with the greatest increase occurring within the first 1-4 days post-ADX. This led to alterations in the molar ratio of POMC primary transcript: nuclear mRNA: cytoplasmic mRNA in the AL at 1 and 4 days after ADX and showed a relative increase in the proportion of POMC RNA transcripts within the nucleus. Acute administration of dexamethasone to ADX rats resulted in rapid 80-90% inhibition of POMC primary transcript levels in the AL that was maximal by 30 min but with no associated change in mature mRNA. No significant changes in POMC RNA were seen in neurointermediate lobe in any of these studies. These studies suggest that following ADX, time-dependent alterations in nuclear transport of mature POMC mRNA and/or changes in POMC mRNA stability, in addition to changes in gene transcription may account for the overall level of POMC mRNA expressed in the AL. Furthermore, we have illustrated the use of exon/intron probes for accurately quantitating rapid alterations in steady-state levels of nuclear precursor RNA that may reflect transcriptional responses and/or changes in post-transcriptional processing of the primary transcript.
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PMID:Changes in rat pituitary nuclear and cytoplasmic pro-opiomelanocortin RNAs associated with adrenalectomy and glucocorticoid replacement. 261 30

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