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)

The effects of forskolin or phorbol-13-myristate (PMA) injected intrathecally (i.t.) or intracerebroventricularly (i.c.v.) on the inhibition of the tail-flick and hotplate responses induced by morphine or beta-endorphin administered i.c.v. were studied. Animals pretreated with forskolin (20 micrograms) i.t. for 10 min had an attenuated inhibition of the tail-flick response induced by i.c.v. administered morphine (2 micrograms) or beta-endorphin (1 microgram). However, i.t. pretreatment with PMA (100 ng) was not effective in reducing the inhibition of the tail-flick response induced by morphine or beta-endorphin administered i.c.v. In addition, i.t. pretreatment with either forskolin or PMA did not affect the inhibition of the hotplate response induced by morphine or beta-endorphin administered i.c.v. Forskolin pretreatment i.c.v. for 10 min attenuated the inhibition of the tail-flick and hotplate responses induced by i.c.v. administered morphine or beta-endorphin. However, i.c.v. pretreatment with PMA was not effective in reducing the inhibition of the tail-flick or hotplate responses induced by morphine or beta-endorphin administered i.c.v. Our results suggest that activation of adenylate cyclase located at both spinal and supraspinal sites appears to be involved in antagonizing antinociception induced by morphine and beta-endorphin administered supraspinally. However, spinal or supraspinal protein kinase C may not be involved in antagonizing antinociception induced by morphine or beta-endorphin administered supraspinally.
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PMID:Differential effects of forskolin and phorbol-13-myristate injected intrathecally or intracerebroventricularly on antinociception induced by morphine or beta-endorphin administered intracerebroventricularly in the mouse. 877 60

Little is known about the effect of alpha-MSH and other melanogenic stimulators on avian melanocytes. Tissue cultures of Barred Plymouth Rock regenerating feather melanocytes were established and the culture medium contained selected concentrations of alpha-MSH and other melanogenic stimulators in Ham's F-10 medium supplemented with antibiotics and 10% new born calf serum. Cultures were maintained at 37 degrees C in 95% air/5% CO2. No increase in melanogenesis over control levels due to the addition of 10(-5) M Forskolin, 10(-4) M IBMX, 10(-3) M c-GMP, and 10(-3) M db-c-AMP was observed in the cultures on days 5 and 7. However, 2.5 (optimum), 5, and 10 micrograms/ml alpha-MSH and 10(-3) M 8-bromo-c-AMP significantly increased melanogenesis over control levels on days 5 and 7. The stimulation of melanogenesis was detectable by a significantly increased number of melanocytes containing numerous stage IV melanosomes. No increase in melanocyte cell number was observed in any of the experimental cultures. The addition of 1, 2 (optimum), or 3 mM calcium did enhance the increased pigmentation effect of 2.5 micrograms/ml alpha-MSH. Two very convincing experiments showed that c-AMP was the second messenger for alpha-MSH in these birds. First, the c-AMP inhibitor, 10(-3) M Rp-c-AMPS, completely inhibited the stimulatory effect of alpha-MSH in these in vitro melanocytes. Second, direct measurements of c-AMP levels in feather tissue showed a significant increase in c-AMP levels 10.min after alpha-MSH treatment. Controls received no alpha-MSH. The results showed that these avian melanocytes have alpha-MSH receptors and were able to respond to the hormone. C-AMP was the second messenger in this system. Apparently db-c-AMP was not able to enter these mature, highly-differentiated cells and c-AMP agonists, Forskolin and IBMX, were also either unable to enter these older cells or, if they did enter the cells, were unable to stimulate c-AMP production. Evidently the more lipophilic 8-bromo-c-AMP was able to enter these cells and stimulate melanogenesis.
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PMID:The role of alpha-MSH, its agonists, and C-AMP in in vitro avian melanocytes. 917 Jan 61

Our previous studies indicate that function of ATP-dependent K+ channels (K(ATP)) in cerebral arterioles is suppressed after ischemia. In the current study, we examined pial arteriolar responses to forskolin, dibutyryl-cAMP, NS-1619, and methionine (met)-enkephalin, activators of calcium-dependent K+ channels (K(Ca)) before and 1 hour after 10 minutes of total, global ischemia in anesthetized piglets. Arteriolar diameters were measured using a closed cranial window and intravital microscopy. All pharmacologic agents were given topically. Baseline diameters were approximately 100 microm, and diameters had returned to normal by 1 hour after ischemia. Forskolin dilated arterioles by 9 +/- 3%, 18 +/- 4%, and 31 +/- 12% at 5 x 10(-8), 5 x 10(-7), and 10(-6) mol/L, respectively (P < 0.05, n = 10). In addition, dibutyryl-cAMP dilated arterioles by 8 +/- 2% at 10(-4) mol/L and 14 +/- 2% at 3 x 10(-4) mol/L (P < 0.05, n = 6). Also, NS-1619 increased diameter of arterioles by 9 +/- 2% at 10(-7) mol/L and 17 +/- 9% at 10(-5) mol/L (P < 0.05, n = 5). Finally, met-enkephalin dilated arterioles by 9 +/- 2% at 10(-8) mol/L and 16 +/- 3% at 10(-6) mol/L (P < 0.05, n = 5). At 1 hour after ischemia, arteriolar dilator effects to forskolin, dibutyryl-cAMP and NS-1619, and met-enkephalin were intact. Thus, in contrast to K(ATP), K(Ca) in cerebral arterioles are resistant to ischemic stress.
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PMID:Calcium-activated K+ channels in cerebral arterioles in piglets are resistant to ischemia. 939 Jun 46

The interaction between corticotropin-releasing factor (CRF) and arginine vasopressin (AVP) is important in the regulation of adrenocorticotropin (ACTH) release from the anterior pituitary (AP). CRF exerts its effect on the AP by activating the adenylate cyclase (AC) complex whereas AVP increases the turnover of phosphatidylinositol. In the rat and in man, CRF is the most potent ACTH secretagogue whereas AVP alone is only a weak agonist. Since recent studies in the sheep indicate a reversal of this order of potency, these studies were undertaken to test the hypothesis that a functional alteration of the AC in the ovine corticotrope might limit the ability of CRF to release ACTH from these cells. When rat AP cells were incubated with CRF, a dose-dependent increase in AC activity was observed. This effect was potentiated either by AVP or PMA, although neither agent alone altered AC activity. In contrast, CRF alone, or in combination with AVP or PMA, did not increase AC activity in ovine AP cells. Both cholera toxin (CT) and pertussis toxin (PT) caused a dose-dependent release of ACTH from rat and ovine AP cells, but the amount of ACTH released from the ovine AP cells by both agents was relatively reduced. In the ovine cells, however, AVP acted synergistically with CT or PT to markedly increase the release of ACTH to levels which approached those obtained when the rat AP cells were exposed to CT or PT alone. Forskolin increased AC activity in AP cells of both species, but to a much lower extent in ovine cells than in the rat cells. However, when the ovine cells were exposed to AVP, the AC response to forskolin became similar to the response observed in the rat cells when incubated with forskolin alone. Forskolin also released significantly less ACTH from the ovine AP cells, but AVP also acted synergistically with forskolin to greatly enhance the amount of ACTH released from these cells. Finally, 8-bromo-cyclic AMP produced a similar release of ACTH from both ovine and rat AP cells. We conclude that: (1) the decreased ability of CRF to increase ACTH release from the ovine AP reflects a net decrease in AC activity and cannot be ascribed to an ovine corticotropic resistance to cAMP; (2) the decreased activity of the ovine corticotropic AC complex may in turn reflect functional alterations at the level of both the G proteins and the catalytic subunit; (3) since AVP causes protein kinase C substrate phosphorylation in the ovine AP, AVP may increase AC activity in this tissue by phosphorylating the G proteins and/or the catalytic subunit.
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PMID:A comparative study of the role of adenylate cyclase in the release of adrenocorticotropin from the ovine and rat anterior pituitary. 939 50

The effects of age on steroidogenesis in rat zona fasciculata-reticularis (ZFR) cells were studied. Young, adult, and middle-aged rats were ovariectomized (Ovx) and received replacement therapy with oil or estradiol benzoate ([EB] 25 microg/mL/kg). Rat ZFR cells were incubated with corticotropin (ACTH), prolactin (PRL), or forskolin at 37 degrees C for 1 hour. The effects of age on the activity of steroidogenic enzymes of ZFR cells were measured by the amount of intermediate steroidal products separated by thin-layer chromatography. Plasma levels were higher for PRL (54% to 254%) and corticosterone (179% to 257%) in middle-aged versus young rats. In oil-treated Ovx rats, basal and ACTH-stimulated corticosterone release by ZFR cells were also greater in middle-aged compared with young rats. Replacement with EB in Ovx rats increased the ACTH-stimulated release of corticosterone. Administration of ovine PRL in vitro resulted in a dose-dependent increase of corticosterone production. In oil-treated middle-aged rats, ovine PRL-stimulated corticosterone release was higher than in young rats. Forskolin-induced production of cyclic adenosine 3',5'-monophosphate (cAMP) was greater in middle-aged versus young rats and correlated with the increase of corticosterone production. The activity of steroidogenic enzymes in rat ZFR cells was unchanged by age. These results suggest that the age-related increase of corticosterone production in female rats is associated with the stimulatory effect of PRL on ZFR cells and is due in part to an increase of cAMP generation.
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PMID:Age-related differences in corticosterone secretion in female rats. 1020 51

Skins of Potamotrygon reticulatus are light in color in vitro, exhibiting punctate melanophores. Alpha-Melanocyte stimulating hormone (EC(50) = 4.58 x 10(-9) M) and prolactin (EC(50) = 1.44 x 10(-9) M) darken the skins in a dose-dependent manner. The endothelins ET-1, ET-2 and ET-3, and the purines, ATP, and uracil triphosphate (UTP) were not able to induce either skin lightening or darkening. Forskolin and the calcium ionophore A23187 promoted a dose-dependent darkening response, whereas N(2), 2'-O-dibutyryl guanosine 3'-5'-cyclic monophosphate (db cyclic GMP), phorbol-12-myristate-13-acetate (TPA), and 1-oleoyl-2-acetyl-sn-glycerol (OAG) were ineffective. The maximal response obtained with the calcium ionophore A23187 was only 76% of maximal darkening. These results indicate that the cyclic adenosine 3'-5'-monophosphate (cAMP) pathway is probably involved in the pigment dispersion of P. reticulatus melanophores. Other experiments should be done to further investigate how cytosolic calcium may be physiologically increased, and the existence of a putative cross-talk between calcium and cAMP signals. In conclusion, the only hormones effective on P. reticulatus melanophores were prolactin and alpha-MSH. No aggregating agent has been shown to antagonize these actions. Prolactin effect on elasmobranch melanophores adds a novel physiological role to this ancient hormone. J. Exp. Zool. 284:485-491, 1999.
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PMID:Elasmobranch color change: A short review and novel data on hormone regulation. 1046 85

The effects of estradiol benzoate (EB) on steroidogenesis in rat zona fasciculata-reticularis (ZFR) cells were studied. Female rats were ovariectomized (Ovx) for 2 weeks and then injected subcutaneously with oil or EB for 3 days before decapitation. ZFR cells were isolated and incubated with adrenocorticotropin (ACTH) or prolactin (PRL) for 1 h. Corticosterone concentrations in plasma and cell media, and adenosine 3',5'-cyclic monophosphate (cAMP) production in ZFR cells were determined by radioimmunoassay. The effects of EB replacement in vivo on the activities of steroidogenic enzymes in ZFR cells were measured by the amounts of intermediate steroidal products separated by thin-layer chromatography. Replacement of EB in vivo resulted in a dose-dependent increase of plasma PRL and corticosterone in Ovx rats. The basal, ACTH-, and PRL-stimulated release of corticosterone by ZFR cells was greater in EB- than in oil-treated animals. Forskolin-induced production of cAMP was greater in the EB-replaced rats than in oil-treated animals, which correlated with the increase of corticosterone production. The 3-isobutyl-l-methylxanthine (IBMX) plus ACTH-, IBMX plus PRL-, and forskolin plus PRL-stimulated productions of cAMP were higher in EB- than in oil-treated rats. The enzyme activities of postpregnenolone were not affected by EB replacement in Ovx rats. These results suggest that the EB-related increase of corticosterone production in Ovx rats is associated with an increase of cAMP generation and the stimulatory effect of PRL on ZFR cells.
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PMID:Effects of estradiol on corticosterone secretion in ovariectomized rats. 1077 12

The pro-opiomelanocortin-derived peptide alpha-melanocyte-stimulating hormone (alpha-MSH) mediates broad anti-inflammatory and immunomodulatory effects, which include inhibition of the production and release of proinflammatory cytokines and nitric oxide (NO) from macrophages. We investigated the effects of alpha-MSH, alpha-MSH(1-10), and alpha-MSH(11-13) on NO production and nuclear factor-kappaB (NF-kappaB) translocation in RAW 264.7 macrophages. After stimulation of the cells with bacterial lipopolysaccharide/interferon-gamma (LPS/IFN-gamma), all three peptides inhibited NO production with an order of potency alpha-MSH > or = alpha-MSH(11-13) > alpha-MSH(1-10). All three MSH peptides inhibited NF-kappaB nuclear translocation with the maximal effect of alpha-MSH and alpha-MSH(11-13) being seen in the range 1 nM-1 microM, and that of alpha-MSH(1-10) at 1 microM. By use of (125)I-(Nle(4),D-Phe(7))alpha-MSH(NDP-MSH) radioligand binding, MC(1) receptor-binding sites were demonstrated on RAW 264.7 cells. alpha-MSH and alpha-MSH(1-10) competed with the (125)I-NDP-MSH binding at these MC(1) receptor-binding sites, but alpha-MSH(11-13) even in concentrations up to 1 mM did not. Moreover, alpha-MSH and alpha-MSH(1-10) caused powerful stimulation of cyclic 3',5'-adenosine monophosphate (cAMP) in the RAW 264.7 cell, whereas alpha-MSH(11-13) was ineffective. Forskolin stimulated cAMP and inhibited NO production to the same extent as alpha-MSH and alpha-MSH(1-10), but did not modify the translocation of NF-kappaB. Whereas the protein kinase A inhibitor H89 did not modify the effect of alpha-MSH on NF-kappaB translocation, H89 caused a partial inhibition of the inhibitory effect of alpha-MSH, alpha-MSH(1-10), alpha-MSH(11-13), and forskolin on NO production. In addition alpha-MSH, alpha-MSH(1-10), alpha-MSH(11-13), and forskolin also inhibited the activity of an NF-kappaB-dependent luciferase reporter and these effects were partially counteracted by H89. We suggest that melanocortin peptides act via dual mechanisms of action: one cAMP-independent and causing inhibition of NF-kappaB translocation and the other dependent on MC(1) receptor/cAMP activation.
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PMID:Effects of melanocortin peptides on lipopolysaccharide/interferon-gamma-induced NF-kappaB DNA binding and nitric oxide production in macrophage-like RAW 264.7 cells: evidence for dual mechanisms of action. 1123 5

The effects and mechanisms of aging on corticosterone secretion in zona fasciculata-reticularis (ZFR) cells of ovariectomized (Ovx) rats were studied. Young (3-month) and old (24-month) female rats were Ovx for 4 days before decapitation. ZFR cells were isolated and incubated with different hormones or reagents at 37 degrees C for 30 min. Aging increased the basal secretion of corticosterone both in vivo and in vitro. The adrenocorticotropin (ACTH)-, forskolin-, 3-isobutyl-l-methylxanthine (IBMX)-, 8-bromo-adenosine 3',5'-cyclic monophosphate (8-Br-cAMP)-, and ovine prolactin (oPRL)-stimulated release of corticosterone by ZFR cells was greater in old than in young Ovx rats. H89, an inhibitor of protein kinase A (PKA), decreased the production of corticosterone in ZFR cells from young but not old Ovx rats. Forskolin-, or IBMX-induced production of cAMP was greater in old than in young Ovx animals, which correlated with the increase of corticosterone production by aging. The activity of 11 beta-hydroxylase that converts deoxycorticosterone (DOC, 10(-9) or 10(-8) M) to corticosterone in rat ZFR cells was decreased by age. However, the corticosterone production in response to high dose of DOC (10(-7) M) was indifferent between young and old groups. These results suggest that aging increases corticosterone production in Ovx rats via a mechanism in part associated with an increase of adenylyl cyclase activity and a decrease of phosphodiesterase activity, and then an increase of the generation of cAMP, but not related to either PKA activity or 11 beta-hydroxylase.
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PMID:Involvement of cAMP but not PKA in the increase of corticosterone secretion in rat zona fasciculata-reticularis cells by aging. 1189 48

The physiologic role of corticotropin-releasing hormone (CRH) was examined in the ovary. We investigated the effects of CRH on steroidogenesis in rat and human granulosa cells in vitro as well as the direct effects of CRH on the ovary in vivo. We further examined the gene expression of CRH in human granulosa cells. CRH significantly inhibited the production of estradiol (E2) and progesterone (P4) in rat and human granulosa cells in vitro. These inhibitory effects were completely abolished by alpha-helical CRH, a CRH receptor antagonist. Forskolin-induced increase in E2 and P4 production was attenuated by CRH. On the other hand, CRH significantly increased serum concentrations of E2 and corticosterone in vivo in hypophysectomized rats, but this increase was completely blocked by adrenalectomy. It is probable that these effects did not result from a direct action on the ovary but were an indirect effect via the adrenal gland. Finally, by reverse transcriptase polymerase chain reaction we demonstrated that CRH mRNA was expressed in human granulosa cells. Our findings indicate that CRH exerts inhibitory effects on steroidogenesis in rat and human granulosa cells, acting through the CRH receptor. These effects are attributed to cellular events downstream of cyclic adenosine monophosphate generation. CRH seems to modulate steroidogenesis via autocrine or paracrine actions in the ovary.
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PMID:Role of corticotropin-releasing hormone in ovarian steroidogenesis. 1245 Mar 17

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