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PubMed1990

Acute phase response to endotoxin: rise in plasma alpha-MSH and effects of alpha-MSH injection.

Endotoxins, cell wall components of bacteria, cause a number of biological effects, presumably via induction of potent cytokines. Previous research suggests that the neuropeptide alpha-melanocyte-stimulating hormone (alpha-MSH) and its COOH-terminal tripeptide reduce the effects of cytokines. These molecules evoke antipyretic and anti-inflammatory effects in vivo. Localization of alpha-MSH within lymphocytes and recent observations that alpha-MSH receptors are widespread and that circulating alpha-MSH increases after systemic injection of endogenous pyrogen, a cytokine-containing extract, suggest that the peptide modulates host defense reactions. One aim of the present experiments was to learn whether a rise in circulating alpha-MSH occurs in synchrony with aspects of the acute phase response (APR) in conscious rabbits given endotoxin. A second aim was to learn whether administration of a single large dose of alpha-MSH inhibits all aspects of the APR induced by a low dose of endotoxin. The results indicate that the concentration of circulating alpha-MSH in rabbits does increase along with other changes in the APR (e.g., increase in corticosterone), which suggests that the peptide is widely available to modulate cytokine effects after endotoxin. Contrary to expectations based on previous results, a large dose of the peptide given intravenously inhibited only fever and not other aspects of the APR. The results suggest that the rise in circulating alpha-MSH is an aspect of the APR and that an acute increase in the circulating peptide caused by intravenous injection does not inhibit all other aspects of the host response to endotoxin.

Acute-Phase Reaction↗
PubMed1986

Stimulation of adenosine 3',5'-monophosphate production in rat Sertoli cells by alpha-melanotropin-stimulating hormone (alpha MSH) and des-acetyl alpha MSH.

Proopiomelanocortin and its derivative peptides alpha MSH and beta-endorphin are produced by Leydig cells. beta-Endorphin or another testicular opiate is believed to suppress Sertoli cell hypertrophy. The goal of this study was to determine the effects of another proopiomelanocortin-derived peptide on Sertoli cells. The activities of both alpha MSH and des-acetyl alpha MSH have been compared, since this latter peptide has been identified in testicular extracts. Both alpha MSH and des-acetyl alpha MSH stimulated cAMP accumulation in the media of primary Sertoli cell cultures when incubated in the presence of a phosphodiesterase inhibitor, FSH or forskolin. Both peptides shifted the FSH dose-response curve to the left, making the cells more sensitive to this gonadotropin. The apparent potencies of alpha MSH and its des-acetyl derivative, as measured in Sertoli cells, were similar. We conclude that the MSHs are one of a group of modulators regulating Sertoli cells via the cAMP system, and Sertoli cells are equally responsive to alpha MSH and des-acetyl alpha MSH, unlike central nervous system and melanocytes which show differential responses to these peptides.

1-Methyl-3-isobutylxanthine↗
PubMed1979

Parallel release of ACTH, beta-endorphin, alpha-MSH and beta-MSH-like immunoreactivities in rat anterior pituitary cells in culture.

Specific radioimmunoassays (RIAs) for ACTH, beta-endorphin, alpha-MSH and beta-MSH were used to identify the immunoreactive components released during incubation of rat anterior pituitary cells in primary culture. Such measurements were performed after separation of the incubation media by chromatography on Sephadex G-50 or G-75. The ACTH-RIA measured approximately equal amounts of 13 and 4.5K ACTH while equal proportions of components migrating at the position of beta-LPH and beta-endorphin were measured in the beta-endorphin RIA system. Immunoreactive components migrating at the position of gamma-LPH and alpha-MSH were measured in the beta-MSH and alpha-MSH RIA systems, resp. 3 purified corticotropin-releasing fractions (CRF) prepared from porcine hypothalami and increasing concentrations of N6,O2'-dibutyryl cyclic AMP and theophylline led to parallel release of ACTH, beta-endorphin, beta-MSH and alpha-MSH immunoreactivities while preincubation with dexamethasone led to a 30-60% inhibition of the release of all peptides. The present data show that the release of ACTH, beta-LPH, beta-endorphin, gamma-LPH and alpha-MSH-like immunoeactivities occurs in parallel in anterior pituitary cells in culture both under basal and acute stimulatory or inhibitory conditions of release.

Adrenocorticotropic Hormone↗
PubMed1983

Catecholaminergic control of alpha-melanocyte-stimulating hormone (alpha MSH) release by frog neurointermediate lobe in vitro: evidence for direct stimulation of alpha MSH release by thyrotropin-releasing hormone.

The role of dopaminergic and adrenergic innervation of the intermediate lobe of amphibian pituitary in the release of alpha MSH has been studied in vitro. Neurointermediate lobes of frog (Rana ridibunda Pallas) have been perifused in amphibian culture medium (ACM) for 5-7 h. alpha MSH released in the effluent perifusate was measured by means of a sensitive and specific RIA. No significant morphological alteration of neurointermediate lobe cells was observed during the perifusion experiment, even at the electron microscopic level. The existence of dopaminergic receptors, responsible for an inhibition of frog melanotrophs, was shown using the dopaminergic agonists apomorphine (10(-6) M) and bromo-2-ergocryptine (10(-8) and 10(-7) M), which initiated a marked reduction of alpha MSH secretion. The effect of apomorphine was obliterated by the dopaminergic antagonist haloperidol. Haloperidol itself induced a dose-related stimulation, and the monoamine oxidase inhibitor nialamide (4 x 10(-3) M) inhibited alpha MSH secretion. In addition, haloperidol led to a complete reversal of the inhibitory effect of nialamide on alpha MSH secretion. These results demonstrate the existence, in the parenchyme of the intermediate lobe, of dopaminergic nerve fibers that are functionally active. The beta-adrenergic agonist isoproterenol was responsible for a dose-related stimulation of alpha MSH secretion; the stimulatory effect was reversed by the beta-adrenergic antagonist propranolol. TRH is a potent stimulator of alpha MSH secretion in amphibians. Since haloperidol and propranolol did not abolish the stimulation of alpha MSH release induced by TRH, it appeared that TRH action was not mediated via an inhibition of dopamine release or via a stimulation of adrenergic nerve fibers.

Animals↗
PubMed1995

Ultraviolet B and melanocyte-stimulating hormone (MSH) stimulate mRNA production for alpha MSH receptors and proopiomelanocortin-derived peptides in mouse melanoma cells and transformed keratinocytes.

Cell lines of cutaneous origin, namely melanocytes and keratinocytes, were previously demonstrated to exhibit functional melanocyte-stimulating hormone (MSH) receptors that are up-regulated by ultraviolet (UV) radiation and by MSH itself. In this study, it is demonstrated that UVB irradiation, exposure to MSH, or exposure to N6,O2-dibutyryl cyclic adenosine monophosphate stimulates production of mRNAs for both alpha MSH receptors and proopiomelanocortin in cultured mouse Cloudman S91 melanoma cells, and that UVB stimulates production and release of MSH and adrenocorticotropin peptides in both melanoma cells and transformed PAM 212 mouse keratinocytes. The results add support to the hypothesis that the effects of UVB on cutaneous melanogenesis are mediated through a series of coordinated events in which MSH receptors and proopiomelanocortin-derived peptides play a central role.

Animals↗
PubMedDate not supplied

Transformation of an irreversible MSH antagonist into an irreversible MSH agonist by differential receptor crosslinking using the photo-affinity technique.

Photocrosslinking of receptors for alpha-melanocyte-stimulating hormone (alpha-MSH) on melanophores of frogs and lizards has been shown to induce long-lasting receptor stimulation whereby the photoreactive alpha-MSH may contain one or two photolabels in positions 1, 7, 9, or 13. The chemical synthesis and biological testing of an alpha-MSH analogue is now described which contains three photoreactive groups in positions 1, 9 and 13, one of which with a cleavable S-S disulphide bridge: [ApSSpr-Ser1, Trp(Naps)9 Pap13]-alpha-MSH. Photocrosslinking of MSH receptors on melanophores of Anolis carolinensis with this analogue led to almost complete receptor blockade which could be transformed into long-lasting receptor stimulation by exposure to a thiol reagent. By contrast, the analogue containing only two photoreactive groups in positions 9 and 13, [Trp(Naps)9, Pap13]-alpha-MSH, produced long-lasting receptor stimulation which was not altered by the thiol reagent. These results demonstrate that one and the same peptide ligand may contain structural information for both receptor activation and inhibition and that the receptor may become arrested in an activated or inhibited state by multiple photocrosslinking, depending on the relative positions of these crosslinks.

Animals↗
PubMed1992

Up-regulation of MSH receptors by MSH in Cloudman melanoma cells.

MSH can up-regulate MSH binding capacity of cultured Cloudman melanoma cells in a dose- and time-dependent fashion. Binding is mediated through proteins exhibiting an apparent molecular weight of 50-53kDa, consistent with previous studies implicating them as the principal MSH receptors on Cloudman cells. Pre-incubation of cells with MSH stimulates expression of the receptor proteins both on the plasma membrane surface as well as in internal sites associated with coated vesicles. The effects of MSH are additive with those of UV light, suggesting that UV and MSH might stimulate receptor expression through separate mechanisms.

Animals↗
PubMed1985

Postnatal development of ACTH and alpha-MSH in the medulla oblongata of rat: alpha-MSH is the predominant peptide.

ACTH and alpha-MSH levels were measured by radioimmunoassays in extracts of the caudal medulla oblongata of developing rats on postnatal (P) days 1-42 at 7 day intervals, and in adult rats. From P1 to adulthood, ACTH increased greater than 11-fold from 7.2 +/- 1.9 fmol to 82.4 +/- 12.6 fmol per medulla section (mean +/- S.E.M.). In comparison, alpha-MSH increased greater than 7-fold from 68.75 +/- 11.0 fmol to 491 +/- 97.8 fmol during this time period. ACTH/microgram of soluble protein decreased during postnatal development from 0.006 +/- 0.01 to 0.005 +/- 0.001 fmol/microgram of protein and alpha-MSH increased from 0.06 +/- 0.01 fmol/microgram of protein to 0.11 +/- 0.009 fmol/microgram of protein between P1 and P7, decreased to 0.015 +/- 0.003 fmol/microgram of protein by P42 and increased to 0.03 +/- 0.006 fmol/protein per unit protein by adulthood. These data indicate a significant shift in the levels of alpha-MSH detected during development with a decrease in the concentration of material occurring from early postnatal development (P1-P7) to adulthood, which does not appear to be solely related to a regional increase in protein. These studies, as well as radioimmunoassays for ACTH and alpha-MSH in combination with sizing chromatography of pooled extracts at P1, P7 and the adult, demonstrated the predominance of alpha-MSH at all ages.

Adrenocorticotropic Hormone↗
PubMed1988

The regulation of the corticomelanotropic cell activity in aves. III--Effect of various peptides on the release of MSH from dispersed, perfused duck pituitary cells. Cosecretion of ACTH with MSH.

1. The melanotropin-releasing activity of arginine-vasopressin (AVP), arginine-vasotocin (AVT), oxitocin (OT), mesotocin (MT) and corticotropin-releasing factor (CRF) was studied in the duck using dispersed, perfused pituitary cells and a specific alpha-MSH RIA. 2. Log dose-response curves were obtained for all the peptides ranging from 5 to 100 ng/ml. All peptides behaved as partial agonists compared to duck median eminence extracts (DME). 3. AVT and MT displayed an alpha-MSH releasing capacity of 60% relative to DME whereas all other peptides behaved as weak agonists with less than 15% capacity relative to DME. 4. AVT and CRF when perfused together acted synergistically on alpha-MSH release yielding a dose response line whose slope approximated that of DME. 5. ACTH was cosecreted together with alpha-MSH in all situations studied with an ACTH to alpha-MSH molar ratio of about 10. 6. It is concluded that CRF and neurohypophyseal peptides may be physiological stimulators of both alpha-MSH and ACTH release in aves.

Adrenocorticotropic Hormone↗
PubMed1979

Serum MSH levels and pituitary MSH content: their fluctuation during pregnancy in the rat.

MSH was measured by a biological assay in the pituitary and serum of the rat during the whole term of pregnancy. The peptide showed changes in early pregnancy in serum, during the middle of pregnancy values of serum MSH became negative, and in late pregnancy it was possible to find high values during days 18 and 19 before delivery. Comparison between the amount of pituitary MSH and that in serum seems to show that between days 10 and 15 there is practically no, or just a litte, MSH synthesis, since the MSH values in serum are negative although the content of pituitary MSH is also low. A relation between the results found by other authors and that found by us was analyzed.

Animals↗
PubMed1978

An improved radioimmunoassay for alpha-melanocyte-stimulating hormone (alpha-MSH) in the rat: serum and pituitary alpha-MSH levels after drugs which modify catecholaminergic neurotransmission.

A modification of our previous radioimmunoassay (RIA) for alpha-melanocyte-stimulating hormone (alpha-MSH) is described that permits the measurement of circulating levels in the rat without the need for an extraction procedure. Using this method, serum and neurointermediate lobe (NIL) immunoreactive alpha-MSH levels were measured in rats after administration of haloperidol, 2-bromo alpha-ergocryptine (CB 154), and alpha-methyl-p-tyrosine (alpha-MPT). Haloperidol caused a rapid increase, alpha-MPT a slow increase, and CB 154 a rapid decrease in serum alpha-MSH. At the time intervals studied none of the drugs had any significant effect on NIL alpha-MSH content. It was concluded from the results of the above drug treatments that modulation of dopaminergic neurotransmission both pre- and postsynaptically produces changes in serum immunoreactive alpha-MSH levels. This supports the suggestion that circulating alpha-MSH in the rat is under an inhibitory control by a catecholaminergic system.

Animals↗
PubMed1986

Immunocytochemical localization of pro gamma MSH, gamma MSH, ACTH and beta endorphin/beta lipotrophin in the fetal sheep pituitary: an ontogenetic study.

An immunocytochemical staining technique was used to localize four fragments [pro gamma MSH, gamma MSH, ACTH and beta endorphin/beta lipotrophin (beta endorphin/beta LPH)] of the proopiomelanocortin molecule in both the adult and fetal sheep pituitary. In the adult sheep anterior pituitary each fragment was localized in cells that were darkly stained, stellate and widely distributed throughout the gland. The same cells, identified in three serial sections, stained with anti-pro gamma MSH, anti-ACTH and anti-beta endorphin/beta LPH. In the fetal sheep anterior pituitary all the proopiomelanocortin derived fragments were present at 38 days gestation. Between about 90 and 130 days of gestation both adult type proopiomelanocortin cells (small, stellate) and uniquely fetal cells (large, columnar) were present. Both adult-type and fetal proopiomelanocortin cells were identified in serial sections of the fetal anterior pituitary, stained with anti-pro gamma MSH, anti-ACTH and anti-beta endorphin/beta LPH. The adult intermediate lobe was immunoreactive with anti-pro gamma MSH and anti-beta endorphin/beta LPH but not with anti-gamma MSH or anti-ACTH. The fetal intermediate lobe was immunoreactive with all four antisera from 60 days gestation.

Adrenocorticotropic Hormone↗
PubMed1996

Domestic cats show episodic variation in plasma concentrations of adrenocorticotropin, alpha-melanocyte-stimulating hormone (alpha-MSH), cortisol and thyroxine with circadian variation in plasma alpha-MSH concentrations.

Blood samples were collected from 31 healthy domestic cats to characterize possible episodic and/or circadian variation in plasma concentrations of adrenocorticotropin (ACTH), cortisol, thyroxine and alpha-melanocyte-stimulating hormone (alpha-MSH). Samples were collected with minimal disturbance through indwelling jugular cannulae at two frequencies: at 20-min intervals for 3 h for evaluation of episodic variation, and at 2-h intervals for 48 or 72 h to identify possible circadian changes. Episodic peaks in profiles of all hormones were found in the majority of cats. When data were compared across four bleed periods (each of 3 h duration), no differences were detected in average hormone concentrations or characteristics of episodic pulses. Correlation analyses showed a significant (p < 0.001) relationship between concentrations of ACTH and cortisol (r = 0.44) when these hormones were measured in the same plasma sample. A weaker but significant correlation (r = 0.13, p < 0.05) was also detected between concentrations of ACTH and alpha-MSH, suggesting that proopiomelanocortin peptide secretion from the pars distalis and pars intermedia occurs at least on occasion in synchrony. No differences in hormonal profiles were noted when comparing data across sexes. Data from the studies designed to evaluate circadian change (48 and 72-h bleed periods) indicated that, of the four hormones, only concentrations of alpha-MSH changed with a significant circadian periodicity. A significant circadian component of period length 24-25 h was detected in 37% (seven of 19) of cats examined. Concentrations of alpha-MSH were greatest coincident with or shortly after the onset of darkness. These findings indicate that pituitary-adrenocortical hormones are secreted episodically in domestic cats and that, in contrast to the patterns shown by ACTH and cortisol, secretion of the pars intermedia product alpha-MSH occurs with a circadian rhythm in about one-third of cats.

Adrenocorticotropic Hormone↗
PubMed1993

Peptides containing multiple photolabels: a new tool for the analysis of ligand-receptor interactions. Reversible long-lasting stimulation and inhibition of MSH receptors by multiple photocrosslinks with alpha-MSH.

Crosslinking of MSH receptors on melanophores of the lizard Anolis carolinensis with analogues of alpha-MSH containing a photoreactive group in position 1, 7, 9 or 13 leads to long-lasting receptor stimulation. Reversibility of this long-lasting stimulation is obtained by employing a disulfide-containing photoreactive group which can be cleaved from the receptor by thiol reagents [Ref. 3]. When two photoreactive groups are simultaneously present on the alpha-MSH molecule (e.g in positions 1 + 9; 1 + 13; 7 + 13, or 9 + 13), identical results were obtained and long-lasting receptor stimulation was not altered after cleavage of one single crosslink. alpha-MSH analogues with three photoreactive groups in positions 1 + 7 + 13 led to irreversible receptor stimulation whereas one compound with the photoreactive groups in positions 1 + 9 + 13 induced reversible receptor inactivation which could be changed into long-lasting stimulation by cleaving the crosslink at position 1 of alpha-MSH. These results demonstrate that one and the same peptide ligand may contain structural information for both receptor activation and inhibition and that the receptor may become arrested in an activated or inhibited state by multiple photocrosslinking, depending on the relative positions of these crosslinks.

Affinity Labels↗
PubMed1980

Possible aminergic mediation of MSH release and of the CNS effects of MSH and MIF-I.

It is well known that the release of melanocyte-stimulating hormone (MSH) from the pituitary gland is mainly controlled by an inhibitory influence from the hypothalamus. In addition to this inhibitory control, there may also be a stimulatory influence. Most, but by no means all, of the evidence is compatible with the possibility that inhibition is mediated by dopaminergic and/or alpha-adrenergic receptors. Gamma-aminobutyric acid also has been shown to have an inhibitory role in some studies. beta-Adrenergic receptors, serotonin, and acetylcholine may be involved in the stimulation of MSH release. Interaction of hypothalamic peptides like Pro-Leu-Gly-NH2(MIF-I) with biogenic amines, however, has not been excluded as a factor in the control of the release of MSH from the pituitary. Just as the evidence for the involvement of amines in the control of MSH release is somewhat puzzling and contradictory, conflicting evidence concerning their involvement in mediating the specific effects of MSH and MIF-I on the CNS remains unresolved.

Acetylcholine↗
PubMed1975

Ontogenesis of the alpha-MSH, beta-MSH and ACTH cells in the foetal hypophysis of the rat. Correlation with the growth of the adrenals and adrenocortical activity.

Pituitary sections from 15 to 21 day-old rat foetuses have been studied with the immunofluorescence technique, using antibodies anti alpha-MSH, anti beta-MSH and anti beta (1-24) ACTH. The first ACTH cells appear on day 17 of pregnancy in the pars distalis of the hypophysis and only on day 18 in the pars intermedia. beta-msh cells have been observed on day 16 in the pars anterior and on day 17 in the pars intermedia, while alpha-MSH cells appear only on day 18 and exclusively in the pars intermedia. The cytodifferentiation of the beta-MSH and ACTH cells occurs in the pars intermedia with about a 24 hours delay in comparison to that of the pars distalis. The first revealed cells are always located in the posterior half of the pituitary gland. The corticostimulating activity of the hypophysis has been tested with the fluorescence intensity of the corticotrophs, the adrenal weight, the adrenal content in corticosterone and the plasma corticosterone level. The fluorescence of the corticotrophs increases on day 18, shows a maximum on day 19 and decreases until term. The adrenal weight rises regularly between day 16 to day 20, thereafer the increase subsides. Adrenal and plasma corticosterone concentrations reach a peak on day 19 of pregnancy. These data suggest that hypophyseal corticostimulating activity is very high between days 18 and 19 and decreases between days 19 and 21.

Adrenal Cortex↗
PubMed1989

L-tyrosine stimulates induction of tyrosinase activity by MSH and reduces cooperative interactions between MSH receptors in hamster melanoma cells.

L-tyrosine, a precurosr to melanin, has recently been shown to be a regulator of the melanogenic pathway in some cultured melanoma cell lines. In this paper we demonstrated that L-tyrosine, besides increasing binding capacity for MSH, decreased cooperativity between MSH receptors and increased the level of tyrosinase induction by MSH. Apparently, regulation of MSH receptor activity by L-tyrosine involves specific changes in the interactions between the receptors and modification of the cellular responsiveness to MSH.

Animals↗
PubMed1987

Phosphorylated isomers of L-dopa stimulate MSH binding capacity and responsiveness to MSH in cultured melanoma cells.

L-dopa is a key metabolite in the process of melanogenesis. However, it is difficult to use in biological experiments because it is subject to auto-oxidation and relatively insoluble at neutral pH. Dopa phosphates contain phosphate ester linkages at positions 3 and/or 4 of the phenylalanine ring of L-dopa, rendering them highly soluble and stable to auto-oxidation when compared to L-dopa. Dopa phosphates are readily taken up by melanoma cells in culture and converted to L-dopa and inorganic phosphate by cellular phosphatases, making them useful for studying L-dopa effects in vivo. Here we investigated the effects of dopa phosphates on receptors for MSH in cultured melanoma cells. We found that dopa phosphates caused a 3-fold stimulation of MSH binding capacity by the cells which probably occurred through an increase in the number of receptors for MSH with no apparent change in affinity of the receptors. The increased binding capacity for MSH was followed by increased cellular tyrosinase activity and melanogenesis. Thus dopa phosphates and/or L-dopa can act as regulators of the MSH receptor system. The observations suggest a novel mechanism for regulation of hormonal responsiveness: hormonal signal amplification by a metabolite in the target pathway.

Animals↗