Selective properties of C- and N-terminals and core residues of the melanocyte-stimulating hormone on binding to the human melanocortin receptor subtypes

1998 ◽  
Vol 349 (2-3) ◽  
pp. 359-366 ◽  
Author(s):  
Helgi B Schiöth ◽  
Felikss Mutulis ◽  
Ruta Muceniece ◽  
Peteris Prusis ◽  
Jarl E.S Wikberg
Keyword(s):  
Melanocortin Receptor ◽  
Receptor Subtypes ◽  
Melanocyte Stimulating Hormone ◽  
C And N ◽  
Stimulating Hormone

scholarly journals Identification of avian alpha-melanocyte-stimulating hormone in the eye: temporal and spatial regulation of expression in the developing chicken

2001 ◽  
Vol 168 (3) ◽  
pp. 527-537 ◽  
Author(s):  
K Teshigawara ◽  
S Takahashi ◽  
T Boswell ◽  
Q Li ◽  
S Tanaka ◽  
...  
Keyword(s):  
In Situ Hybridization ◽  
Neural Retina ◽  
Melanocortin Receptor ◽  
Receptor Subtypes ◽  
Peripheral Tissues ◽  
Rpe Cells ◽  
Melanocyte Stimulating Hormone ◽  
Cone Cells ◽  
Stimulating Hormone

The presence and possible physiological roles of alpha-melanocyte-stimulating hormone (alpha-MSH) in the peripheral tissues of birds have not been established. By a combination of RT-PCR, immunocytochemistry and in situ hybridization, we have examined alpha-MSH expression in the eye of the chicken during development. In the 1-day-old chick, alpha-MSH was expressed in the retinal pigment epithelial (RPE) cells, and also at a lower level in the cone cells. The melanocortin receptor subtypes, CMC1, CMC4 and CMC5, were expressed in the layers of the choroid and the neural retina, but not in the RPE cells. It is probable that the RPE cells secrete alpha-MSH to exert paracrine effects on the choroid and neural retina. During embryonic development, alpha-MSH immunoreactivity in the RPE cells was initially detected at embryonic day 10, and increased in intensity as development proceeded. No cone cells were stained with anti-alpha-MSH antiserum in any of the embryonic stages tested. The immunoreactivities for two prohormone convertases, PC1 and PC2, were co-localized to the RPE cells with a pattern of staining similar to that of alpha-MSH. Despite containing alpha-MSH immunoreactivity, the RPE cells in 1-day-old chicks expressed no immunoreactivity for the endoproteases. Furthermore, in a 3-day-old chick, pro-opiomelanocortin mRNA was detectable by in situ hybridization only in the photoreceptor layer and not in the RPE cells. These results suggest that the RPE cells and the cone cells are intraocular sources of alpha-MSH in the embryonic and postnatal life of the chicken respectively. Embryonic expression of alpha-MSH in the RPE cells implies a possible role for the peptide in ocular development.

Regulation of c-met expression in B16 murine melanoma cells by melanocyte stimulating hormone

1999 ◽  
Vol 112 (5) ◽  
pp. 623-630
Author(s):  
D. Rusciano ◽  
P. Lorenzoni ◽  
M.M. Burger
Keyword(s):  
Melanoma Cells ◽  
Parental Cell ◽  
Melanocortin Receptor ◽  
Parental Cell Line ◽  
Melanocyte Stimulating Hormone ◽  
Murine Melanoma ◽  
The One ◽  
Murine Melanoma Cells ◽  
Stimulating Hormone

B16 murine melanoma cells selected in vivo for enhanced liver metastatic ability (B16-LS9) show on the one hand an increased expression and constitutive activation of the proto-oncogene c-met (the receptor for hepatocyte growth factor/scatter factor), and on the other hand a more differentiated phenotype, when compared to the parental cell line, B16-F1. Following this observation, we have tried to establish whether there is a direct relationship between differentiation and c-met expression in B16 melanoma cells. Treatment of these cells with differentiating agents indicated that c-met expression was strongly induced by melanocyte stimulating hormone, while retinoic acid had almost no influence. c-met induction was triggered by engagement of the melanocortin receptor, cAMP elevation and PKA/PKC(α) activation, as respectively shown by the effects of ACTH, cAMP elevating agents and specific PK inhibitors. Regulation of c-met expression via the melanocortin receptor and cAMP raises the intriguing possibility that autocrine and/or paracrine mechanisms acting in vivo on this circuit might influence (through c-met expression and activation) the metastatic behavior of these tumor cells, which we have shown to be dependent on their c-met expression.

Analogs of α-melanocyte stimulating hormone with high agonist potency and selectivity at human melanocortin receptor 1b: The role of Trp9 in molecular recognition

Biopolymers ◽  
2008 ◽  
Vol 89 (5) ◽  
pp. 401-408 ◽  
Author(s):  
Maria A. Bednarek ◽  
Tanya MacNeil ◽  
Rui Tang ◽  
Tung M. Fong ◽  
M. Angeles Cabello ◽  
...  
Keyword(s):  
Molecular Recognition ◽  
Melanocortin Receptor ◽  
Melanocyte Stimulating Hormone ◽  
Stimulating Hormone

scholarly journals The Melanocortin System in Control of Inflammation

2010 ◽  
Vol 10 ◽  
pp. 1840-1853 ◽  
Author(s):  
Anna Catania ◽  
Caterina Lonati ◽  
Andrea Sordi ◽  
Andrea Carlin ◽  
Patrizia Leonardi ◽  
...  
Keyword(s):  
Receptor Activation ◽  
Brain Regions ◽  
New Drugs ◽  
Melanocortin Receptor ◽  
Receptor Subtypes ◽  
Melanocortin System ◽  
Inflammatory Disorders ◽  
Melanocyte Stimulating Hormone ◽  
Common Precursor ◽  
Anti Inflammatory

Melanocortin peptides, the collective term for α-, β-, and γ-melanocyte-stimulating hormone (α-, β-, γ-MSH) and adrenocorticotropic hormone (ACTH), are elements of an ancient modulatory system. Natural melanocortins derive from the common precursor pro-opiomelanocortin (POMC). Five receptor subtypes for melanocortins (MC1-MC5) are widely distributed in brain regions and in peripheral cells. Melanocortin receptor activation by natural or synthetic ligands exerts marked anti-inflammatory and immunomodulatory effects. The anticytokine action and the inhibitory influences on inflammatory cell migration make melanocortins potential new drugs for treatment of inflammatory disorders. Effectiveness in treatment of acute, chronic, and systemic inflammatory disorders is well documented in preclinical studies. Further, melanocortins are promising compounds in neuroprotection. This review examines the main signaling circuits in anti-inflammatory and immunomodulatory actions of melanocortins, and the potential therapeutic use of these molecules.

scholarly journals Depletion of Alpha-Melanocyte-Stimulating Hormone Induces Insatiable Appetite and Gains in Energy Reserves and Body Weight in Zebrafish

Biomedicines ◽  
2021 ◽  
Vol 9 (8) ◽  
pp. 941
Author(s):  
Yang-Wen Hsieh ◽  
Yi-Wen Tsai ◽  
Hsin-Hung Lai ◽  
Chi-Yu Lai ◽  
Chiu-Ya Lin ◽  
...  
Keyword(s):  
Body Weight ◽  
Energy Homeostasis ◽  
Body Weight Gain ◽  
Genetically Engineered ◽  
Melanocortin Receptor ◽  
Synthetic Analog ◽  
Melanocortin System ◽  
Releasing Hormone ◽  
Melanocyte Stimulating Hormone ◽  
Stimulating Hormone

The functions of anorexigenic neurons secreting proopiomelanocortin (POMC)/alpha-melanocyte-stimulating hormone (α-MSH) of the melanocortin system in the hypothalamus in vertebrates are energy homeostasis, food intake, and body weight regulation. However, the mechanisms remain elusive. This article reports on zebrafish that have been genetically engineered to produce α-MSH mutants, α-MSH−7aa and α-MSH−8aa, selectively lacking 7 and 8 amino acids within the α-MSH region, but retaining most of the other normal melanocortin-signaling (Pomc-derived) peptides. The α-MSH mutants exhibited hyperphagic phenotypes leading to body weight gain, as observed in human patients and mammalian models. The actions of several genes regulating appetite in zebrafish are similar to those in mammals when analyzed using gene expression analysis. These include four selected orexigenic genes: Promelanin-concentrating hormone (pmch), agouti-related protein 2 (agrp2), neuropeptide Y (npy), and hypothalamic hypocretin/orexin (hcrt). We also study five selected anorexigenic genes: Brain-derived neurotrophic factor (bdnf), single-minded homolog 1-a (sim1a), corticotropin-releasing hormone b (crhb), thyrotropin-releasing hormone (trh), and prohormone convertase 2 (pcsk2). The orexigenic actions of α-MSH mutants are rescued completely after hindbrain ventricle injection with a synthetic analog of α-MSH and a melanocortin receptor agonist, Melanotan II. We evaluate the adverse effects of MSH depletion on energy balance using the Alamar Blue metabolic rate assay. Our results show that α-MSH is a key regulator of POMC signaling in appetite regulation and energy expenditure, suggesting that it might be a potential therapeutic target for treating human obesity.

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