MSH inhibits growth in a line of amelanotic hamster melanoma cells and induces increases in cyclic AMP levels and tyrosinase activity without inducing melanogenesis

1989 ◽  
Vol 92 (4) ◽  
pp. 551-559
Author(s):  
A. Slominski ◽  
G. Moellmann ◽  
E. Kuklinska
Keyword(s):  
Cyclic Amp ◽  
Cyclic Gmp ◽  
Melanoma Cells ◽  
Amelanotic Melanoma ◽  
Tyrosinase Activity ◽  
Melanin Synthesis ◽  
Melanocyte Stimulating Hormone ◽  
Inhibit Cell Growth ◽  
Hamster Melanoma ◽  
Peak Increase

In Bomirski Ab amelanotic hamster melanoma cells, L-tyrosine and/or L-dopa induce increases in tyrosinase activity as well as synthesis of melanosomes and melanin. L-tyrosine also modifies melanocyte-stimulating hormone (MSH) binding. In this paper we show that in the Bomirski amelanotic melanoma system MSH and agents that raise intracellular cyclic AMP induce dendrite formation, inhibit cell growth, and cause substantial increases in tyrosinase activity without inducing melanin synthesis. Tyrosinase activity is detected only in broken cell preparations, or cytochemically in fixed cells. In the continued absence of mature melanosomes, the induced enzyme remains in elements of the trans-Golgi reticulum. Comparative measurements of cyclic AMP in amelanotic and tyrosine-induced melanotic cells show similar basal levels. L-tyrosine and L-dopa have little or no effect, whereas MSH may cause a 1000% peak increase in cyclic AMP levels both in amelanotic and melanotic cells. None of these agents influences cyclic GMP or inositol trisphosphate (InsP3) levels. In agreement with the InsP3 assays, phorbol ester (TPA) has no effect on melanization, tyrosinase activity or cell proliferation. In conclusion, in the Bomirski amelanotic melanoma, MSH induces only partial cell differentiation associated with raised levels of cyclic AMP. Induction of melanosome synthesis and melanization by L-tyrosine or L-dopa appear to follow pathways unrelated to cyclic AMP, cyclic GMP or InsP3.

Melanocyte-stimulating hormone and the regulation of tyrosinase activity in hair follicular melanocytes of the mouse

1986 ◽  
Vol 111 (2) ◽  
pp. 225-232 ◽  
Author(s):  
S. A. Burchill ◽  
A. J. Thody
Keyword(s):  
Cyclic Amp ◽  
Cyclic Gmp ◽  
Hair Growth ◽  
Yellow Pigment ◽  
Tyrosinase Activity ◽  
Melanocyte Stimulating Hormone ◽  
Golden Yellow ◽  
Skin Explants ◽  
Low Levels ◽  
Old Mice

ABSTRACT Skin tyrosinase activity increases during hair growth in C3H–HeA*vy mice and reaches higher levels in young (30- to 35-day-old) mice when the hair follicular melanocytes synthesize the black pigment, eumelanin, than in older (6-month-old) mice when they produce the golden yellow pigment, phaeomelanin. To examine the regulation of the melanocytes at these different stages we have compared the effect of α-MSH and other agents that act, through cyclic AMP-dependent mechanisms, on skin tyrosinase activity in both young and old mice during hair growth, initiated by plucking. Daily administration of α-MSH, isoprenaline or theophylline increased coat darkness, and skin tyrosinase activity in the younger mice 7–9 days after plucking, but they were ineffective in the older mice. Similarly α-MSH, 8-bromo-cyclic AMP or theophylline increased tyrosinase activity in skin explants from the younger mice incubated for up to 24 h but had no effect in explants from older mice. Cyclic GMP had no effect on tyrosinase activity in skin explants from both young and old mice. It is suggested that whereas cyclic AMP-dependent mechanisms may operate to regulate tyrosinase activity in the hair follicular melanocytes of younger mice that produce eumelanin these systems may not operate in the older mice when these melanocytes synthesize phaeomelanin. Phaeomelanin synthesis, unlike that of eumelanin, may not depend upon tyrosinase and its regulation by cyclic AMP and this could explain the low levels of this enzyme in the skin and its failure to respond to α-MSH and other activators of the cyclic AMP system during periods of phaeomelanin production. J. Endocr. (1986) 111, 225–232

INTERACTION OF α-MELANOCYTE-STIMULATING HORMONE, MELATONIN, CYCLIC AMP AND CYCLIC GMP IN THE CONTROL OF MELANOGENESIS IN HAIR FOLLICLE MELANOCYTES IN VITRO

1981 ◽  
Vol 90 (1) ◽  
pp. 89-96 ◽  
Author(s):  
BRIAN WEATHERHEAD ◽  
ANN LOGAN
Keyword(s):  
Cyclic Amp ◽  
Cyclic Gmp ◽  
Phosphodiesterase Inhibitors ◽  
Hair Follicles ◽  
Tyrosinase Activity ◽  
Melanin Production ◽  
Melanocyte Stimulating Hormone ◽  
Dependent Mechanism ◽  
Stimulating Hormone

In short-term (48 h) cultures of hair follicles α-melanocyte-stimulating hormone (α-MSH) and cyclic AMP stimulated melanogenesis through an increase in tyrosinase activity. In contrast cyclic GMP mimicked the effects of melatonin by inhibiting melanin production without causing a concomitant decrease in tyrosinase activity. Both cyclic GMP and melatonin blocked the stimulatory effects of cyclic AMP and α-MSH on melanin production but they left the increased levels of tyrosinase activity unaffected. Phosphodiesterase inhibitors (3-isobutyl-1-methylxanthine and papaverine) simultaneously stimulated tyrosinase activity and inhibited melanin production, presumably by allowing endogenous cyclic AMP and cyclic GMP to accumulate intracellularly. It is suggested that whereas MSH stimulates melanogenesis through a cyclic AMP-dependent mechanism there must also be an inhibitory cyclic GMP-dependent mechanism, perhaps activated by melatonin, which operates at some post-tyrosinase step in the melanin biosynthetic pathway.

MSH binding in bomirski amelanotic hamster melanoma cells is stimulated by L-tyrosine

1987 ◽  
Vol 7 (12) ◽  
pp. 949-954 ◽  
Author(s):  
Andrzej Slominski ◽  
John Pawelek
Keyword(s):  
Culture Medium ◽  
De Novo ◽  
Binding Capacity ◽  
Fold Increase ◽  
Insulin Binding ◽  
Melanoma Cells ◽  
Amelanotic Melanoma ◽  
Tyrosinase Activity ◽  
Regulatory Pathways ◽  
Hamster Melanoma

Bomirski Ab amelanotic melanoma cells have recently been shown to undergo striking phenotypic changes when precursors of the melanogenic pathway, L-tyrosine and L-dopa, are added to the culture medium. The changes include increased tyrosinase activity and de novo synthesis of melanosomes and melanin. L-tyrosine and L-dopa appeared to elicit these responses through separate but overlapping regulatory pathways. Here we show an additional effect of L-tyrosine: stimulation of MSH binding capacity. Cells cultured for 24–48 hours in the presence of 200 μM L-tyrosine display a 3–4 fold increase in their ability to bind125l-β-MSH. L-dopa did not stimulate MSH binding under the same conditions. In control experiments neither L-tyrosine nor L-dopa had any effect on insulin binding. The amelanotic cells respond to MSH with increased dendrite formation, increased tyrosinase activity without melanin production, and decreased growth rate.

scholarly journals The Organogermanium Compound THGP Suppresses Melanin Synthesis via Complex Formation with L-DOPA on Mushroom Tyrosinase and in B16 4A5 Melanoma Cells

2019 ◽  
Vol 20 (19) ◽  
pp. 4785
Author(s):  
Junya Azumi ◽  
Tomoya Takeda ◽  
Yasuhiro Shimada ◽  
Hisashi Aso ◽  
Takashi Nakamura
Keyword(s):  
Gene Expression ◽  
Kojic Acid ◽  
Biological Activities ◽  
Melanoma Cells ◽  
Tyrosinase Activity ◽  
Melanin Synthesis ◽  
Mushroom Tyrosinase ◽  
Melanin Production ◽  
Organogermanium Compound ◽  
Or Gene

The organogermanium compound 3-(trihydroxygermyl)propanoic acid (THGP) has various biological activities. We previously reported that THGP forms a complex with cis-diol structures. L-3,4-Dihydroxyphenylalanine (L-DOPA), a precursor of melanin, contains a cis-diol structure in its catechol skeleton, and excessive melanin production causes skin darkening and staining. Thus, the cosmetic field is investigating substances that suppress melanin production. In this study, we investigated whether THGP inhibits melanin synthesis via the formation of a complex with L-DOPA using mushroom tyrosinase and B16 4A5 melanoma cells. The ability of THGP to interact with L-DOPA was analyzed by 1H-NMR, and the influence of THGP and/or kojic acid on melanin synthesis was investigated. We also examined the effect of THGP on cytotoxicity, tyrosinase activity, and gene expression and found that THGP interacted with L-DOPA, a precursor of melanin with a cis-diol structure. The results also showed that THGP inhibited melanin synthesis, exerted a synergistic effect with kojic acid, and did not affect tyrosinase activity or gene expression. These results suggest that THGP is a useful substrate that functions as an inhibitor of melanogenesis and that its effect is enhanced by combination with kojic acid.

An In-Vitro Assay Estimating Changes in Melanin Content of Melanoma Cells due to Ultra-Dilute, Potentized Preparations

Homeopathy ◽  
2019 ◽  
Vol 108 (03) ◽  
pp. 183-187 ◽  
Author(s):  
Renuka Munshi ◽  
Samidha Joshi ◽  
Gitanjali Talele ◽  
Rajesh Shah
Keyword(s):  
In Vitro Study ◽  
Melanoma Cells ◽  
Tyrosinase Activity ◽  
Melanin Content ◽  
B16f10 Melanoma ◽  
Vitro Assay ◽  
Melanocyte Stimulating Hormone ◽  
B16f10 Melanoma Cells ◽  
Physiological Dose

Introduction The authors had previously conducted an in-vitro study to observe the effect of homeopathic medicines on melanogenesis, demonstrating anti-vitiligo potential by increasing the melanin content in murine B16F10 melanoma cells. A similar experiment was performed using further homeopathic preparations sourced from kojic acid (KA), hydrogen peroxide (H2O2; HP), 6-biopterin (BP), and [Nle4, D-Phe7]-α-melanocyte-stimulating hormone (NLE), some of which are known to induce vitiligo or melano-destruction at physiological dose. Materials and Methods The homeopathic preparations of BP, KA, NLE, and HP were used in 30c potency. Alcohol and potentized alcohol were used as vehicle controls. Prior to starting the main experiment, the viability of B16F10 melanoma cells after treatment with study preparations was assayed. Melanin content (at 48 h and 96 h) and tyrosinase activity in melanocytes were determined. Results At the end of 48 hours, NLE and HP in 30c potency had a significantly greater melanin content (p = 0.015 and p = 0.039, respectively) compared with controls; BP and KA in 30c potency had no significant effects. No significant changes were seen at the end of 96 hours. KA, NLE, HP, and vehicle controls showed an inhibition of tyrosinase activity. Conclusion The study demonstrated melanogenic effects of two homeopathic preparations. Further research to evaluate the therapeutic efficacy of these medicines is warranted.

Effect of apigenin-7-glucoside, genkwanin and naringenin on tyrosinase activity and melanin synthesis in B16F10 melanoma cells

Life Sciences ◽  
2016 ◽  
Vol 144 ◽  
pp. 80-85 ◽  
Author(s):  
Nouha Nasr Bouzaiene ◽  
Fadwa Chaabane ◽  
Aicha Sassi ◽  
Leila Chekir-Ghedira ◽  
Kamel Ghedira
Keyword(s):  
Melanoma Cells ◽  
Tyrosinase Activity ◽  
Melanin Synthesis ◽  
B16f10 Melanoma ◽  
B16f10 Melanoma Cells

ABILITY OF VARIOUS FACTORS TO OPPOSE THE STIMULATORY EFFECT OF DIBUTYRYL CYCLIC AMP ON THE RELEASE OF MELANOCYTE-STIMULATING HORMONE BY THE RAT PITUITARY IN VITRO

1976 ◽  
Vol 68 (2) ◽  
pp. 283-287 ◽  
Author(s):  
BRIDGET I. BAKER
Keyword(s):  
Cyclic Amp ◽  
Cyclic Gmp ◽  
Inhibitory Effect ◽  
Aminobutyric Acid ◽  
Intermediate Lobe ◽  
Dibutyryl Cyclic Amp ◽  
Melanocyte Stimulating Hormone ◽  
Rat Pituitary ◽  
Stimulating Hormone

SUMMARY Various agents were tested for their ability to oppose the stimulatory effect of dibutyryl cyclic AMP on the release of the melanocyte-stimulating hormone from the rat neuro-intermediate lobe in vitro. Only dopamine exhibited an inhibitory effect; serotonin, γ-aminobutyric acid, tocinoic acid, tocinamide, the tripeptide Pro-Leu-Gly-NH2 and dibutyryl cyclic GMP were all ineffective.

Stimulation of tyrosinase in human melanocytes by pro-opiomelanocortin-derived peptides

1995 ◽  
Vol 146 (3) ◽  
pp. 439-447 ◽  
Author(s):  
S D McLeod ◽  
C Smith ◽  
R S Mason
Keyword(s):  
Extracellular Matrix ◽  
Corneal Endothelium ◽  
Adrenocorticotropic Hormone ◽  
Test System ◽  
Tyrosinase Activity ◽  
Melanin Synthesis ◽  
Melanocyte Stimulating Hormone ◽  
Kinase C ◽  
Human Melanocytes ◽  
Stimulation Of

Abstract Human melanocytes, maintained on bovine corneal endothelium-derived extracellular matrix for at least 4 days in the absence of phorbol 12-myristate 13-acetate (PMA) and cholera toxin (CT), displayed increased tyrosinase activity when exposed to several pro-opiomelanocortinderived (POMC) peptides. Melanocytes from 9 of 14 donors showed significantly increased tyrosinase activity after treatment with adrenocorticotropic hormone (ACTH; mean increase 320±107 (s.e.m.)% of control, P<0·005), while melanocytes from 8 of 13 donors increased tyrosinase in the presence of diacetyl-melanocyte stimulating hormone (di-MSH; mean increase 223±31 (s.e.m.)% of control, P<0·005). Maximal increases in tyrosinase were seen after treatment with 10−10 m ACTH and with 10−6 m di-MSH. In two cell cultures which showed tyrosinase stimulation, melanin synthesis was similarly increased in the presence of added POMC peptides. PMA but not CT increased tyrosinase activity in melanocytes cultured under these conditions. In the presence of staurosporine, an inhibitor of protein kinase C (PKC), the magnitude of the increase in tyrosinase due to PMA, ACTH and di-MSH was significantly reduced. These results indicate that tyrosinase activity in melanocytes from most human donors, under appropriate conditions, is susceptible to the stimulatory effects of POMC peptides, that ACTH is considerably more potent than di-MSH in this test system and that in human cells the PKC pathway may be important in modulating melanogenesis. Journal of Endocrinology (1995) 146, 439–447

Sign in / Sign up

Export Citation Format

Share Document