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

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

1986 ◽  
Vol 109 (1) ◽  
pp. 15-21 ◽  
Author(s):  
S. A. Burchill ◽  
A. J. Thody ◽  
S. Ito
Keyword(s):  
Dopamine Agonist ◽  
Hair Growth ◽  
Coat Colour ◽  
Tyrosinase Activity ◽  
Melanocyte Stimulating Hormone ◽  
Adult Mice ◽  
Dark Hair ◽  
Golden Yellow ◽  
Dopaminergic Mechanisms ◽  
Yellow Hair

ABSTRACT Skin tyrosinase levels and the eumelanin and phaeomelanin contents of the hair were measured in pubertal and adult C3H–HeA*vy mice that grow dark and golden yellow hair respectively. Hair growth was initiated by plucking and the skin tyrosinase levels, which increased during the growth of new hair and peaked at around 9 days after plucking, were higher during the growth of dark hair in the pubertal mice than during the growth of yellow hair in the adult mice. Although there was only a twofold difference in the phaeomelanin contents of these two types of hair, the dark hair of the pubertal mice contained over 20 times more eumelanin than the golden-yellow hair of the adult mice. These results suggest that the changes in coat colour in C3H–HeA*vy mice are due mainly to changes in eumelanin synthesis by the hair follicular melanocytes and that the production of this pigment requires higher levels of the enzyme tyrosinase than does the production of phaeomelanin. These changes did not appear to be related to plasma α-MSH levels. Nevertheless, administration of α-MSH increased skin tyrosinase activity in the pubertal mice that were growing dark hair and produced a twofold increase in the eumelanin content of the hair. However, it had no such effects in adult mice and also failed to affect the phaeomelanin content of the hair in both groups of mice. In contrast to α-MSH, bromocriptine decreased skin tyrosinase levels and the eumelanin content and increased the phaeomelanin content of the hair in pubertal mice. These effects of bromocriptine were unrelated to plasma immunoreactive α-MSH levels and were not restored when α-MSH was administered together with the dopamine agonist. Although the present results support the idea that α-MSH increases coat darkening in the C3H–HeA*vy mouse through its actions on tyrosinase activity and eumelanin synthesis, it seems that these actions are more dependent on changes at the melanocyte level than changes in circulating α-MSH. The present results further suggest that dopaminergic mechanisms may also play a direct regulatory role in the control of coat colour in this mouse. J. Endocr. (1986) 109, 15–21

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.

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.

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.

Effect of Cyclic AMP and Cyclic GMP on Thromboplastin (Factor III) Synthesis in Human Monocytes In Vitro

1983 ◽  
Vol 50 (04) ◽  
pp. 804-809 ◽  
Author(s):  
Torstein Lyberg
Keyword(s):  
Cyclic Amp ◽  
Cyclic Gmp ◽  
Immune Complexes ◽  
Phosphodiesterase Inhibitors ◽  
Inhibitory Effect ◽  
Intracellular Camp ◽  
Human Monocytes ◽  
Purified Protein Derivative ◽  
A 23187

SummaryHuman monocytes in vitro respond to various agents (immune complexes, lectins, endotoxin, the divalent ionophore A 23187, 12-0-tetradecanoyl-phorbol 13-acetate [TPA], purified protein derivative [PPD] of Bacille Calmette-Guerin) with an increased synthesis of the protein component of thromboplastin. The effect of cyclic AMP and cyclic GMP on this response has been studied. Dibutyryl-cyclic AMP, prostaglandin E1 and the phosphodiesterase inhibitors 3-butyl-1-methyl-xanthine (MIX) and rac -4-(3-butoxy-4-methoxybenzyl)-2-imidazolidinone (Ro 201724), separately and in combination have a pronounced inhibitory effect on the response to immune complexes and PPD, and a moderate effect on the response to endotoxin and lectins. The effect on TPA response and on the response to A 23187 was slight. Dibutyryl-cyclic GMP (1 mM) gave a slight inhibition of the TPA arid IC response, but had essentially no effect on the response to other inducers. The intracellular cAMP level increased when monocytes were incubated with IC, TPA or A 23187 followed by a decrease to basal levels within 1-2 hr, whereas lectin (PHA) and PPD did not induce such changes. The cAMP response to endotoxin varied. Stimulation with IC induced an increase in monocyte cGMP levels, whereas the other stimulants did not cause such changes.

scholarly journals Cellular localization of cyclic AMP and cyclic GMP in rat bone marrow

1979 ◽  
Vol 29 ◽  
pp. 85
Author(s):  
Nobuyoshi Yoshida ◽  
Kohtaro Taniyama ◽  
Chikako Tanaka
Keyword(s):  
Bone Marrow ◽  
Cyclic Amp ◽  
Cyclic Gmp ◽  
Cellular Localization ◽  
Rat Bone
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