Effects Of Melanocyte-stimulating Hormone Research Articles

The Effect of Melanocyte Stimulating Hormone and Hydroxyapatite on Osteogenesis in Pulp Stem Cells of Human Teeth Transferred into Polyester Scaffolds

Presently, tissue engineering is employed in the restoration and repair of tissue defects. Degradable scaffolds, stem cells and stimulating factors are employed in this method. In this study, the effect of melanocyte-stimulating hormone (MSH) and/or hydroxyapatite (HA) on proliferation, osteoblast differentiation, and mineralization of human dental pulp stem cells (hDPSCs) seeded on PLLA-PCL nanofibrous scaffolds was evaluated. For this aim, PLLA-PCL-HA nanofibrous scaffolds were fabricated using electrospinning method. FE-SEM images exhibited that all nanofibers had bead-free morphologies with average diameters ranging from 150–205 nm. Human DPSCs seeded into PLLA-PCL nanofibers were treated with MSH. Cell viability, proliferation, morphology, osteogenic potential, and the expression of tissue-specific genes were assessed by means of MTT assay, FE-SEM, alizarin red S staining, and RT-PCR analysis. hDPSCs exhibited improved adhesion and proliferation capacity on the PLLA-PCL-HA nanofibers treated with MSH compared to other groups (p<0.05). Additionally, PLLA-PCL-HA nanofibers treated with MSH exhibited significantly higher mineralization and alkaline phosphatase activity than other groups. RT-PCR results confirmed that PLLA-PCL-HA nanofibers enriched with MSH could significantly unregulated the gene expression of BMP2, osteocalcin, RUNX2 and DSPP that correlated to osteogenic differentiation (p<0.05). Based on results, incorporation of HA nanoparticles in PLLA-PCL nanofibers and addition of MSH in media exhibited synergistic effects on the adhesion, proliferation, and osteogenesis differentiation of hDPSCs, and therefore assumed to be a favorable scaffold for bone tissue engineering applications.

Endocrinology of osmoregulation and thermoregulation of Australian desert tetrapods: A historical perspective

Many Australian tetrapods inhabit desert environments characterised by low productivity, unpredictable rainfall, high temperatures and high incident solar radiation. Maintaining a homeostatic milieu intérieur by osmoregulation and thermoregulation are two physiological challenges faced by tetrapods in deserts, and the endocrine system plays an important role in regulating these processes. There is a considerable body of work examining the osmoregulatory role of antidiuretic hormones for Australian amphibians, reptiles and mammals, with particular contributions concerning their role and function for wild, free-living animals in arid environments. The osmoregulatory role of the natriuretic peptide system has received some attention, while the role of adrenal corticosteroids has been more thoroughly investigated for reptiles and marsupials. The endocrinology of thermoregulation has not received similar attention. Reptiles are best-studied, with research examining the influence of arginine vasotocin and melatonin on body temperature, the role of prostaglandins in heart rate hysteresis and the effect of melanocyte-stimulating hormone on skin reflectivity. Australian mammals have been under-utilised in studies examining the regulation, development and evolution of endothermy, and there is little information concerning the endocrinology of thermoregulation for desert species. There is a paucity of data concerning the endocrinology of osmoregulation and thermoregulation for Australian desert birds. Studies of Australian desert fauna have made substantial contributions to endocrinology, but there is considerable scope for further research. A co-ordinated approach to examine arid-habitat adaptations of the endocrine system in an environmental and evolutionary context would be of particular value.

Melanocyte-stimulating hormone facilitates hypermelanosis on the non-eyed side of the barfin flounder, a pleuronectiform fish

A pleuronectiform fish, the barfin flounder, Verasper moseri, is promising for aquaculture and resource enhancement in Northern Japan due to its high commercial value. Hypermelanosis of its non-eyed side, which frequently occurs under culture conditions, diminishes its commercial value. Two peptide hormones, melanin-concentrating hormone (MCH) and melanocyte-stimulating hormone (MSH), having opposing actions, are associated with the color changes of fish. We have previously reported the positive effect of MCH in preventing hypermelanosis. Here, we examined the effects of MSH on the occurrence of hypermelanosis. A single injection of Des-Ac-α-MSH [0.01 nmol/g–10 nmol/g (0.016 μg–16 μg/g)] did not change the eyed-side body color, while a single injection of MCH [0.1 nmol/g (0.21 μg/g)] made the eyed-side color paler. No difference was observed in eyed-side lightness between fish injected with MCH (0.1 nmol/g) and those receiving MCH (0.1 nmol/g) and an increased amount of Des-Ac-α-MSH (0.01 nmol/g–10 nmol/g) simultaneously. These results indicate that MSH does not suppress the in vivo body color-paling effects of MCH in barfin flounders. On the other hand, implantation of a cholesterol pellet containing Des-Ac-α-MSH (280 μg, twice at 29-day interval) increased hypermelanosis of the non-eyed side of barfin flounders compared to control fish. Eyed-side bodies of MSH-treated fish were darker than control fish; thus, MSH is involved in morphological color change including ectopic melanin synthesis in non-eyed-side skin.

Effects of Melanocyte-stimulating Hormone on Serum Levels of Thyroid Hormones in Short-term Alloxan-induced Diabetic Rats

Effects of Melanocyte-stimulating Hormone on Serum Levels of Thyroid Hormones in Short-term Alloxan-induced Diabetic Rats

Effects of Melanocyte-stimulating Hormone on Plasma Levels of Testosterone and Estradiol Hormones in Alloxan-Induced Diabetic Rats

Effects of Melanocyte-stimulating Hormone on Plasma Levels of Testosterone and Estradiol Hormones in Alloxan-Induced Diabetic Rats

Effects of Desacetyl-α-MSH on Lipid Mobilization in the Rainbow Trout, Oncorhynchus mykiss

Effects of melanocyte-stimulating hormone (MSH) and beta-endorphin on lipid mobilization were examined in the rainbow trout (Oncorhynchus mykiss). Plasma levels of fatty acid (FA) were measured after intra-arterial administration of alpha-MSH, desacetyl-alpha-MSH, beta-MSH, or beta-endorphin through a cannula in the dorsal aorta. Desacetyl-alpha-MSH at 1 ng/g body weight resulted in an increase in plasma FA levels 1-3 hr after the injection, whereas the other three peptides showed no significant effect at the same dose. There was no significant change in plasma levels of cortisol after administration of any of the peptides. Lipolytic enzyme activity in the liver was significantly increased in a dose-related manner 1 hr after single intra-peritoneal injection of desacetyl-alpha-MSH. The direct effect of desacetyl-alpha-MSH on lipolysis was examined in liver slices incubated in vitro. Lipase activity in the liver slice was stimulated in the medium containing desacetyl-alpha-MSH in a dose-related manner. The results indicate that desacetyl-alpha-MSH is a potent stimulator of lipid mobilization in the rainbow trout.

Experimental metastasis and differentiation of murine melanoma cells: actions and interactions of factors affecting different intracellular signalling pathways.

Various factors that modulate the differentiation of malignant cells are known to affect their experimental metastatic potential (EMP), or lung colonization after intravenous injection into syngeneic animals. However, some results and conclusions on the relation between cell differentiation and metastasis have appeared to conflict. We have reanalysed this by measurement of EMP of B16 melanoma sublines after culture with agents or conditions that acted on differentiation through various intracellular pathways. All tested agents did affect the EMP. EMP was usually positively correlated with differentiation under diverse conditions, but exceptions showed that there is no direct causal connection. Nor could all findings be explained in terms of cell proliferation or expression of major histocompatibility antigens. Some data helped to explain disparities between previous reports. Specific novel findings included the following. The stimulation of EMP by melanocyte-stimulating hormone (MSH) as well as all other tested effects of MSH were prevented by extended exposure to 12-O-tetradecanoyl phorbol acetate (TPA), suggesting a requirement for protein kinase C activity as well as G-protein coupling in MSH action. Cells grown with cholera toxin were always more differentiated than untreated cells, but the EMP could be either markedly increased or markedly decreased by cholera toxin under different conditions. The basic culture medium apparently determined this striking reversal. The EMP was also significantly affected by the extracellular pH.

Melanin biosynthesis patterns following hormonal stimulation.

The effect of melanocyte-stimulating hormone (MSH) on the differentiation of mammalian melanocytes has been widely studied since the early 1950s. There have been many reports about the stimulatory effect of MSH on melanin production and specifically on the activity of tyrosinase, the critical enzyme in the melanogenic pathway. However, few and variable results have been obtained concerning the effect of this hormone on the regulation of DOPAchrome tautomerase (TRP2), another melanogenic enzyme which functions later in the melanogenic pathway, or on other melanogenic activities, such as TRP1. In this study, we show that the MSH-induced stimulation of tyrosinase is accompanied by no significant change in the synthesis or catalytic activities of other melanogenic enzymes such as TRP1 or TRP2. This in turn elicits a dramatic increase in melanin production accompanied by a significant decrease in the incorporation of carboxylated precursors into that melanin biopolymer, although the biological implication of that is still unclear.

Effects of melanocyte-stimulating hormone on tyrosinase expression and melanin synthesis in hair follicular melanocytes of the mouse.

Tyrosinase mRNA, synthesis and activity were measured in the skin during the first 2 weeks of life of C3H-HeAvy mice. Tyrosinase mRNA levels were found to peak on days 3-4 and were followed by increases in tyrosinase synthesis and activity which peaked on days 6-7 and 7-8 respectively. These changes in tyrosinase expression were presumably associated with the growth of the first coat of hair that in neonatal C3H-HeAvy mice is yellow in colour as a result of the increased proportion of phaeomelanin. By the time hair growth had ceased there was no expression of tyrosinase at both mRNA and protein levels. Daily administration of alpha-melanocyte stimulating hormone (alpha-MSH) enhanced the expression of tyrosinase mRNA transcripts, tyrosinase synthesis and activity. The increase in tyrosinase activity paralleled the change in the amount of tyrosinase, suggesting that the primary action of alpha-MSH is to stimulate new synthesis of the enzyme. This induction of tyrosinase was associated with the growth of hair that was darker in colour than that of the controls and contained an increased proportion of eumelanin. This increase in eumelanin reflected a decrease in phaeomelanin content. It was concluded that, through its actions on the enzyme tyrosinase, alpha-MSH is able to switch the synthesis of phaeomelanin to that of eumelanin in hair follicular melanocytes.

Differentiation and the tumorigenic and metastatic phenotype of murine melanoma cells

Using B16 F10 murine melanoma cells and sublines generated from the JB/MS melanoma which exhibit various degrees of melanogenesis, the relationships among differentiation, tumorigenicity, and metastatic potential were examined. The effect of melanocyte-stimulating hormone (MSH), which specifically stimulates differentiation of melanocytes, was also studied. All melanoma lines tested were capable of growing as experimental pulmonary metastases but, surprisingly, the undifferentiated and amelanotic JB/MS-w cells failed to grow as primary subcutaneous tumors. JB/MS-w cells, which had few surface MSH receptors, did not respond to MSH with an increase in melanin production, unlike the other cell lines. Although in vitro treatment with MSH did not change the rates of growth of primary tumors by these cell lines, such treatment decreased the number of pulmonary metastases from B16 F10, JB/MS cells, JB/MS-b1 cells and JB/MS-w cells. Conversely, MSH treatment significantly increased the rates of pulmonary metastases from JB/MS-p cells. The expression of surface melanoma antigens, urokinase-type plasminogen activity and susceptibility to natural killer cells were examined. MSH did not significantly alter surface melanoma antigen expression, but increased the natural killer cell susceptibility of B16 F10, JB/MS and JB/MS-b1 cells, cells which possess abundant surface MSH receptors. There was an inverse correlation between differentiation (pigmentation) and proliferation in vitro, and the more pigmented melanoma cells (B16 F10, JB/MS and JB/MS-b1) expressed relatively lower levels of class-I MHC, relatively higher levels of class-II MHC and the highest metastatic capacity. These results demonstrate that MSH possesses the capacity to regulate not only melanogenesis, but also other factors critical to the metastatic growth of the cells.

Stimulation of Follicular Melanogenesis in the Mouse by Topical and Injected Melanotropins

The effects of melanocyte-stimulating hormone (alpha-MSH) and related analogs on follicular melanogenesis in the mouse (C57BL/6JA gamma) were studied. [Nle4, D-Phe7]-alpha-MSH and the related fragment analogues Ac-[Nle4, D-Phe7]-alpha-MSH4-11-NH2 and Ac-[Nle4, D-Phe7]-alpha-MSH4-10-NH2, stimulated the conversion of pheomelanogenesis to eumelanogenesis when subcutaneously injected at concentrations 100-fold lower than the native hormone, alpha-MSH. In addition, the melanotropin analogs stimulated follicular eumelanogenesis when applied topically to the skin of mice. The melanotropins were transdermally delivered to the systemic circulation as evidenced by the fact that eumelanogenesis was stimulated in hair follicles in areas distant from the site of topical application. These results demonstrate that peptide hormone analogs can be transported across the skin. The unique actions of the melanotropin analogs may relate to the fact that these peptides are nonbiodegradable and thus exert prolonged actions on melanocytes. These compounds may prove important for studies on normal integumental melanogenesis and for the treatment of hypopigmentary disorders in humans.

Effects of melanocyte-stimulating hormone and epinephrine on proliferating melanophores of bullfrog tadpole in vitro

All melanophores of bullfrog tadpoles in in vitro nonsynchronously proliferating populations showed melanin dispersion by the addition of melanocyte-stimulating hormone (MSH) or epinephrine. The cells before mitosis (in G 2 phase), after mitosis (in G 1 phase), and synthesizing DNA (S phase) showed the responses. It was concluded that MSH and epinephrine receptor were available in all phases of the cell cycle, and the machinery for melanosome translocation was also available in all phases of the cell cycle except M phase.

Possible interaction of melanocyte-stimulating hormone (MSH) and the pineal in the control of territorial aggression in mice

The fighting of male mice (TO), housed in groups (3 + 3), was observed and a group aggression score (attacks/latency) recorded. There was no significant difference between the scores of untreated and saline injected groups. Pinealectomy (PX) and MSH injections (100 μg/kg IP) potentiated fighting, and raised the aggressiveness of PX groups to control level. Combined injections of MSH + MT increased aggressive behaviour to the same extent as did MT alone. MSH + PX treatment did not suggest that the two anti-aggressive treatments were additive: these groups fought less than controls, but not less than after either treatment alone. Sham operated (SO) groups fought as much as the MT injected ones, and MSH reduced this response to control levels. No consistent pattern was found in the effects of the treatments on open field activity, tail-pinch responding, or body, adrenal and testicular weights. The results support the hypothesis that the anti-aggressive effect of MSH is due to inhibition of pineal MT secretion. The increased aggressiveness shown by SO groups is assumed to be caused by leakage of MT from a partially damaged pineal.

Behavioral effects of melanocyte stimulating hormone

Consideration of the isolation, structure, localization, and biological actions of melanocyte stimulating hormone are followed by a review of its behavioral effects. Evidence pertaining to various hypotheses offered in explanation of these behavioral effects is examined and evaluated. It is concluded that MSH affects the neurophysiological processes that give rise to the phenomena which include the concept of attention.

Effects of melanocyte-stimulating hormone (MSH) and melatonin on passive avoidance and on an emotional response

The present experiment investigated the opposite effects of synthetic α-MSH and Melatonin on acquisition and extinction of a passive avoidance response (PAR) and on emotionality, as indexed by defecation, in the PA box. It was found that intraperitoneal (IP) administration of α-MSH delayed extinction and increased defecation responses whereas IP administration of Melatonin facilitated extinction of the PAR and decreased defecation. The present experiment confirmed MSH-Melatonin opposition on memory and on the defecation response.

Effects of melanocyte stimulating hormone and theophylline on human melanocytes in vitro

The effects of MSH on the human melanocyte in vitro were studied. The addition of MSH up to the concentration of 40 mug/ml into the culture medium did not produce appreciable change on the morphology of the melanocyte. The melanocyte, however, responded to the simultaneous addition of MSH and theophylline with marked increase in the length and complexity of the dendritic process. Melanin synthesis, as indicated by the uptake of tyrosine in the presence of an inhibitor of protein synthesis, was remarkably activated by the simultaneous addition of MSH and theophylline. MSH alone activated the melanin synthesis only slightly, but the increase in the uptake of tyrosine was significant statistically. These results were discussed in terms of the MSH-cyclic AMP cascade in which theophylline worked as an inhibitor of cyclic AMP phosphodiesterase, and increased the intracellular level of cyclic AMP by inhibiting catabolism of cyclic AMP.

Cholera toxin mimics melanocyte stimulating hormone in inducing differentiation in melanoma cells.

Cholera toxin (choleragen) and melanocyte stimulating hormone alter within hours the morphology of melanoma cells in culture, and they slow the growth of serum-stimulated cells. After 7-10 days, cells exposed to choleragen or hormone show increased size and a fibroblastic growth pattern. Tyrosinase (EC 1.14.18.1; monophenol monooxygenase) activity increases after 3 days in the presence of 10(-8) M hormone or 10(-10) M choleragen. Binding studies with (125)I-labeled choleragen indicate that although a melanoma cell can bind a maximum of 10(6) molecules of cholera toxin, only about 4000 binding sites must be occupied to achieve maximum stimulation of tyrosinase activity. Melanocyte stimulating hormone and choleragen probably have different membrane-binding sites. After exposure to choleragen for 5 min, membrane adenylate cyclase (EC 4.6.1.1) activity increases dramatically upon further incubation of intact cells for several hours at 37 degrees and falls slowly to basal values over a period of more than 10 days. Hormone stimulation of adenylate cyclase is rapidly reversed by washing the cells, but subsequent restimulation of cyclase by the hormone is impaired. These studies indicate that cAMP mediates the effects of melanocyte stimulating hormone on growth and morphology as well as on tyrosinase activity. Cholera toxin may permanently activate the available adenylate cyclase molecules, and the protracted decay of stimulation that follows may reflect the biological turnover of adenylate cyclase molecules in these cells.

Response of mouse melanoma cells to melanocyte stimulating hormone.

WE have recently described a mouse melanoma cell line which responds to melanocyte stimulating hormone (MSH) with dramatic increases in tyrosinase activity and melanin content, as well as changes in cellular morphology and growth characteristics1–3. The increase in pigmentation following exposure to MSH is shown in Fig. 1. Cyclic AMP or dibutyryl cyclic AMP may be substituted for MSH in eliciting these responses; consistent with other work suggesting that MSH acts through cyclic AMP in the control of pigmentation in vertebrates4–7. In our previous studies we used non-synchronised mouse melanoma cells grown in monolayer culture. Martin et al.8 have shown that synchronised mouse HTC cells respond to corticosteroids with increased tyrosine amino transferase synthesis in the late Gl and early S periods of the cell cycle; similarly, Buell and Fahey9 have shown, using a synchronised human lymphoid cell line, that immunoglobulins G and M are expressed in late Gl and S. We wished to investigate the effects of MSH on tyrosinase activity and endogenous cyclic AMP levels in synchronised cells to determine if there is a particular hormone-sensitive phase of the melanoma cell cycle. We report here that melanoma cells responded maximally to MSH with increased tyrosinase activity and cyclic AMP content during the G2 phase.

General activity in intact and hypophysectomized rats after administration of melanocyte-stimulating hormone (MSH), melatonin, and Pro-Leu-Gly-NH 2

The effects of melanocyte-stimulating hormone (MSH), melatonin, and Pro-Leu-Gly-NH 2 on levels of general locomotor activity were investigated in hypophysectomised and intact rats. General activity was not altered by the hormones studied. Body weight, food ingestion, and water intake were also measured and found to be unchanged. The findings reduce the possibility that alterations in activity account for the behavioral changes previously observed after administration of MSH, melatonin, or Pro-Leu-Gly-NH 2.

Behavioral Aspects of Melanocyte-Stimulating Hormone (MSH)

Publisher Summary This chapter explores the behavioral aspects of melanocyte-stimulating hormone (MSH). The pituitary hormone MSH is tested in several different behavioral systems. MSH is a hormone(s) whose presence has persisted in the pituitary gland of vertebrates from very low forms to man. The primary function of MSH in higher mammals no longer seems to be pigmentary, but this is not sufficient reason to assume that MSH has no role in mammals or that the effects of MSH can be ascribed to corticotrophin (ACTH). Although MSH is known to play a vital role in amphibians such as the frog, an important function for MSH in mammals such as the rat is not well recognized. The frog better adapts to the environment by changing the color of its skin, an effect mediated by MSH. Extra-pigmentary effects of MSH upon bodily processes other than the central nervous system (CNS) are described by several investigators, including ourselves. It is speculated that during the course of evolution, MSH has maintained its “adaptive” value for the organism, but that this may apply only to simple tasks. The conclusion is reached that in mammals MSH exhibits definite extra-pigmentary actions upon behavior.