Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01189 (beta-endorphin)
 21,003 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

alpha-MSH was found to decrease the recently characterized dopachrome tautomerase activity in cultures of B16/F10 mouse melanoma cells. Other stimulating agents of melanogenesis, like dibutyryl cyclic AMP, 3-isobutyl-1-methylxanthine, theophylline, retinol, and retinoic acid, caused the same effect. The grade of inhibition depended on the nature of the agent and the time of exposure. In all cases, both melanin production and tyrosinase activity were activated by these treatments, although the grade of tyrosine hydroxylase and dopa oxidase stimulation was different. Moreover, no correlation among the intensities of dopachrome tautomerase inhibition and tyrosinase activation by the tested agents could be obtained. The significance of these results in the regulation of mammalian melanogenesis is discussed.
J Invest Dermatol 1992 Oct
PMID:Alpha-MSH and other melanogenic activators mediate opposite effects on tyrosinase and dopachrome tautomerase in B16/F10 mouse melanoma cells. 132 99

Although alpha-MSH increases skin darkening in humans, there are several reports that it fails to have melanogenic effects on human melanocytes in vitro. The purpose of this study was to see whether cultured human melanocytes express MSH receptors. Human melanocytes were grown in the absence of artificial mitogens such as 12-O-tetradecanoyl phorbol-13-acetate (TPA) and cholera toxin (CT) and incubated for 2 h at room temperature with increasing amounts of 125I-labelled Nle4DPhe7-alpha-MSH with and without excess cold peptide. Binding was saturable and specific: Scatchard analysis gave a Kd of 4.9 x 10(-11) M and approximately 700 binding sites/cell. Human keratinocytes and fibroblasts showed no specific binding. The addition of 1 mM dibutyryl cAMP to the culture medium caused a 62% increase in MSH binding to human melanocytes. A smaller increase (25%) was seen with 10(-9) M CT while 25 mM TPA caused a 24% decrease. These results show that human melanocytes in culture express MSH receptors and that this expression can be modulated by mitogens.
Arch Dermatol Res 1992
PMID:The expression of functional MSH receptors on cultured human melanocytes. 133 93

According to the present state of findings there are melanocyte-stimulating hormones (MSH) alpha, beta, gamma and delta with hormone alpha-MSH special physiological importance for man. Our study of special literature shows that the secretion of MSH is affected by exogene factors, different biorhythms and some diseases. Numerous investigation with melanocytes and melanoma cell cultures clearly show the impact of MSH on the function, regulation and the proliferation of pigment cells. The results presented contribute to the discussion of possibilities of improving diagnostics or therapy of malignant melanoma.
Dermatol Monatsschr 1990
PMID:[Importance and function of the melanocyte-stimulating hormone in malignant melanoma. Importance of MSH]. 196 35

The extent to which alpha melanocyte-stimulating hormone (MSH) is a true in vivo regulator of melanogenesis in mice is unknown. The objective of this study was to determine if MSH-induced eumelanogenesis in hairbulb melanocytes of yellow (Ay/a) mice mimics the natural program of eumelanogenesis occurring in genetically black (a/a) hairbulb melanocytes. We conducted quantitative transmission electron microscopy on melanosome differentiation within MSH-treated regenerating 9-d hairbulbs of Ay/a and a/a mice. Results of exogenous alpha-MSH injections (5 d at 0.15 mM MSH) showed that the striking visual darkening of hair was accompanied by an incomplete transformation of phaeo- to eumelanogenesis. Ontogenetic data on developmental stages I-IV of 3678 melanosomes based on geometric considerations (length, width, shape, and area) showed that MSH did not induce a complete transformation from spherical phaeomelanosomes to elliptical eumelanosomes. Also, observations on the number of vesiculoglobular bodies and matrix organization reveled that MSH-treated Ay/a melanosomes retained distinct features of phaeomelanogenesis even after 5 d of MSH treatment. Thus, MSH induced a partial but incomplete pattern of eumelanogenesis in regenerating hairbulb melanocytes of Ay/a mice. The continued investigation of the dynamics of melanin synthesis in MSH-induced Ay/a mice melanocytes possessing "mosaic" melanosomes could be productive in understanding fundamental relationships between tyrosinase activity, matrix function, matrix structure, and regulation of melanin (phaeo- and/or eumelanin) synthesis.
J Invest Dermatol 1991 Jan
PMID:Effects of exogenous MSH on the transformation from phaeo- to eumelanogenesis within C57BL/6J-Ay/a hairbulb melanocytes. 198 99

The role of melanocyte stimulating hormone (MSH) as a mediator of the melanogenic response to ultraviolet radiation (UVR) was examined in C57 BL/6 mice. While exposure to UVR (250-300 nm) for 7, 14 and 27 days increased tyrosinase activity in epidermal melanocytes of the ear MSH had no effect and failed to alter the response to UVR. Plasma alpha-MSH concentrations were unchanged following UVR. Theophylline, a phosphodiesterase inhibitor, also had no effect on epidermal tyrosinase activity in non-irradiated and UV irradiated mice. Prostaglandin E2 and arachidonic acid were also ineffective in non-irradiated and UV irradiated mice and indomethacin, an inhibitor of prostaglandin synthesis, failed to increase epidermal tyrosinase activity after UVR. On the other hand, 12-0-tetradecanoyl phorbol 13 acetate, an activator of protein kinase C, increased epidermal tyrosinase activity in non-irradiated mice and also enhanced the effect of UVR.
J Dermatol Sci 1990 Jul
PMID:The effect of ultraviolet radiation and melanocyte-stimulating hormone on tyrosinase activity in epidermal melanocytes of the mouse. 212 69

A superpotent analogue of alpha-MSH, (Nle4,D-Phe7)-alpha-MSH, when applied topically to mice induces darkening of follicular melanocytes throughout the skin. In vitro studies have demonstrated delivery of the peptide across mouse but not rat skin. This variation in permeability of skin of animal models prompted us to use human skin in vitro. The melanotropin was applied to the surface of human skin samples through a permeation apparatus and allowed to penetrate for 24 h at 36 degrees C. Passage of the analogue was shown by both bioassay and radioimmunoassay. These assays correlated well and demonstrated both the presence and the biologic integrity of the peptide after transdermal passage. Regional differences were noted in the degree of transdermal penetration. In addition, split thickness skin allowed greater penetration suggesting dermal binding of the hormone. This study is the first to show that a melanotropic peptide can be delivered transdermally through human skin in vitro. This has potential importance in the development of therapies for hypopigmentary disorders and for the stimulation of skin tanning without ultraviolet light.
J Invest Dermatol 1990 Apr
PMID:In vitro transdermal delivery of a melanotropic peptide through human skin. 215 69

Tyrosinase synthesis and its regulation in human melanocytes was studied by measuring the incorporation of [35S] methionine into incubated skin biopsies. Tyrosinase was detected in all skin samples with the highest levels in skin type IV and the lowest levels in skin type I. Following psoralen ultraviolet A (PUVA) therapy for several weeks, significant increases in the amounts of tyrosinase were found in skin types III and IV. The presence of alpha-melanocyte-stimulating hormone (alpha-MSH) (100 mumol/l) or the long-acting analogue [Nle4, DPhe7] alpha-MSH (1-10 mumol/l) in the incubation medium failed to alter tyrosinase levels in the skin biopsies taken from patients both before and after receiving PUVA therapy. Bromo-adenosine 3,5-cyclic monophosphate sodium salt (8-bromo-cAMP) (10 mmol/l), on the other hand, increased the amounts of tyrosinase both before and after PUVA, but these effects were only seen in biopsies of type III and IV skin. These results indicate that MSH fails to stimulate tyrosinase synthesis in human melanocytes. Nevertheless, tyrosinase synthesis and its regulation by cyclic AMP-dependent mechanisms could be important control points in the pigmentary response.
J Invest Dermatol 1990 Nov
PMID:Tyrosinase synthesis in different skin types and the effects of alpha-melanocyte-stimulating hormone and cyclic AMP. 217 91

The release of neuropeptides, such as substance P (SP) and somatostatin (SOM), from primary sensory nerve fibers has been implicated in the modulation of local immune responses in surface tissues, such as the skin, the pulmonary airways, and the gastrointestinal mucosa. We have investigated the influence of six neuropeptides substance P (SP), somatostatin (SOM), substance K (SK), vasoactive intestinal peptide (VIP), bombesin (BOM), and adrenocorticotropic hormone (ACTH) on the proliferation of resting and partially stimulated human peripheral blood mononuclear leukocytes (PBMLs) and T lymphocytes. Neuropeptides in concentrations from 10(-7) to 10(-12) M were added to either resting or partially stimulated cells [interleukin-2 (IL-2), concanavalin A (Con A), and phytohemagglutinin (PHA)]. Cellular proliferation was assessed by incorporation of 3H-thymidine after 72 h. With the exception of SP, no significant effect of any of these neuropeptides on 3H-thymidine incorporation was found. In resting cells, 10(-9) MSP elicits an 80...maximal increase of 3H-thymidine incorporation, whereas no statistically significant effect on partially stimulated leukocytes was found. These results contradict a previous report on a significant mitogenic effect of SP on partially stimulated T cells. Considering the very minimal effect of SP on resting cells and, particularly, the absence of an effect on partially stimulated cells, we would question a significant modulatory role for SP and the five other neuropeptides in the proliferation of immunocompetent cells in skin.
Arch Dermatol Res 1988
PMID:Effect of neuropeptides present in skin on the proliferation of human peripheral blood mononuclear cells and T cells. 246 35

Radioimmunologic examination of the hypophyseo-adrenal system in patients suffering from disseminated lupus erythematosus with insulin glycemia has revealed changes in the system's reactivity, confirmed by a slow reduction of the blood plasma corticotropin and somatotropin, reaching the initial values by the 120th minute after insulin injection. Decreased functional activity of the adrenal cortex was revealed, manifesting by a slow rise of the blood plasma hydrocortisone by the 30th minute after insulin injection. The examined reserve potentials of the hypophyseo-adrenal system indicate not so much an impairment of the corticotropin secretion central mechanisms, but mostly a decrease of the adrenocortical functional activity.
Vestn Dermatol Venerol 1989
PMID:[The function of the hypophyseo-adrenal system in patients with disseminated lupus erythematosus]. 255 57

At the final step of melanocyte differentiation in mouse hair follicles, the cells produce melanin. The type of melanin they produce is, however, determined by the tissue environment of hair follicles. In wild-type mice, melanocytes located in hair bulbs synthesize eumelanin at the beginning of hair growth. They subsequently produce pheomelanin and finally produce eumelanin again. Therefore, the hair is characterized by a subterminal band of yellow, with the rest of it displaying black. This characteristic is called the agouti pattern and is known to be determined by the wild-type allele, A at the a (agouti) locus, which is considered to function in the follicular cells. Expression of the agouti pattern is altered by genetic substitutions at the a locus and the e (extension) locus. Animals heterozygous for the Ay (lethal yellow) allele exhibit yellow coat color; those homozygous for the e (recessive yellow) also produce yellow hair exclusively. By using an organ culture method, we demonstrated that alpha-MSH and cholera toxin, as well as forskolin, induced eumelanin synthesis in explants from lethal yellow mice (Ay/a). On the other hand, these reagents did not induce eumelanogenesis in the hair follicles of recessive yellow (e/e) mice. Therefore, we assume that the product of the a locus, which probably functions in follicle cells, interacts with alpha-MSH at the alpha-MSH receptor and that the e locus controls the functionality of adenylate cyclase in the membrane of mouse melanocytes.
J Invest Dermatol 1989 May
PMID:Genetic control of signal transduction in mouse melanocytes. 271 58


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