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)

In an attempt to clarify the mechanisms underlying the lack of melanin formation in hair bulb melanocytes of chinchilla mice (genotype a/a, cch/cch, strain PW), we studied the effect of exogenous melanogenic stimulants such as theophylline (Tp), dibutyryl cyclic AMP (db-cAMP), and alpha-melanocyte-stimulating hormone (alpha-MSH) on the induction of melanization. Skin explants excised from the dorsa of chinchilla or lethal yellow C57BL/6J, Ay/a) mice at 7 to 9 days of age were cultured in the presence of Tp (2 mM), db-cAMP (2 mM), or alpha-MSH (1.0 microgram/ml). After 2 to 5 days, melanin formation was induced in hair bulb melanocytes of chinchilla mutant in response to both Tp and db-cAMP, but alpha-MSH did not produce new melanin formation. In contrast, yellow mutant increased the melanin formation in response to all stimulants. Electron microscopic studies demonstrated that while non-treated hair bulb melanocytes of chinchilla mutant contain a large number of stage II-III melanosomes without melanin deposition, a hair bulb treated with Tp exhibits the new formation of melanin within melanosomes that appears both as typical eumelanosomes with striated longitudinal matrices and as pheomelanosomes with vacuolar melanization. Quantitative analysis of melanin has revealed that in chinchilla mutant, Tp and db-cAMP induce a severalfold increase in the formation of both eumelanin [pyrrole-2,3,5-tricarboxylic acid (PTCA)] and pheomelanin (aminohydroxyphenylalanine), whereas alpha-MSH does not stimulate production of either melanin. In yellow mutant, db-cAMP induced a remarkable increase in eumelanin (PTCA), in contrast to the fewfold increase induced by alpha-MSH and Tp. All stimulants induced a slight increase in pheomelanin to a similar extent. These different reactions to melanogenic stimulation suggest a possible defect in the tyrosinase activation system within hair bulb melanocytes in chinchilla mutants.
J Invest Dermatol 1988 Aug
PMID:Induction of melanization within hair bulb melanocytes in chinchilla mutant by melanogenic stimulants. 284 Apr 69

Normal and malignant pigment cells are known targets for many hormones. Besides alpha-melanocyte-stimulating hormone and the steroidal hormones estrogen, testosterone, and glucocorticoids, factors produced by other epidermal cells can affect melanization and proliferation of pigment cells. Among those factors are the prostaglandins, vitamin D3, ETAF, and interleukin-1.
Dermatol Clin 1988 Apr
PMID:Endocrine factors as effectors of integumental pigmentation. 313 40

Since the initial clinical presentation of visceral neuroendocrine carcinoma is occasionally a cutaneous metastasis, diagnostic confusion with primary neuroendocrine carcinoma of the skin (Merkel cell carcinoma) may ensue. In this study, seven cases of secondary cutaneous neuroendocrine carcinoma were immunohistochemically compared with twenty-one Merkel cell carcinomas for ten antigenic moieties that have been associated with endocrine tumors. Six of seven secondary tumors stained for bombesin, leucine enkephalin, methionine enkephalin, or beta-endorphin, none of which was detected in the primary cutaneous neuroendocrine carcinomas. These data suggest that immunohistochemical study may be useful in separating primary from secondary neuroendocrine tumors of the skin and may assist in directing clinical attention to the most probable site of visceral neoplasia.
J Am Acad Dermatol 1985 Jul
PMID:Secondary neuroendocrine carcinomas of the skin. An immunohistochemical comparison with primary neuroendocrine carcinoma of the skin ("Merkel cell" carcinoma). 316 11

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.
J Invest Dermatol 1987 Sep
PMID:Stimulation of follicular melanogenesis in the mouse by topical and injected melanotropins. 362 99

Since met-enkephalin-like substance has been demonstrated only in Merkel cells of some rodents but not of cat, dog, pig, and humans, Merkel cells of these species were analyzed by immunohistochemistry using a variety of different antisera for the occurrence of neuropeptides different from met-enkephalin. In various locations of all species investigated Merkel cells were found to be immunoreactive exclusively to vasoactive intestinal polypeptide (VIP) but not to any of the other antisera used. Thus, in mammalian Merkel cells, neuropeptides occur that are different from met-enkephalin. It is suggested that the Merkel cell-axon complex represents a complex regulatory system involving a presumptive receptor or modulator function whereby the Merkel cell may influence the threshold of the sensory nerve ending via release of a neuropeptide (VIP- or met-enkephalin-like material).
J Invest Dermatol 1983 Oct
PMID:Immunohistochemical localization of vasoactive intestinal polypeptide (VIP) in Merkel cells of various mammals: evidence for a neuromodulator function of the Merkel cell. 613 3

The effect of various opioid or putative neurotransmitter peptides on histamine-induced itch and flare responses was studied in humans after intradermal injection. Significant enhancement of the histamine responses was induced by the stable methionine-enkephalin analogue FK 33-824, beta-endorphin and morphine. The putative neurotransmitters substance P and vasoactive intestinal polypeptide (VIP)--which moreover are potent histamine liberators--had no enhancing effect. The potentiation induced by FK 33-824 was induced neither by local pretreatment with Compound 48/80 to deplete the local stores of mast-cell-bound histamine, nor by oral pretreatment with indomethacin to inhibit prostaglandin formation in the skin. Thus, the enhancement did not seem to be due to histamine release or to prostaglandin formation and the mechanism of the effect remains to be shown. The specific morphine antagonist naloxone did not inhibit the potentiation by FK 33-824, which might indicate that ordinary opiate receptors were not involved. The results support the idea that pain and itch are qualitatively separate processes and suggest possible mechanisms of morphine-induced pruritus. The findings are of particular interest in view of recent reports on the presence of methionine-enkephalin in Merkel cells.
Arch Dermatol Res 1982
PMID:Potentiation of histamine-induced itch and flare responses in human skin by the enkephalin analogue FK-33-824, beta-endorphin and morphine. 618 98

The association of acanthosis nigricans with pituitary tumors and insulin-resistant diabetes suggests that a pituitary peptide may promote papillomatosis and acanthosis characteristic of acanthosis nigricans. Although such a peptide has not been isolated, it may derive by sequential cleavage from the 31,000-dalton precursor peptide to ACTH and beta-lipotropin (beta-LPH). In order to evaluate the role of pituitary peptides in the pathogenesis of acanthosis nigricans, we compared plasma levels of beta-endorphin (beta-EP) and ACTH in plasma of 8 fasting patients with obesity-associated benign acanthosis nigricans and 7 fasting normal controls utilizing sensitive radioimmunoassay procedures. Mean plasma beta-EP levels for the acanthosis nigricans and control subjects were not significantly different (90 pg/ml vs. 140 pg/ml), nor was any significant difference observed between plasma ACTH levels of the 2 groups (42.3 and 31.2 pg/ml, respectively.) Our data indicate that plasma levels of the pituitary-derived peptides ACTH and beta-EP are not increased in obesity-associated benign acanthosis nigricans, and suggest that its proposed hormonal mediator might originate independently from the large peptide precursor of ACTH, beta-LPH and their fragments.
J Invest Dermatol 1983 Jan
PMID:Neuropeptides in the pathogenesis of obesity-associated benign acanthosis nigricans. 629 89

Using a special selection technique, normal guinea-pig melanocytes were maintained in highly purified but sparse cultures (approximately 10(4) cells/25 cm2 culture vessel) which showed little proliferative activity. The applicability of the Pomerantz tyrosinase assay was tested in this in vitro model system using three different approaches, namely crude cell extracts and viable cell cultures either in situ or in suspension. The latter modifications both proved too insensitive, whereas crude cell extracts allowed accurate measurements of the basal tyrosinase activity and its stimulation by various agents. In unstimulated cultures basal tyrosinase activities ranged from 30% to 700% (mean 260%) above the blank values; intra-assay and inter-assay variability were 4.2% and 77.5%, respectively. Stimulation with alpha-MSH (10(-5) M, 10(-6) M), beta-MSH (10(-5) M), choleratoxin (10(-11) M) and cAMP (10(-4) M) plus theophylline (10(-4) M) resulted in an increase of tyrosinase activity 30-65% above basal values. Melanotropin potentiating factor (10(-8) M) enhanced the effects of alpha-MSH (10(-6) M) by 20%. This assay modification provides a sensitive tool for comparative studies of melanogenesis in normal melanocytes, malignant melanocytes and otherwise altered melanocytes.
Br J Dermatol 1983 Oct
PMID:Application of the tyrosinase assay to normal melanocytes in culture. 631 31

White horses are subject to age-dependent coat depigmentation. They are dark gray or black at birth and lose their coloring between their second and fourth year. Beginning at about age 10 their coat takes on a characteristic silver-gray coloring. The purpose of this paper was to find out to what extent the endogenic alpha-MSH level changes with the change in pigmentation. alpha-MSH plasma levels were determined by radioimmunologic analysis in 3 age groups of white Camarque horses: age group 1 consisted of dark horses with a mean age of 1.2 years and a mean alpha-MSH level of 106.4 pg/ml +/- 18.2, age group 2 consisted of gray horses with a mean age of 7.5 years and with a mean alpha-MSH level of 73.6 pg/ml +/- 4.8, and age group 3 consisted of silver-gray horses with a mean age of 13.5 years and a mean alpha-MSH level of 65.0 pg/ml +/- 5.3. Highly significant differences (p less than 0.001) were found between the means of age group 1 and age group 2 and between the means of age group 1 and age group 3. Determination of the ACTH plasma levels in this breed of horses showed no statistically significant differences between the various age groups. Determination of alpha-MSH and ACTH levels in a control group (n = 56) of other breeds of horses (10 black, 28 brown, and 18 sorrel) resulted in no significant differences for either hormone with regard to age or coat color. On the basis of these results it may be concluded that the degree of coat pigmentation in white Camarque horses correlates directly with the alpha-MSH plasma level.
J Invest Dermatol 1984 Feb
PMID:The relationship between alpha-MSH level and coat color in white Camarque horses. 631 3

Thirty-two patients with various severe or selected dermatoses were chosen for treatment with cortisone acetate by mouth. The criteria for selection included refractoriness to previous therapy and absence of ascertainable contraindications. The initial dose of cortisone acetate varied between 100 and 200 mg. per day. The dose was reduced as quickly as each patient's response permitted, with the object of reaching the lowest effective dose as quickly as possible. Response of most patients to the hormone was dramatic, with abatement of symptoms within 24 hours and substantial improvement of clinical signs within 24 to 48 hours. Details of the results are tabulated. Adverse effects, possibly attributable to the hormone, were noted in five patients. In two instances, moon facies developed, one with hypertrichosis and a 20-lb. (9.1-kg.) gain in weight. However, both of these patients had received corticotropin (ACTH) prior to the cortisone. A third patient showed hyperpigmentation of the areas of skin usually exposed and not covered by clothing. Two additional patients each complained of hyperexcitability and insomnia. All these undesirable effects diminished or disappeared after the dose was reduced or administration of cortisone was discontinued. The effectiveness of this new therapeutic approach in a wide variety of skin diseases is clearly demonstrated by the excellent response noted in this series of selected cases. No other modality known to us has comparable beneficial effects. It is to be stressed, however, that the benefits generally stop soon after cortisone therapy is discontinued, unless the disease or the attack is one with spontaneous remissions. Disagreeable and sometimes dangerous effects still preclude the use of this treatment except in serious diseases and situations, and unless the patient can be kept under sufficiently close and expert surveillance.
Arch Dermatol 1983 Oct
PMID:Centennial Paper. November 1951 (Arch Dermatol Syphilol: Cortisone acetate administered orally in dermatologic therapy by Marion B. Sulzberger, Victor H. Witten and Stanley N. Yaffe. 635 55


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