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)

A detailed review of the hormonal effects on intraocular pressure is presented. There is evidence that corticotropin, vasopressin, thyroxin, insulin, glucocorticoids and mineralocorticoids may play a role in the physiologic regulation of intraocular pressure. Growth hormone, melanocyte stimulating hormone, progesterone, estrogen, chorionic gonadotropin and relaxin may influence intraocular pressure when administered in pharmacologic doses. Whether the key to understanding primary open-angle glaucoma lies in recognizing abnormal endocrine mechanisms, especially involving glucocorticoids, remains unclear at the present time.
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PMID:Hormonal regulation of intraocular pressure. 41 3

Levels of melatonin in rabbit eye tissues were detected by radioimmunoassay. Solutions of met-enkephalin, leu-enkephalin, alpha-endorphin and beta-endorphin were given topically. Met-Enkephalin and alpha-endorphin lowered levels of melatonin in the iris, iris root-ciliary body, retina and choroid; leu-enkephalin raised levels in the retina and lowered them in other tissues. beta-Endorphin only lowered levels in the iris root-ciliary body. DAGO (a mu agonist) given i.v. lowered levels of melatonin in the iris, iris root-ciliary body and retina. The delta and sigma agonists given i.v. only lowered levels in the iris root-ciliary body, and a kappa agonist given i.v. raised levels in the ciliary body. No opiate binding sites could be detected in the rabbit iris or iris root-ciliary body for any class of receptor. Our data suggest opioids may be useful for treating glaucoma.
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PMID:Effects of some opiates and opioid peptide eyedrops on ocular melatonin regulation in rabbits. 830 77

Several prostaglandin analogues used for glaucoma treatment cause increased pigmentation of the iris. The purpose of the present study was investigate whether latanoprost, a PGF(2 alpha) analogue, has any effect on the production of endogenous prostaglandins in iridial melanocytes, which could be important in the mechanism leading to increased pigmentation. Bovine and human iridial melanocytes in culture were used for the experiments. Production of endogenous prostaglandins was measured by enzyme immunoassay, and the melanin content was measured spectrophotometrically. In bovine iridial melanocytes, latanoprost acid caused a significant increase of the PGE(2) production, which could be blocked by indomethacin and NS398, indicating an involvement of cyclo-oxygenase 2. In order to study the selectivity of the phenomenon other endogenous substances/drugs were tested, e.g., acetylcholine, carbachol, noradrenaline, neuropeptide Y, substance P and alpha-MSH, but none was found to have any significant effect. Human iridial melanocytes also responded to latanoprost acid with increased production of PGE(2) and in 1 out of 5 individuals increased melanogenesis coincided with increased PGE(2) production. In bovine iridial melanocytes, latanoprost acid did not stimulate melanogenesis. These results indicate that latanoprost acid cause enhanced formation of endogenous prostaglandins that may have auto- and/or paracrine effects in the melanocytes, possibly associated with melanogenesis.
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PMID:Production of prostaglandin e(2) by iridial melanocytes exposed to latanoprost acid, a prostaglandin F(2 alpha) analogue. 1241 90

Our study included 71 patients (38 males and 33 females) with diagnosed open angle glaucoma and healthy 71 persons for control group. Their age ranged from 45 to 70. The patients and healthy persons were divided into three groups: I group--45-55 years old persons, II group--55-65 years old persons, III group--65-75 years old persons. Examination included ophthalmologic and hormonal research. To assess the function of pituitary-adrenal axis, we measured the concentrations of cortisol, aldosterone and adrenocorticotropic hormone (ACTH) in the plasma of patients and control groups by radioimmunoassay method. The level of ACTH was decreased in I and II groups of females and in III group of males. The level of cortisol was increased in all--I, II and III groups of males. Aldosterone was decreased in III group of males and in I and III groups of females. According to our studies there were some changes in secretion of these hormones as well as in their regulation. The findings confirmed the role pituitary-adrenal axis of in the regulation of IOP. In compliance to our data, the investigation of the hormonal status of patients with glaucoma is recommended for complete understanding of glaucoma etiology and pathogenesis.
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PMID:[Pituitary-adrenal axis system condition in patients with open angle glaucoma]. 1623 2

Gpnmb is a glycosylated transmembrane protein implicated in the development of glaucoma in mice and melanoma in humans. It shares significant amino acid sequence homology with the melanosome protein Pmel-17. Its extracellular domain contains a RGD motif for binding to integrin and its intracellular domain has a putative endosomal and/or melanosomal-sorting motif. These features led us to posit that Gpnmb is associated with melanosomes and involved in cell adhesion. We showed that human Gpnmb is expressed constitutively by melanoma cell lines, primary-cultured melanocytes and epidermal melanocytes in situ, with most of it found intracellularly within melanosomes and to a lesser degree in lysosomes. Our newly developed monoclonal antibody revealed surface expression of Gpnmb on these pigment cells, albeit to a lesser degree than the intracellular fraction. Gpnmb expression was upregulated by UVA (but not UVB) irradiation and by alpha-melanocyte-stimulating hormone (MSH) (but not beta-MSH); its cell surface expression on melanocytes (but not on melanoma cells) was increased markedly by IFN-gamma and TNF-alpha. PAM212 keratinocytes adhered to immobilized Gpnmb in a RGD-dependent manner. These results indicate that Gpnmb is a melanosome-associated glycoprotein that contributes to the adhesion of melanocytes with keratinocytes.
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PMID:Gpnmb is a melanosome-associated glycoprotein that contributes to melanocyte/keratinocyte adhesion in a RGD-dependent fashion. 1932 Jul 36