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)

Repeated exposure to stressors was reported to increase the expression of arginine-vasopressin (AVP), especially in corticotropin-releasing hormone (CRH) neurons co-expressing AVP, within the hypothalamus. This may increase the potential for subsequent stressor-elicited enhancement of hypothalamic-pituitary-adrenal (HPA) functioning as these peptides synergistically stimulate pituitary ACTH secretion. Likewise, members of the bombesin (BB) family of peptides (including its mammalian analogues gastrin-releasing peptide (GRP) and neuromedin B (NMB)) stimulate the release of ACTH and may play a role in the mediation and/or modulation of the CRH stress response. In the present investigation, chronic stressor exposure (daily restraint over 14 days) was associated with increased co-expression of CRH and AVP at the median eminence. In addition, in vivo interstitial levels of anterior pituitary AVP, GRP and NMB (but not CRH) were elevated following chronic stressor exposure. Basal pituitary corticosterone levels, in contrast, were unaffected by chronic stressor exposure. Following consumption of a highly palatable snack, interstitial levels of CRH, GRP, NMB and corticosterone (but not AVP) were elevated at the pituitary; however, a cross-sensitization was not apparent among rats previously exposed to the stressor and then provided with the snack. As the CRH, AVP and BB-like peptide systems have been associated with altered anxiety and depressive symptoms, the sustained peptidergic alterations observed in the chronically stressed rats may have implications for the development of these stressor-related disorders.
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PMID:Impact of repeated stressor exposure on the release of corticotropin-releasing hormone, arginine-vasopressin and bombesin-like peptides at the anterior pituitary. 1901 76

The hypothalamic-pituitary-adrenal (HPA) axis is a major part of the neuroendocrine system that controls responses to stress, and has an important function in the regulation of various body processes. We previously created a mouse line deficient in the melanocortin 2 receptor (MC2R). MC2R-deficient mice (MC2R(-/-) mice) have high adrenocorticotropic hormone (ACTH) levels because of undetectable corticosterone levels. Increased neuromedin B (NMB) expression was recently reported in the pituitary gland of adrenalectomized mice, a model for acute adrenal insufficiency. To investigate gene expression in the pituitary gland under chronic adrenal deficiency, we examined the pituitary gland of MC2R(-/-) mice, a model of chronic adrenal insufficiency. To understand the molecular background of pituitary cells under chronic adrenal deficiency, we first performed DNA microarray analyses using the pituitary glands of the MC2R(-/-) mice. The DNA microarray analysis and real-time polymerase chain reaction showed that NMB expression was higher in the MC2R(-/-) than in the wild-type (WT) mice. We detected NMB expression in the MC2R(-/-) pituitary corticotrophs by immunohistochemistry using the specific antibodies for ACTH and NMB. In addition, the plasma NMB concentration was significantly higher in the MC2R(-/-) mice than in the WT mice. Subcutaneous implantation of a sustained-release corticosterone pellet decreased the expression of NMB mRNA as well as pituitary proopiomelanocortin mRNA. In isolated anterior pituitary cells, NMB mRNA expression was increased by the administration of corticotropin-releasing hormone (CRH) and was suppressed by dexamethasone treatment. In this study, we first demonstrate NMB expression in corticotrophs and its regulation by CRH and glucocorticoids. Furthermore, corticotrophs seemed to secrete NMB into the systemic circulation.
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PMID:Expression and regulation of neuromedin B in pituitary corticotrophs of male melanocortin 2 receptor-deficient mice. 2474 95