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 the Alzheimer disease (AD) brain, senile plaques contain several proteins and cytokines, such as beta-amyloid protein (A beta), interleukin 1, transforming growth factor beta 1 (TGF beta 1), and apolipoprotein E, which may contribute to the process of neurodegeneration. Clusterin is also known to colocalize with A beta deposits in neuritic plaques. Clusterin is a multifunctional protein that causes cell aggregation, binds to beta-endorphin, and inhibits the terminal complex formation of complement. Clusterin mRNA and protein are increased in the brains of AD patients. Cytokines such as TGF beta 1 and interleukin 1 enhance the expression of clusterin, which may link clusterin to inflammatory mechanisms in AD. A beta, a 39-43 amino acid peptide, is a major component of the senile plaques that are characteristic of AD. Highly aggregated A beta is implicated in neurodegeneration, e.g., A beta aggregates spontaneously into fibrillar forms resembling those in plaques that, in experimental models, cause neurotoxicity through oxidative stress. Clusterin inhibits the aggregation of A beta, which might be neuroprotective according to the aggregation-toxicity hypothesis of A beta. However, clusterin enhanced the oxidative stress of A beta. This may extend its neurotoxicity to locations distal from plaques wherever A beta is present.
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PMID:Relationship between multifunctional protein "clusterin" and Alzheimer disease. 889 44

Sulfated glycoprotein-2 (SGP-2 or clusterin) is a complex multifunctional molecule that has been recently been implicated in neuronal degeneration and remodeling. We have shown that estradiol treatment results in a selective destruction of beta-endorphin neurons in the hypothalamic arcuate nucleus. We have used immunocytochemistry to determine the distribution of SGP-2 immunoreactivity in the rat hypothalamus and to assess the effects of the estradiol-induced destruction of beta-endorphin neurons on SGP-2 expression. We have found that SGP-2-immunopositive neurons normally occur in the medial preoptic area (MPOA), supraoptic nucleus (SON), paraventricular nucleus (PVN), dorsomedial nucleus (DM), and the lateral hypothalamic area (LHA) in both males and females. The neuropil appears free of label. Treatment with estradiol valerate results in the appearance of immunopositive punctate deposits in the neuropil in the MPOA, PVN and DM. The number and distribution of SGP-2-positive neurons are unaffected by estradiol treatment except in the MPOA, where there are twice as many SGP-2-positive neurons as in controls. These effects are precluded by treatment with vitamin E, with blocks the cytotoxic action of estradiol on beta-endorphin neurons. Thus, we interpret these changes as responses to the loss of beta-endorphin afferents.
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PMID:The effect of estradiol-induced hypothalamic pathology on sulfated glycoprotein-2 (clusterin) expression in the hypothalamus. 903 92

Clusterin is a sulfated glycoprotein abundantly expressed in the pituitary gland and hypothalamus of mammals. However, its physiological role in neuroendocrine function is largely unknown. In the present study, we investigated the effects of intracerebroventricular (ICV) administration of clusterin on plasma pituitary hormone levels in normal rats. Single ICV injection of clusterin provoked neurohormonal changes seen under acute stress condition: increased plasma adrenocorticotropic hormone (ACTH), corticosterone, GH and prolactin levels and decreased LH and FSH levels. Consistently, hypothalamic and pituitary clusterin expression levels were upregulated following a restraint stress, suggesting an involvement of endogenous clusterin in stress-induced neurohormonal changes. In the pituitary intermediate lobe, clusterin was coexpressed with proopiomelanocortin (POMC), a precursor of ACTH. Treatment of clusterin in POMC expressing AtT-20 pituitary cells increased basal and corticotropin-releasing hormone (CRH)-stimulated POMC promoter activities and intracellular cAMP levels. Furthermore, clusterin treatment triggered ACTH secretion from AtT-20 cells in a CRH-dependent manner, indicating that increased clusterin under stressful conditions may augment CRH-stimulated ACTH production and release. In summary, hypothalamic and pituitary clusterin may function as a modulator of neurohormonal responses under stressful conditions.
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PMID:Hypothalamic and pituitary clusterin modulates neurohormonal responses to stress. 2408 Aug 98