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)

Although opioid peptides are involved in the regulation of the hypothalamic-pituitary-adrenal axis, their role in pro-opiomelanocortin (POMC) gene expression at the pituitary level is not known. We therefore examined the effects of opioid receptor agonists, including recently discovered endogenous opioid peptides, on POMC gene expression using the AtT20PL cell line, a subclone of AtT20 in which the rat POMC 5'-promoter-luciferase fusion gene was stably incorporated. The endogenous mu-opioid receptor agonists endomorphin 1 and 2 had no effect on either basal or corticotropin-stimulating-hormone-induced POMC expression. This was also the case with the delta-agonist BUBUC, the kappa-agonist U50488H and the orphan receptor agonist orphanin FQ. In contrast, the synthetic mu-agonist loperamide significantly inhibited basal and yet enhanced cAMP-induced POMC expression. The inhibitory effect of loperamide was mimicked by the calmodulin antagonist W7 and antagonized by the calcium channel blocker nifedipine, whereas neither the inhibitory nor the enhancing effect of loperamide was influenced by the opioid antagonist naloxone. These results suggest that the synthetic mu-agonist loperamide has a modulatory effect on the 5'-promoter activity of the POMC gene. This effect does not seem to be mediated through the classical mu-opioid receptor but rather in part through a calcium/calmodulin-related mechanism.
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PMID:Effects of loperamide and other opioid-related substances on the transcriptional regulation of the rat pro-opiomelanocortin gene in AtT20 cells. 1147 16

Nowadays the cardiovascular diseases particularly ischaemic heart disease (IHD) are the most frequent causes of death in Poland. Some of patients with IHD are completely asymptomatic. These subjects are more susceptible to sudden coronary events due to lack of diagnosis and treatment. Cohn divided patients with asymptomatic ischaemia (AI) into three groups: completely asymptomatic, asymptomatic patients after myocardial infarction, patients with painful angina who have some ischaemic events asymptomatic. Some causes of AI are: increased pain threshold, increased beta-endorphin levels, impairment of pain pathways, smaller ischaemic regions in comparison with painful angina, psychological factors, transient platelet microaggregates. Estimated prevalence of AI is about 2-4% of total population and is larger in the group of patients with multiple coronary disease risk factors especially with diabetes mellitus (autonomic neuropathy). In the patients after myocardial infarction the prevalence of AI is between 30-70% and it is associated with poorer prognosis. In subjects with painful angina 70-80% of total ischaemic episodes detected by 24-hour ECG monitoring is asymptomatic. The most useful methods for diagnosis of AI are ECG exercise test and ambulatory 24-hour ECG monitoring, although they may sometimes produce false positive results. Other tests are not widely performed and their use is restricted to specific circumstances. Some cases are finally solved by coronary angiography. Although screening in whole population is not cost-effective, but in some groups is necessary (people with many risk factors of IHD, people of certain professions--plane pilots, etc.). Treatment of AI does not vary from treatment of symptomatic IHD. Basic drugs used are: aspirin, beta-blockers, calcium channel blockers, long time acting nitrates. Positive effect of statins is also observed. The most beneficial is invasive treatment--CABG is more efficient than PTCA. Moreover the treatment of symptomatic IHD should be oriented not only to eliminate the symptoms but also to withdraw episodes of silent ischaemia confirmed by 24-h ECG monitoring or ECG exercise test.
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PMID:[Silent myocardial ischemia]. 1147 58

Although it is known that the expression of proopiomelanocortin, a precursor protein of adrenocorticotropic hormone, can be affected by a variety of drugs, the effects of calcium channel blockers have not been studied. This study examined the effect of calcium channel blockers on proopiomelanocortin gene expression. Mouse pituitary tumor cells stably transfected with approximately 0.7 kb of the rat proopiomelanocortin 5' promoter-luciferase fusion gene were stimulated by potassium chloride, corticotropin-releasing hormone (CRH) or forskolin, in the presence or absence of calcium channel blockers (nifedipine, verapamil and diltiazem). Assessments were made of proopiomelanocortin gene promoter activity and cyclic adenosine 3',5'-monophosphate (cyclic AMP) efflux. A dose-dependent enhancement of CRH- or forskolin-stimulated proopiomelanocortin promoter activity was observed with nifedipine and verapamil, but not diltiazem. Cyclic AMP efflux induced by CRH or forskolin was also enhanced by nifedipine and verapamil. In the presence of isobutylmethylxanthine, a phosphodiesterase inhibitor, enhancement of proopiomelanocortin promoter activity and cyclic AMP efflux by nifedipine and verapamil was not observed. It was concluded that the inhibition of phosphodiesterase is a probable mechanism for the effect of nifedipine and verapamil on CRH or forskolin induction of proopiomelanocortin gene expression.
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PMID:Potentiation of cyclic AMP-mediated proopiomelanocortin gene promoter activity by calcium channel blockers in a pituitary cell line. 1719 58

The acrosome reaction occurs in vivo following sperm capacitation and is essential for the acquisition of sperm fertilization ability. However, little is known about the molecular identity of the physiological acrosome reaction regulators. In addition to progesterone, which is produced by cumulus oophorus cells and known to regulate acrosome reaction by activating the specific calcium channel CatSper, endogenous opioid peptides such as beta-endorphin and met-enkephalin are present at high concentrations in the follicular fluid suggesting that the opioid system may be involved in the mechanisms regulating the acrosome reaction in humans. By using Reverse Transcription-PCR, western blot and immunofluorescence approaches, we described the presence and localization of the beta-endorphin precursor, pro-opiomelanocortinin the middle section and in flagellum of human spermatozoa, and inside the seminiferous tubules of human testis. Flow cytometry and intracellular calcium analyses showed that beta-endorphin causes an inversely dose-dependent increase in the percentage of acrosome-reacted sperm cells by a calcium-independent protein kinase C pathway. These findings are important for future studies of sperm physiology and provide new insight into the function of the opioid system as a target of fertility management.
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PMID:The opioid peptide beta-endorphin stimulates acrosome reaction in human spermatozoa. 2666 9


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