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)

At the beginning of the 70-ties various studies showed the existence of endogenous opiates in central nervous system. The chemical structure of first endogenous pentapeptides called enkephalins (met-enkephalin and leu-enkephalin) and their receptor was already known in 1975. Further investigations confirmed the existence of opiates (endorphins) in brain, pituitary gland, spinal cord and other tissues. Endorphins may exert various effects: analgesic (especially dynorphin and b-endorphin), antidiuretic, depressive on respiratory center, constipative, they also cause physical and mental dependence. These peptides, which are not known thoroughly may play a big part in the regulation of many biochemical and hemodynamic processes. Many of these mechanisms are already described and changes in concentrations of endorphins, for example in patients with silent myocardial ischaemia, are basic in the pathogenesis of this disease. Many of these mechanisms are controversial, the role of endogenous opiates in pathogenesis of hypertension or congestive heart failure is still unknown. This study summerizes the present knowledge endorphins and tries to answer whether changes in the concentration of endorphins are primary or secondary to the biochemical and hemodynamic disturbances in 2 diseases.
Pol Merkur Lekarski 1999 Aug
PMID:[The role of endorphins in the etiopathogenesis of circulatory diseases]. 1052 12

The paper contains a review of reports concerned with how for hormones, epileptic seizures and antiepileptic drugs can be influenced by one another. Hormones influence brain excitability but, on the other hand, both epileptic seizures and antiepileptic drugs may alter hormone secretion and metabolism. Effect of hormones on seizures--Experimental studies revealed the properties which inhibit or stimulate convulsive reactivity of different hormones. Progesterone, testosterone, adrenocorticotropin and desoxycorticosterone are responsible for an increase in seizure threshold, while estradiol, cortisol and thyroid hormones cause a reduction. Effect of seizures on hormones--Epileptic seizures, chiefly tonic-clonic, also complex partial and sometimes simple partial seizures, result in "the hormonal storm". Immediately after an epileptic seizure, an increase is found in serum concentrations of prolactin, cortisol, adrenocorticotropin, triidothyronine, thyroxin, thyrotropin, luteotropin, follicular stimulating hormone and growth hormone. These changes may persist for two hours, while prolactin concentration even for 24 hours after a seizure. Effect of antiepileptic drugs on hormones--Antiepileptic drugs may affect hypothalamus-pituitary function directly or indirectly through neurotransmitter system. By induction of hepatic microsomal enzymes, some antiepileptic drugs cause acceleration of hormone metabolism, reducing hormone serum concentrations. Moreover, antiepileptic drugs enhance sex hormone binding globulin SHBG/synthesis, increase binding of these hormones and reduce their active fraction concentration in serum. Recognition of the relationship between epilepsy and hormonal system is necessary to obtain better understanding of this disease.
Neurol Neurochir Pol 2000
PMID:[Epilepsy and hormones]. 1076 43

Apart from its regulatory role in release of adrenocorticotropic hormone (ACTH) and beta-endorphin, corticotropin-releasing factor (CRF) is implicated in behavioral functions. This review summarizes the present knowledge of the role of CRF in anxiety and discusses probable sites and receptors involved in the anxiogenic-like effect of CRF as well as possible interactions between the CRF system and other peptides. The role of the CRF system in human psychopathological conditions associated with anxiety is also reviewed. Based on the available literature, we suggest that the CRF system may interact with antianxiety drugs and that this interaction may be of importance in the development of anxiety induced by ethanol or cocaine withdrawal.
Pol J Pharmacol
PMID:Role of corticotropin-releasing factor (CRF) in anxiety. 1094 16

In order to test if antidepressant drugs can directly influence corticotropin-releasing hormone (CRH) gene expression, their effect on CRH gene promoter activity was evaluated in neuro-2A cells stably transfected with a human CRH - chloramphenicol acetyl-transferase plasmid. Forskolin (an activator of adenylate cyclase), but not phorbol 12-myristate 13-acetate (an activator of protein kinase C), ca. 3-fold increased reporter gene activity, which confirms the critical role of the cAMP-responsive element in regulation of the CRH gene. Imipramine and fluoxetine present in the medium for 5 days, in a concentration-dependent manner (3-30 microM) inhibited the basal activity of CRH gene promoter, while tianeptine was inactive. The obtained results indicate that inhibition of the human CRH gene promoter activity by imipramine and fluoxetine, but not tianeptine, may play a role in a mechanism by which the former drugs attenuate HPA axis activity.
Pol J Pharmacol
PMID:Effect of antidepressant drugs on the human corticotropin-releasing-hormone gene promoter activity in neuro-2A cells. 1286 30

Clinical and experimental studies on animals indicate that depression is associated with increased plasma cytokine acute phase protein concentrations and hypothalamic-pituitary-adrenal axis (HPA) activation. Additionally it has been detected that immunological activation induces stress-like behavioural and neurochemical changes in organisms of animals and humans. Hypersecretion of cytokines in response to stress or to endogenous trigger factors may induce depressive symptoms. Corticotropin releasing hormone (CRH) overproduction in the brain also may participate in cytokine-induced behavioural and neurochemical changes. Treatment with antidepressants conferred protection against cytokine-induced depressive-like biological and behavioural changes. This is mainly due to alterations of the pro-/anti-inflammatory cytokine balance. There is a substantial body of evidence that the immune system plays a major role in aetiology of depression and that cytokines participate in neurochemical, behavioural and endocrine changes in this illness.
Psychiatr Pol
PMID:[The role of cytokines in depression]. 1463 99

The use of nucleotides and their analogs in the pharmacological studies of nucleotide receptors (P2 class) should be preceded by detailed studies on their degradation connected with ecto-enzymes of a given cell type. In the present studies we have analyzed stability of some phosphorothioate and phosphonate analogs of ATP and ADP in the HeLa epitheloid carcinoma and endothelial HUVEC cells cultures. Our studies have revealed that ecto-nucleotide pyrophosphatase (E-NPP) is one of the main enzymes involved in the extracellular degradation of ATP and other nucleotides in the HeLa cells. On the other hand, the ecto-ATPDase is responsible for the hydrolysis of extracellular nucleotides in human endothelial cell cultures, while the E-NPP-like enzymes of the HUVEC cells are not essential to this degradation. The concerted action of the aforementioned ecto-enzymes and nucleotide pyrophosphatase, 5'-nucleotidase and adenosine deaminase present in fetal bovine serum (FBS) supplied to the culture medium, results in partial or complete degradation of the phosphorothioate (ATPgammaS) and phosphonate analogs of adenosine nucleotides (alpha,beta-methylene-ATP and beta,gamma-methylene-ATP) in the cell cultures. Only ADPbetaS appears to be resistant to these enzymes. The influence of some nucleotides and their analogs on the proliferation of the HeLa cells in presence or absence of FBS is also discussed.
Acta Biochim Pol 2003
PMID:Degradation of extracellular nucleotides and their analogs in HeLa and HUVEC cell cultures. 1473 90

Cytochrome P450c17, encoded by the CYP17 gene, is a component of the 17alpha-hydroxylase/17,20-lyase enzyme complex essential for production of adrenal glucocorticoids and androgens as well as gonadal androgens. The expression of CYP17 in adrenocortical cells is stimulated by corticotropin (ACTH) via the signal transduction pathway involving cAMP and protein kinase A (PKA). Thus, in addition to glucocorticoids, ACTH stimulates formation of adrenal androgens, which are known to induce transforming growth factor beta (TGF-beta) secretion. TGF-b in turn inhibits steroid hormone output by attenuating both basal and ACTH-dependent expression of CYP17. The present study revealed that treatment of bovine and human H295R adrenocortical cells with androgens resulted in a decrease in the basal level of CYP17 transcript and cortisol secretion, without affecting forskolin-stimulated levels. We also demonstrated that in H295R cells TGF-beta inhibited both basal and forskolin-stimulated accumulation of CYP17 mRNA. Determination of promoter activity, directing luciferase reporter gene expression in H295R cells transfected with deletion fragments of bovine CYP17 promoter, indicated that the -483 to -433 bp fragment of the promoter was necessary for the inhibitory action of TGF-beta on CYP17 expression. It is concluded that in bovine and human adrenocortical cells, androgens inhibit basal CYP17 expression probably at the transcriptional level and independently of the effect of TGF-beta.
Acta Biochim Pol 2004
PMID:Inhibition of CYP17 expression by adrenal androgens and transforming growth factor beta in adrenocortical cells. 1562 62

The role of glucocorticoids and the repressor isoform of cAMP response element (CRE) modulator (CREM), inducible cAMP early repressor (ICER), in limiting corticotropin-releasing hormone (CRH) transcription during restraint stress were examined in both intact and adrenalectomized rats receiving glucocorticoid replacement. CRH primary transcript, measured by intronic in situ hybridization, increased after 30 min of restraint and returned to basal levels by 90 min, despite the persistent stressor. The decline was independent of circulating glucocorticoids, because adrenalectomized rats displayed an identical pattern. ICER mRNA in the hypothalamic paraventricular nucleus (PVN) increased after 30 min and remained elevated for up to 4 h in a glucocorticoid-independent manner. Western blot and electrophoretic mobility shift assay analyses showed increases in endogenous ICER in the PVN of rats subjected to restraint stress for 3 h. Chromatin immunoprecipitation assays showed the recruitment of CREM by the CRH CRE in conjunction with decreases in RNA polymerase II (Pol II) binding in the PVN region of rats restrained for 3 h. These data show that stress-induced glucocorticoids do not mediate the limitation of CRH transcription. Furthermore, the ability of CREM to bind the CRH CRE and the time relationship between elevated CREM and reduced Pol II recruitment by the CRH promoter suggest that inhibitory isoforms of CREM induced during stress contribute to the decline in CRH gene transcription during persistent stimulation.
 ...
PMID:Role of glucocorticoids and cAMP-mediated repression in limiting corticotropin-releasing hormone transcription during stress. 1584 9

The objective of our study was to investigate the effect of stimulation of the cAMP-dependent pathway on the expression of an orphan nuclear receptor, SF-1/Ad4BP in mouse adrenal tumour, Y-1 cells in culture. We evaluated the temporal pattern of the effects of corticotropin (ACTH) and the adenylyl cyclase activator forskolin on the level of SF-1 mRNA, and compared the time course of induction of SF-1 with that of CYP11A1. Forskolin, corticotropin and 8-Br-cAMP significantly elevated the level of the SF-1 transcript, after 1.5 h of incubation, with a concomitant increase of SF-1 protein level, observed after 6 h. The CYP11A1 transcript increased gradually over the incubation period, and reached the maximal level after 12 to 24 h. The steady-state level of the SF-1 transcript was unaffected by forskolin when the cells were incubated with actinomycin D, indicating that stimulation of the cAMP pathway results in enhanced transcription of the gene. The effect of forskolin was augmented by cycloheximide, suggesting that an inhibitory protein, whose synthesis was inhibited by cycloheximide, could be involved in negative regulation of SF-1 expression. It is concluded that SF-1 expression is positively regulated by the cAMP pathway at the transcriptional level, and can represent the primary event in cAMP-mediated induction of steroid hormone synthesis in Y-1 cells.
Acta Biochim Pol 2005
PMID:Temporal pattern of the induction of SF-1 gene expression by the signal transduction pathway involving 3',5'-cyclic adenosine monophosphate. 1591 8

Factors which induce the corpus luteum persistent (CLP) creation in animal ovaries are located in the hypothalamic-pituitary-ovarian axis and also in the uterus. In cows and likewise in others animals, various mediators of inflammatory reaction are released, mainly proinflammatory cytokines from inflamed uterus into the blood and lymph. Afterwards the cytokines cross the blood-brain barrier, and though the brain mediators alter the hormonal profile and amplitude pulses of the hormones release in the hypothalamus and the pituitary. Until it is known, that cytokines: IL-1, IL-2, IL-6, TNF-alpha and also IFN-alpha, administered into the median eminence, cause an increase in corticotrophin-releasing hormone (CRH) and adrenocorticotropic hormone (ACTH) concentrations and decrease in the pituitary gland hormones secretion. The immune system, represented in the corpora lutea (CL) by numerous macrophages/monocytes, limphocytes and neutrophils plays an important role in the luteolysis process. The stimulating factor of the infiltration of these cells is an increased PRL level. The preovulatory increase in PRL level regulates the number of macrophages in newly-formed CL and later influences the number of these cells in the luteolysis period. The pulsatory release and high levels of the hypophyseal oxytocin (OT) and uterine PGF2alpha ensure the beginning and the normal course of the luteolysis period. The cytokines decrease OT concentration and disorder its pulsatory release from the pituitary. In these circumstances the quantity of the uterine PGF2alpha reaching ovaries, is insufficient to begin luteolysis. In the inflamed uterus, the elevation of PGE2 and PGI2 synthesis takes place. Both prostaglandins cause smooth uterine muscles relaxation and the dilatation of blood and lymph vessels in this organ. In these conditions, the blood and lymph outflow from the uterus is several times slower than in the control animals. The secretion of P4 and E2 from CLP, in comparison with control animals, is significantly lower. Decreased P4 concentration during the luteal phase of the estrous cycle, and E2 in the initiation of the luteolysis period, may cause the insufficient preparation of the endometrium for hypophyseal OT activity. Finally, we can assume that the creation of the CLP in the animal ovary is an exceptionally complex and not yet fully understood process.
Pol J Vet Sci 2005
PMID:Immuno-endocrine mechanisms connected with the creation of corpora lutea persistent in animal ovaries. 1618 May 88


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