Biological signals and receptors最新文献

{"title":"Effects of somatostatin and its analogues on tyrosine kinase activity in rodent tumors.","authors":"A Lachowicz-Ochedalska,&nbsp;E Rebas,&nbsp;J Kunert-Radek,&nbsp;K Winczyk,&nbsp;M Pawlikowski","doi":"10.1159/000014647","DOIUrl":"https://doi.org/10.1159/000014647","url":null,"abstract":"<p><p>The effects of native somatostatin-14 (SS-14) and of its two analogues, octreotide and CH-275, on the activity of tyrosine kinases (TK) in two rodent tumors (rat pituitary tumor and murine colonic cancer) were studied in vitro. The activity of TK was measured in tissue homogenates using gamma[(32)P]ATP as the donor of the phosphoryl group and poly(Glu(80), Tyr(20)) as a substrate. It was found that native SS-14 inhibited TK activity in both investigated tumors. Octreotide, which acts preferentially via somatostatin receptor subtype 2 (SSTR2), was very effective in inhibiting TK activity in the rat pituitary tumor, but it is a rather weak inhibitor of TK activity in murine colonic cancer. CH-275, a selective ligand of the SSTR1 subtype of SS receptors, suppressed TK activity in the pituitary tumor but was ineffective in the colonic cancer. It is hypothesized that the effect of neuropeptide somatostatin (SS-14) on murine colonic cancer is exerted via the subtype of receptor which does not interact with CH-275 and has no or low affinity for octreotide (SSTR 4, 3 or 5?).</p>","PeriodicalId":79565,"journal":{"name":"Biological signals and receptors","volume":"9 5","pages":"255-9"},"PeriodicalIF":0.0,"publicationDate":"2000-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000014647","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"21801204","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Nonradioisotope assay of glucose uptake activity in rat skeletal muscle using enzymatic measurement of 2-deoxyglucose 6-phosphate in vitro and in vivo.","authors":"A Ueyama,&nbsp;T Sato,&nbsp;H Yoshida,&nbsp;K Magata,&nbsp;N Koga","doi":"10.1159/000014649","DOIUrl":"https://doi.org/10.1159/000014649","url":null,"abstract":"<p><p>We investigated a nonradioisotope method for the evaluation of glucose uptake activity using enzymatic measurement of 2-deoxyglucose 6-phosphate (2DG6P) content in isolated rat soleus muscle in vitro and in vivo. The 2DG6P content in isolated rat soleus muscle after incubation with 2-deoxyglucose (2DG) was increased in a dose-dependent manner by insulin (ED(50) = 0.6 mU/ml), the maximum response being about 5 times that of the basal content in vitro. This increment was completely abolished by wortmannin (100 nM), with no effect on basal 2DG6P content. An insulin-mimetic compound, vanadium, also increased 2DG6P content in a dose-dependent manner. In isolated soleus muscle of Zucker fa/fa rats, well known as an insulin-resistant model, insulin did not increase 2DG6P content. The 2DG6P content in rat soleus muscle increased after 2DG (3 mmol/kg) injection in vivo, and conversely, the 2DG concentration in plasma was decreased in a dose-dependent manner by insulin (ED(50) = 0.11 U/kg). The maximum response of the accumulation of 2DG6P in soleus muscle was about 4 times that of the basal content. This method could be useful for evaluating glucose uptake (transport plus phosphorylation) activity in soleus muscle in vitro and in vivo without using radioactive materials.</p>","PeriodicalId":79565,"journal":{"name":"Biological signals and receptors","volume":"9 5","pages":"267-74"},"PeriodicalIF":0.0,"publicationDate":"2000-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000014649","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"21801210","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Immunoglobulin G1 Fc fragment-tagged human opioid receptor-like receptor retains the ability to inhibit cAMP accumulation.","authors":"L Y Yung, K W Tsim, G Pei, Y H Wong","doi":"10.1159/000014645","DOIUrl":"10.1159/000014645","url":null,"abstract":"<p><p>The human opioid receptor-like (ORL(1)) receptor was tagged with the immunoglobulin G1 Fc fragment at the carboxy-terminus and expressed in human embryonic kidney 293 cells. Expression of the ORL(1)-Fc receptor was confirmed by immunohistochemical staining. The fusion protein was enriched by affinity chromatography and then verified by immunodetection. The function of the ORL(1)-Fc receptor was determined by examining nociceptin/OFQ-induced inhibition of cAMP accumulation. The ORL(1)-Fc receptor inhibited the forskolin-stimulated cAMP accumulation. The inhibitory response was selectively induced by nociceptin/OFQ in a dose-dependent and pertussis toxin-sensitive manner. Our results indicate that the carboxy-terminal Fc-tagged ORL(1) receptor retained the ability to interact with G(i) proteins to inhibit adenylyl cyclase.</p>","PeriodicalId":79565,"journal":{"name":"Biological signals and receptors","volume":"9 5","pages":"240-7"},"PeriodicalIF":0.0,"publicationDate":"2000-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000014645","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"21801207","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Melatonin and biological rhythms.","authors":"P Pévet","doi":"10.1159/000014640","DOIUrl":"https://doi.org/10.1159/000014640","url":null,"abstract":"<p><p>Circadian and seasonal rhythms are a fundamental feature of all living organisms. The functional mechanism involved is built around internal biological clock(s) and the hormone melatonin (Mel) is one of its critical components. Although numerous other sources have been identified (retina, harderian gland, gut), in vertebrates Mel is primarily produced by the pineal gland during the dark period of the light-dark cycle. This rhythmic Mel is generated directly by circadian clock(s). The Mel rhythm is thus an important efferent hormonal signal from the clock. The periodic secretion of Mel might thus be used as a circadian mediator of a system that can 'read' the message. The duration of the nocturnal Mel production is directly proportional to the length of the dark period. It is through these changes in duration that the brain integrates the photoperiodic information. In essence, the Mel rhythm appears to be an endocrine code of the environmental light-dark cycle conveying photic information that is used by organisms for both circadian and seasonal temporal organization. The major question arising from this effect of Mel concerns it precise mechanism of action. From the data reported in the present minireview, it appears that the photoneuroendocrine mechanism is not fundamentally different in vertebrates at least as far as the role of Mel is concerned.</p>","PeriodicalId":79565,"journal":{"name":"Biological signals and receptors","volume":"9 3-4","pages":"203-12"},"PeriodicalIF":0.0,"publicationDate":"2000-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000014640","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"21741417","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Pharmacology and physiology of melatonin in the reduction of oxidative stress in vivo.","authors":"R J Reiter,&nbsp;D X Tan,&nbsp;W Qi,&nbsp;L C Manchester,&nbsp;M Karbownik,&nbsp;J R Calvo","doi":"10.1159/000014636","DOIUrl":"https://doi.org/10.1159/000014636","url":null,"abstract":"<p><p>This brief resume summarizes the evidence which shows that melatonin is a significant free radical scavenger and antioxidant at both physiological and pharmacological concentrations in vivo. Surgical removal of the pineal gland, a procedure which lowers endogenous melatonin levels in the blood, exaggerates molecular damage due to free radicals during an oxidative challenge. Likewise, providing supplemental melatonin during periods of massive free radical production greatly lowers the resulting tissue damage and dysfunction. In the current review, these findings are considered in terms of neurodegenerative diseases, cancer, ischemia/reperfusion injury and aging. Besides being a highly effective direct free radical scavenger and indirect antioxidant, melatonin has several features that make it of clinical interest. Thus, melatonin is readily absorbed when it is administered via any route, it crosses all morphophysiological barriers, e.g., blood-brain barrier and placenta, with ease, it seems to enter all parts of every cell where it prevents oxidative damage, it preserves mitochondrial function, and it has low toxicity. While blood melatonin levels are normally low, tissue levels of the indoleamine can be considerably higher and at some sites, e.g., in bone marrow cells and bile, melatonin concentrations exceed those in the blood by several orders of magnitude. What constitutes a physiological level of melatonin must be redefined in terms of the bodily fluid, tissue and subcellular compartment being examined.</p>","PeriodicalId":79565,"journal":{"name":"Biological signals and receptors","volume":"9 3-4","pages":"160-71"},"PeriodicalIF":0.0,"publicationDate":"2000-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000014636","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"21740512","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Nuclear receptors are involved in the enhanced IL-6 production by melatonin in U937 cells.","authors":"J M Guerrero,&nbsp;D Pozo,&nbsp;S García-Mauriño,&nbsp;A Carrillo,&nbsp;C Osuna,&nbsp;P Molinero,&nbsp;J R Calvo","doi":"10.1159/000014639","DOIUrl":"https://doi.org/10.1159/000014639","url":null,"abstract":"<p><p>This report shows that melatonin enhances IL-6 production by U937 cells via a nuclear receptor-mediated mechanism. Resting U937 cells only express membrane (mt1) melatonin receptors. In these cells, melatonin did not modify basal production of IL-6 or when activated by PMA plus lipopolysaccharide, a treatment that downregulates the expression of mt1 receptor. However, in U937 cells activated with IFN-gamma, which induces the expression of the ROR alpha 1 and ROR alpha 2 nuclear receptors and represses the expression of the mt1 receptor, melatonin can activate IL-6 production. These results show that the expression of nuclear melatonin receptor but not membrane receptors is sufficient for melatonin to activate cytokine production in human lymphocytic and monocytic cell lines.</p>","PeriodicalId":79565,"journal":{"name":"Biological signals and receptors","volume":"9 3-4","pages":"197-202"},"PeriodicalIF":0.0,"publicationDate":"2000-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000014639","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"21740438","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Photic regulation of mt(1) melatonin receptors and 2-iodomelatonin binding in the rat and Siberian hamster.","authors":"M Masson-Pévet,&nbsp;F Gauer,&nbsp;C Schuster,&nbsp;H Y Guerrero","doi":"10.1159/000014638","DOIUrl":"https://doi.org/10.1159/000014638","url":null,"abstract":"<p><p>We have investigated the photic regulation of melatonin receptors both at the level of binding capacity and mt(1) mRNA expression in the suprachiasmatic nucleus (SCN) and the pars tuberalis (PT) of the pituitary of two species: a highly photoperiodic one, the Siberian hamster, and a nonphotoperiodic one, the Wistar rat. This study has been performed by looking at the effect of a light pulse applied during the night on the two receptor parameters. The results show that the photic regulations of mt(1) mRNA expression and receptor density are distinct from each other in both the SCN and PT of the two species studied. They also show that, depending on the species and the structure, this regulation may implicate either the circadian clock or melatonin.</p>","PeriodicalId":79565,"journal":{"name":"Biological signals and receptors","volume":"9 3-4","pages":"188-96"},"PeriodicalIF":0.0,"publicationDate":"2000-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000014638","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"21740435","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Biological basis and possible physiological implications of melatonin receptor-mediated signaling in the rat epididymis.","authors":"S Y Shiu,&nbsp;L Li,&nbsp;S W Siu,&nbsp;S C Xi,&nbsp;S W Fong,&nbsp;S F Pang","doi":"10.1159/000014637","DOIUrl":"https://doi.org/10.1159/000014637","url":null,"abstract":"<p><p>The mammalian epididymis plays an important role in sperm maturation, an important process of male reproduction. Specific high-affinity 2-[(125)I]iodomelatonin binding sites, satisfying the pharmacokinetic properties of specific receptors, have been found in the rat corpus epididymis, suggesting a direct melatonin action on epididymal physiology. Subsequent molecular and cell biology studies have identified these 2-[(125)I]iodomelatonin binding sites to be mt(1) (MEL(1A)) and MT(2) (MEL(1B)) melatonin receptor subtypes. Changes in the binding characteristics of these receptors in the rat corpus epididymis in response to castration and steroid hormones like testosterone and hydrocortisone indicated that these membrane melatonin receptors are biologically functional receptors, whose activities are differentially regulated by testosterone and hydrocortisone. These melatonin receptors are coupled to pertussis toxin (PTX)-sensitive G(i) protein and probably participate in androgenic and adrenergic regulation of rat corpus epididymal epithelial cell functions. Furthermore, rat corpus epididymal epithelial cell proliferation was stimulated by melatonin, whose action was dependent on the concentration and duration of exposure to the hormone. Interestingly, an MT(2) receptor ligand (4-phenyl-2-propionamidotetraline, 4-P-PDOT) induced a stimulatory effect on epididymal epithelial cell proliferation similar to that produced by melatonin. In contrast, a nuclear melatonin receptor agonist (1-[3-allyl-4-oxo-thiazolidine-2-ylidene]-4-methyl-thiosemi-car bazone , CGP52608) and 8-bromo-cAMP inhibited epididymal epithelial cell proliferation. Taken together, our data lead us to postulate that one of the possible physiological functions of melatonin on the rat epididymis is the stimulation of mt(1) and MT(2) melatonin receptors resulting in the inhibition of cAMP signaling and an increase in epithelial cell proliferation.</p>","PeriodicalId":79565,"journal":{"name":"Biological signals and receptors","volume":"9 3-4","pages":"172-87"},"PeriodicalIF":0.0,"publicationDate":"2000-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000014637","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"21740433","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Significance of melatonin in antioxidative defense system: reactions and products.","authors":"D X Tan,&nbsp;L C Manchester,&nbsp;R J Reiter,&nbsp;W B Qi,&nbsp;M Karbownik,&nbsp;J R Calvo","doi":"10.1159/000014635","DOIUrl":"https://doi.org/10.1159/000014635","url":null,"abstract":"<p><p>Melatonin is a potent endogenous free radical scavenger, actions that are independent of its many receptor-mediated effects. In the last several years, hundreds of publications have confirmed that melatonin is a broad-spectrum antioxidant. Melatonin has been reported to scavenge hydrogen peroxide (H(2)O(2)), hydroxyl radical (HO(.)), nitric oxide (NO(.)), peroxynitrite anion (ONOO(-)), hypochlorous acid (HOCl), singlet oxygen ((1)O(2)), superoxide anion (O(2)(-).) and peroxyl radical (LOO(.)), although the validity of its ability to scavenge O(2)(-). and LOO(.) is debatable. Regardless of the radicals scavenged, melatonin prevents oxidative damage at the level of cells, tissues, organs and organisms. The antioxidative mechanisms of melatonin seem different from classical antioxidants such as vitamin C, vitamin E and glutathione. As electron donors, classical antioxidants undergo redox cycling; thus, they have the potential to promote oxidation as well as prevent it. Melatonin, as an electron-rich molecule, may interact with free radicals via an additive reaction to form several stable end-products which are excreted in the urine. Melatonin does not undergo redox cycling and, thus, does not promote oxidation as shown under a variety of experimental conditions. From this point of view, melatonin can be considered a suicidal or terminal antioxidant which distinguishes it from the opportunistic antioxidants. Interestingly, the ability of melatonin to scavenge free radicals is not in a ratio of mole to mole. Indeed, one melatonin molecule scavenges two HO. Also, its secondary and tertiary metabolites, for example, N(1)-acetyl-N(2)-formyl-5-methoxykynuramine, N-acetyl-5-methoxykynuramine and 6-hydroxymelatonin, which are believed to be generated when melatonin interacts with free radicals, are also regarded as effective free radical scavengers. The continuous free radical scavenging potential of the original molecule (melatonin) and its metabolites may be defined as a scavenging cascade reaction. Melatonin also synergizes with vitamin C, vitamin E and glutathione in the scavenging of free radicals. Melatonin has been detected in vegetables, fruits and a variety of herbs. In some plants, especially in flowers and seeds (the reproductive organs which are most vulnerable to oxidative insults), melatonin concentrations are several orders of magnitude higher than measured in the blood of vertebrates. Melatonin in plants not only provides an alternative exogenous source of melatonin for herbivores but also suggests that melatonin may be an important antioxidant in plants which protects them from a hostile environment that includes extreme heat, cold and pollution, all of which generate free radicals.</p>","PeriodicalId":79565,"journal":{"name":"Biological signals and receptors","volume":"9 3-4","pages":"137-59"},"PeriodicalIF":0.0,"publicationDate":"2000-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000014635","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"21740511","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The regulation of apoptosis in preantral ovarian follicles.","authors":"E A McGee","doi":"10.1159/000014626","DOIUrl":"https://doi.org/10.1159/000014626","url":null,"abstract":"<p><p>Less than 1% of ovarian follicles ever mature to ovulation. The remainder undergo atretic degeneration via apoptosis during development. Though the regulation of antral and preovulatory survival has been studied for many years, very little is known about the regulation of survival and development of preantral follicles. This review discusses recent findings regarding preantral follicle development with emphasis on the regulation of preantral follicle apoptosis.</p>","PeriodicalId":79565,"journal":{"name":"Biological signals and receptors","volume":"9 2","pages":"81-6"},"PeriodicalIF":0.0,"publicationDate":"2000-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000014626","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"21656436","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}