Relevant bibliographies by topics / Nucleotide extracellulaire

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Academic literature on the topic 'Nucleotide extracellulaire'

Author: Grafiati
Published: 4 June 2021
Last updated: 14 February 2022

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Journal articles on the topic "Nucleotide extracellulaire"

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Gendaszewska-Darmach, Edyta, Maria Maszewska, Małgorzata Zakłos, and Maria Koziołkiewicz. "Degradation of extracellular nucleotides and their analogs in HeLa and HUVEC cell cultures." Acta Biochimica Polonica 50, no. 4 (2003): 973–84. http://dx.doi.org/10.18388/abp.2003_3627.

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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.
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Gounaris, Kleoniki. "Nucleotidase Cascades Are Catalyzed by Secreted Proteins of the Parasitic Nematode Trichinella spiralis." Infection and Immunity 70, no. 9 (2002): 4917–24. http://dx.doi.org/10.1128/iai.70.9.4917-4924.2002.

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ABSTRACT Extracellular nucleotides are signaling molecules whose receptor-mediated effects are involved in a variety of physiological responses in mammalian tissues. An overwhelming body of data indicate that inflammatory and other immune responses can be modulated by the availability and local concentrations of nucleotides via nucleotide receptor signaling, but this is only just beginning to be investigated in the context of infectious disease. Evidence is provided here that the parasitic nematode Trichinella spiralis can catalyze the conversion and thus modulate both the availability and concentration of extracellular nucleotides by means of the following secreted exoenzymes: apyrase, 5′-nucleotidase, and adenosine deaminase. These enzymes were characterized in terms of substrate specificity, kinetic behavior, pH, divalent cation preferences, and response to a series of compounds. The secreted 5′-nucleotidase was identified as a protein with an apparent molecular mass of 67 kDa after N-terminal amino acid sequencing of the purified protein. The presence of adenosine deaminase was confirmed in the secreted products by Western blotting with an antibody against a mammalian enzyme, as a protein with an apparent molecular mass of 38 kDa. These secreted proteins constitute an enzymatic cascade which catalyzes the degradation of extracellular nucleotides, with a potential physiological role in the regulation of purinergic signaling.
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Opdebeeck, Britt, Isabel R. Orriss, Ellen Neven, Patrick C. D’Haese, and Anja Verhulst. "Extracellular Nucleotides Regulate Arterial Calcification by Activating Both Independent and Dependent Purinergic Receptor Signaling Pathways." International Journal of Molecular Sciences 21, no. 20 (2020): 7636. http://dx.doi.org/10.3390/ijms21207636.

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Arterial calcification, the deposition of calcium-phosphate crystals in the extracellular matrix, resembles physiological bone mineralization. It is well-known that extracellular nucleotides regulate bone homeostasis raising an emerging interest in the role of these molecules on arterial calcification. The purinergic independent pathway involves the enzymes ecto-nucleotide pyrophosphatase/phosphodiesterases (NPPs), ecto-nucleoside triphosphate diphosphohydrolases (NTPDases), 5′-nucleotidase and alkaline phosphatase. These regulate the production and breakdown of the calcification inhibitor—pyrophosphate and the calcification stimulator—inorganic phosphate, from extracellular nucleotides. Maintaining ecto-nucleotidase activities in a well-defined range is indispensable as enzymatic hyper- and hypo-expression has been linked to arterial calcification. The purinergic signaling dependent pathway focusses on the activation of purinergic receptors (P1, P2X and P2Y) by extracellular nucleotides. These receptors influence arterial calcification by interfering with the key molecular mechanisms underlying this pathology, including the osteogenic switch and apoptosis of vascular cells and possibly, by favoring the phenotypic switch of vascular cells towards an adipogenic phenotype, a recent, novel hypothesis explaining the systemic prevention of arterial calcification. Selective compounds influencing the activity of ecto-nucleotidases and purinergic receptors, have recently been developed to treat arterial calcification. However, adverse side-effects on bone mineralization are possible as these compounds reasonably could interfere with physiological bone mineralization.
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Beckenkamp, Aline, Danielle Bertodo Santana, Alessandra Nejar Bruno, et al. "Ectonucleotidase expression profile and activity in human cervical cancer cell lines." Biochemistry and Cell Biology 92, no. 2 (2014): 95–104. http://dx.doi.org/10.1139/bcb-2013-0051.

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Cervical cancer is the third most frequent cancer in women worldwide. Adenine nucleotide signaling is modulated by the ectonucleotidases that act in sequence, forming an enzymatic cascade. Considering the relationship between the purinergic signaling and cancer, we studied the E-NTPDases, ecto-5′-nucleotidase, and E-NPPs in human cervical cancer cell lines and keratinocytes. We evaluated the expression profiles of these enzymes using RT-PCR and quantitative real-time PCR analysis. The activities of these enzymes were examined using ATP, ADP, AMP, and p-nitrophenyl-5′-thymidine monophosphate (p-Nph-5′-TMP) as substrate, in a colorimetric assay. The extracellular adenine nucleotide hydrolysis was estimated by HPLC analysis. The hydrolysis of all substrates exhibited a linear pattern and these activities were cation-dependent. An interesting difference in the degradation rate was observed between cervical cancer cell lines SiHa, HeLa, and C33A and normal imortalized keratinocytes, HaCaT cells. The mRNA of ecto-5′-nucleotidase, E-NTPDases 5 and 6 were detectable in all cell lines, and the dominant gene expressed was the Entpd 5 enzyme, in SiHa cell line (HPV16 positive). In accordance with this result, a higher hydrolysis activity for UDP and GDP nucleotides was observed in the supernatant of the SiHa cells. Both normal and cancer cells presented activity and mRNAs of members of the NPP family. Considering that these enzymes exert an important catalytic activity, controlling purinergic nucleotide concentrations in tumors, the presence of ectonucleotidases in cervical cancer cells can be important to regulate the levels of extracellular adenine nucleotides, limiting their effects.
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Vettenranta, K., and K. O. Raivio. "Extracellular adenine nucleotides in human trophoblastic purine nucleotide synthesis." Placenta 10, no. 5 (1989): 472. http://dx.doi.org/10.1016/0143-4004(89)90091-x.

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Parabucki, Ana, Danijela Savic, Danijela Laketa, et al. "Expression of major ectonucleotidases after cortical stab brain injury in rats: A real-time PCR study." Archives of Biological Sciences 66, no. 1 (2014): 149–55. http://dx.doi.org/10.2298/abs1401148p.

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Ectonucleotidases are cell surface-located enzymes responsible for the extracellular degradation of nucleotides. They are comprised of several protein families: ectonucleoside triphosphate diphosphohydrolases (E-NTPDase), ectonucleotide pyrophosphatase/phosphodiesterases (E-NPPases) and ecto-5?-nucleotidase. Previously we showed that cortical stab injury alters ectonucleotidase activities in the rat brain, but that the specific enzymes responsible for these changes were not identified. In this study we investigated the gene expression of the specific ectonucleotidase enzymes, NTPDase1- 3, NPP1-3 and ecto-5?-nucleotidase, two and seven days after cortical stab injury in rats, using real-time PCR. Two days after the injury we observed only one significant change: the downregulation in NTPDase2 mRNA expression. Our results indicate that traumatic brain injury induces significant upregulation of NTPDase1, NTPDase2 and ecto-5?-nucleotidase transcripts, and the downregulation of NPP1, seven days after the injury. Thus, traumatic brain injury has diverse impacts on ectonucleotidases gene expression, which may be reflected in the enzyme activities and extracellular nucleotide concentrations in the perilesional tissue.
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YEGUTKIN, Gennady G., Tiina HENTTINEN, Sergei S. SAMBURSKI, Jozef SPYCHALA, and Sirpa JALKANEN. "The evidence for two opposite, ATP-generating and ATP-consuming, extracellular pathways on endothelial and lymphoid cells." Biochemical Journal 367, no. 1 (2002): 121–28. http://dx.doi.org/10.1042/bj20020439.

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Extracellular purines are important signalling molecules in the vasculature that are regulated by a network of cell surface ectoenzymes. By using human endothelial cells and normal and leukaemic lymphocytes as enzyme sources, we identified the following purine-converting ectoenzymes: (1) ecto-nucleotidases, NTP diphosphohydrolase/CD39 (EC 3.6.1.5) and ecto-5′-nucleotidase/CD73 (EC 3.1.3.5); (2) ecto-nucleotide kinases, adenylate kinase (EC 2.7.4.3) and nucleoside diphosphate kinase (EC 2.7.4.6); (3) ecto-adenosine deaminase (EC 3.5.4.4). Evidence for this was obtained by using enzyme assays with 3H-labelled nucleotides and adenosine as substrates, direct evaluation of γ-phosphate transfer from [γ-32P]ATP to AMP/NDP, and bioluminescent measurement of extracellular ATP synthesis. In addition, incorporation of radioactivity into an approx. 20kDa surface protein was observed following incubation of Namalwa B cells with [γ-32P]ATP. Thus two opposite, ATP-generating and ATP-consuming, pathways coexist on the cell surface, where basal ATP release, re-synthesis of high-energy phosphoryls, and selective ecto-protein phosphorylation are counteracted by stepwise nucleotide breakdown with subsequent adenosine inactivation. The comparative measurements of enzymic activities indicated the predominance of the nucleotide-inactivating pathway via ecto-nucleotidase reactions on the endothelial cells. The lymphocytes are characterized by counteracting ATP-regenerating/adenosine-eliminating phenotypes, thus allowing them to avoid the lymphotoxic effects of adenosine and maintain surrounding ATP at a steady-state level. These results are in agreement with divergent effects of ATP and adenosine on endothelial function and haemostasis, and provide a novel regulatory mechanism of local agonist availability for nucleotide- or nucleoside-selective receptors within the vasculature.
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Eltzschig, Holger K., Linda F. Thompson, Jorn Karhausen, et al. "Endogenous adenosine produced during hypoxia attenuates neutrophil accumulation: coordination by extracellular nucleotide metabolism." Blood 104, no. 13 (2004): 3986–92. http://dx.doi.org/10.1182/blood-2004-06-2066.

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Abstract Hypoxia is a well-documented inflammatory stimulus and results in tissue polymorphonuclear leukocyte (PMN) accumulation. Likewise, increased tissue adenosine levels are commonly associated with hypoxia, and given the anti-inflammatory properties of adenosine, we hypothesized that adenosine production via adenine nucleotide metabolism at the vascular surface triggers an endogenous anti-inflammatory response during hypoxia. Initial in vitro studies indicated that endogenously generated adenosine, through activation of PMN adenosine A2A and A2B receptors, functions as an antiadhesive signal for PMN binding to microvascular endothelia. Intravascular nucleotides released by inflammatory cells undergo phosphohydrolysis via hypoxia-induced CD39 ectoapyrase (CD39 converts adenosine triphosphate/adenosine diphosphate [ATP/ADP] to adenosine monophosphate [AMP]) and CD73 ecto-5′-nucleotidase (CD73 converts AMP to adenosine). Extensions of our in vitro findings using cd39- and cd73-null animals revealed that extracellular adenosine produced through adenine nucleotide metabolism during hypoxia is a potent anti-inflammatory signal for PMNs in vivo. These findings identify CD39 and CD73 as critical control points for endogenous adenosine generation and implicate this pathway as an innate mechanism to attenuate excessive tissue PMN accumulation. (Blood. 2004;104:3986-3992)
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Kennedy, Eileen J., Lorraine Pillus, and Gourisankar Ghosh. "Pho5p and Newly Identified Nucleotide Pyrophosphatases/ Phosphodiesterases Regulate Extracellular Nucleotide Phosphate Metabolism in Saccharomyces cerevisiae." Eukaryotic Cell 4, no. 11 (2005): 1892–901. http://dx.doi.org/10.1128/ec.4.11.1892-1901.2005.

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ABSTRACT Extracellular nucleotides play many biological roles, including intercellular communication and modulation of nucleotide receptor signaling, and are dependent on the phosphorylation state of the nucleotide. Regulation of nucleotide phosphorylation is necessary, and a specialized class of enzymes, nucleotide pyrophosphatases/phosphodiesterases (E-NPPs), has been identified in mammals to perform this function. Although the E-NPP class is conserved among complex eukaryotes, this system has not yet been identified in Saccharomyces cerevisiae. Using genetic and biochemical experiments, we show that two orthologs of the E-NPP family, referred to as Npp1p and Npp2p, exist in budding yeast and can perform nucleotide phosphate hydrolysis. This activity is enhanced during phosphate starvation, where hydrolyzed phosphates can be imported from extracellular sources and utilized to overcome phosphate starvation through the activity of the Pho5p acid phosphatase. The added compensatory effect by Pho5p is also a newly established role for Pho5p. This study demonstrates that extracellular nucleotide phosphate metabolism appears to be controlled by at least two independent regulatory mechanisms, uniting phosphate starvation with extracellular nucleotide regulation.
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Dawicki, D. D., J. McGowan-Jordan, S. Bullard, S. Pond, and S. Rounds. "Extracellular nucleotides stimulate leukocyte adherence to cultured pulmonary artery endothelial cells." American Journal of Physiology-Lung Cellular and Molecular Physiology 268, no. 4 (1995): L666—L673. http://dx.doi.org/10.1152/ajplung.1995.268.4.l666.

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Adenosine, ATP, and various nucleotides were examined for their effects on the adherence of leukocytes to bovine pulmonary artery endothelial cells. Extracellular ATP enhanced adherence of HL-60 cells and human neutrophils to endothelial cells in a dose-dependent fashion. Maximal adherence occurred after 15 min coincubation of ATP and HL-60 cells or neutrophils with endothelial cells. ATP stimulation was mediated by direct effects on both HL-60 cells and endothelial cells. The potency profile of various nucleotides was ATP = 2-MeSATP > beta,gamma-CH2ATP, indicative of a P2y receptor. Interestingly, UTP was as potent as ATP in stimulating HL-60 cell adherence, suggesting the presence of a pyrimidine nucleotide receptor. Photoaffinity labeling of endothelial cells with 8-Az-[alpha-32P]ATP showed the presence of two ATP binding proteins of 48 and 87 kDa. ATP and 2-MeSATP inhibited binding by both proteins. Labeling of the 87-kDa protein was inhibited by beta,gamma-CH2ATP, whereas UTP blocked binding by the 48-kDa protein. Thus photoaffinity labeling experiments support the proposal that endothelial cells possess two ATP receptors, one of which is a P2u nucleotide receptor. These findings show that extracellular nucleotides enhance leukocyte adherence to endothelial cells. Nucleotide release into the extracellular space may be one mechanism of exacerbating vascular cell injury relevant to conditions such as adult respiratory distress syndrome and septic shock.
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Dissertations / Theses on the topic "Nucleotide extracellulaire"

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Djerada, Zoubir. "Récepteurs P2Y et Cardioprotection : implication du récepteur P2Y11-like dans le préconditionnement pharmacologique induit par le NAADP extracellulaire." Thesis, Reims, 2013. http://www.theses.fr/2013REIMM201.

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L’infarctus du myocarde (IC) représente plus de 15 % de la mortalité mondiale liés aux maladies cardiovasculaires (MC). En absence d’une rapide reperfusion des coronaires occluses, aucune intervention thérapeutique n’est capable de limiter les effets délétères de l’IC. Un des moyens les plus efficaces de la cardioprotection, étudié en recherche, est le préconditionnement cardiaque ischémique (PCI). L’adénosine libérée au cours du PCI active via ces récepteurs P1 les voies de cardioprotection. Des études mettent en évidence également l’implication des purinorécepteurs P2Y dans la cardioprotection. Les récepteurs P2Y2, 4 et 6 sont les plus étudiés dans la cardioprotection. Les récepteurs P2Y sont sensibles aux nucléotides comme l’ATP et l’UTP libérés au cours de l’ischémie. Parmi les récepteurs P2Y seul le récepteur P2Y11 est doublement couplé à l’adénylate cyclase et à la phospholipase C (PLC). Il est également le seul récepteur dont le polymorphisme génétique, induisant une perte du signal métabotropique, prédispose à plus de risques d’IC et d’inflammation dans toutes les catégories d’âge indépendamment des facteurs de risques variables de l’IC (Amisten et al., 2007). Ceci suggère un important rôle du récepteur P2Y11 dans la prévention primaire et comme cible thérapeutique de l’infarctus du myocarde. Le β-NAD, nucléotide à base de pyridine, est libéré au cours de l’ischémie comme les médiateurs de cardioprotection notamment l’adénosine, l’ATP et l’UTP. Cependant, aucune étude ne s’est intéressée spécifiquement aux rôles du P2Y11 et des nucléotides pyridiniques, comme médiateurs, dans la cardioportection alors que le NAADP, un métabolite du β-NAD, est rapporté comme agoniste (Moreschi et al., 2008) du récepteur P2Y11. Dans ce travail, nous avons mis en évidence pour la première fois l’augmentation des concentrations interstitielles des métabolites du β-NAD comme le NAADP au cours de l’ischémie. L’augmentation des concentrations du NAADP décrit une cinétique comparable à celle de l’adénosine. Le NAADP extracellulaire ([NAADP]e), appliqué avant un cycle d’ischémie/reperfusion (I/R), déclenche une cardioprotection envers les effets délétères de l’I/R. En effet, le [NAADP]e améliore les fonctions contractiles, réduit les contractures, les arythmies de reperfusion et la taille de l’infarctus, dans un modèle d’I/R cardiaque chez le rat. Ce préconditionnement pharmacologique induit par le [NAADP]e implique les récepteurs P2Y11-like. Dans un modèle de cardiomyocytes, nous mettons en évidence l’activité métabotropique spécifique du récepteur P2Y11-like déclenché par le [NAADP]e. Le [NAADP]e déclenche via le récepteur P2Y11-like l’activation de la PKCε, ERK1/2, AKT et GSK-3β, des protéines kinases de prosurvie cellulaire, ce qui explique ses effets cardioprotecteurs. La phosphorylation des protéines de prosurvie cellulaire nécessite la médiation de la PKA, de la PLC et de la src. Le NF546, un nouvel agoniste sélectif du récepteur P2Y11, déclenche une activité métabotropique semblable à celle du [NAADP]e, confirmant ainsi l’existence fonctionnelle du récepteur P2Y11-like au niveau des cardiomyocytes de rat. L’activation du récepteur P2Y11-like, que ce soit par le [NAADP]e ou le NF546, induit une augmentation des concentrations intracellulaires du β-NAD et de ses métabolites, le NADP, le NAADP, le NAAD et l’ADP ribose cyclique. Le β-NAD, le NAADP comme le NAAD, ont été impliqués dans le déclenchement au niveau intracellulaire des voies de cardioprotection comme la voie des sirtuines et de l’autophagie. Ces mécanismes peuvent être complementaires de l’effet cardioprotecteur du [NAADP]e. L’ensemble de nos données conforte le rôle cardioprotecteur du récépteur P2Y11 et suggère que le NAADP interstitiel accumulé au cours de l’ischémie pourrait avoir un rôle de facteur paracrine de survie cellulaire améliorant la survie des cardiomyocytes au cours des évènements ischémiques
Myocardial infarction (MI) accounts for more than 15 % of global deaths related to cardiovascular diseases (CD). In the absence of a prompt reperfusion of occluded coronary arteries, none of therapeutic interventions is able to limit the deleterious effects of MI. One of the most effective means of cardioprotection, studied in research, is the ischemic cardiac preconditioning (ICP). Adenosine released during ICP triggers, via P1 receptors, cardioprotective effects. Involvement of the purinoceptors (P2Y) in cardioprotective effects has been also reported. P2Y2,4,6 receptors, the most studied P2Y receptors in cardioprotection, are activated by the nucleotides released during ischemia such as ATP and UTP. Among the P2Y receptors, P2Y11 is dually coupled to Gs and Gq proteins and is the single P2Y receptor which has been linked, via a genetic polymorphism, to an increased risk of acute myocardial infarction and elevated levels of C-reactive protein in humans in all age groups (Amisten et al., 2007). This suggests for the P2Y11 receptor an important role in primary prevention and as a therapeutic target of the P2Y11 receptor for myocardial infarction. β-NAD, a pyridine nucleotide, is released during ischemia like adenosine, ATP and UTP. However, no study has focused on the roles of P2Y11 receptor and pyridine nucleotide in mediating cardioprotective effects while NAADP, a β-NAD metabolite, has been reported as an agonist (Moreschi et al., 2008) of the P2Y11 receptor. In this work, we show, for the first time, increased interstitial concentrations of NAADP during ischemia. Interstitial kinetics of NAADP is similar to adenosine. Using a pharmacological preconditioning protocol, triggered by extracellular NAADP ([NAADP]e) before a prolonged ischemia/reperfusion (I/R), rat hearts rapidly recovered post-ischemic contractile function and displayed attenuated contracture, infarct size and arrhythmogenesis. This pharmacological preconditioning involves the P2Y11-like receptor. In cardiomyocytes culture, [NAADP]e induces specific metabotropic response of the P2Y11-like receptor. [NAADP]e triggers via the P2Y11-like receptor prosurvival protein kinases activation such as PKCε, ERK1/2, AKT and GSK-3β which explains its protective effects. Phosphorylation of prosurvival protein kinases requires the mediation of PKA, PLC and src. As with [NAADP]e, the NF546, a new selective agonist of P2Y11 receptor, triggers a metabotropic activity, thus confirming the functional existence of P2Y11-like receptor in rat cardiomyocytes. Activation of the P2Y11-like receptor, either by [NAADP]e or NF546 induced an increase in intracellular concentrations of β-NAD and its metabolites, NADP, NAADP, NAAD and cyclic ADP ribose. More, β-NAD, NAADP as well as NAAD have been involved in activation of cardioprotective pathways such as sirtuine pathways and autophagy. Taken together, our data demonstrate for the first time that the P2Y11 receptor mediates cardioprotective effects induced by [NAADP]e. NAADP is released during ischemia suggesting that [NAADP]e may act as a paracrine survival factor, prolonging cardiomyocytes lifespan during ischemic events
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Pillois, Xavier. "Modulation de l'expression des récepteurs nucléotidiques P2 de la cellule musculaire lisse artérielle." Bordeaux 2, 1998. http://www.theses.fr/1998BOR28626.

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Chaulet, Hervé. "L'ostéopontine dans la paroi artérielle : rôle dans la calcification et la réponse aux nucléotides extracellulaires." Bordeaux 2, 1999. http://www.theses.fr/1999BOR28703.

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Kennedy, Eileen Jeanne. "Understanding modulation of nucleotide binding by PKA and regulation of extracellular nucleotides in saccharomyces cerevisiae /." Diss., Connect to a 24 p. preview or request complete full text in PDF formate. Access restricted to UC campuses, 2005. http://wwwlib.umi.com/cr/ucsd/fullcit?p3208636.

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Golding, Sarah Louise. "Extracellular nucleotides and Interleukin-8 : potential mediators in psoriasis." Thesis, University of Liverpool, 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.417304.

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Orriss, Isabel. "The regulation of bone cell function by extracellular nucleotides." Thesis, University College London (University of London), 2005. http://discovery.ucl.ac.uk/1445760/.

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Extracellular nucleotides, acting via P2 receptors, modulate bone remodelling by inhibiting osteoblast and stimulating osteoclast activity. The aim of this thesis was to investigate further the effects of extracellular nucleotides on bone cell function under both normal and stress situations. Nucleotide agonists were shown to evoke intracellular Ca2+ responses in rat osteoblasts from > 0.2 uM. The approximate order of potency was ATP > UTP = ATPyS > ADP > UDP > 2-MeSATP = BzATP > a0- meATP, consistent with the expression of functional P2X2, P2X5, P2X7, P2Yi, P2Y2, P2Y4 and P2Y6 receptors. A dramatic increase in intracellular Ca responses to ATP or UTP was observed in osteoblasts cultured for 8-10 days compared to 4 days, indicating that osteoblast responsiveness to nucleotides increases with cell differentiation. P2 receptor mRNA and protein expression in osteoblasts was shown to be differentiation dependent and was characterised by a shift from P2X to P2Y expression, with mature osteoblasts strongly expressing P2Y2, P2Y4 and P2Y6 receptors. Closer investigation revealed ATP and UTP decrease alkaline phosphatase expression and activity, indicating that extracellular nucleotides primarily inhibit mineralisation rather than organic matrix synthesis. Taken together these data suggest the P2Y2 receptor, and possibly the P2Y4 receptor could function as "off-switches" for mineralised bone formation. Constitutive ATP release from primary rat osteoblasts was found to occur via vesicular exocytosis in a differentiation dependent manner. Moreover, transient exposure to hypoxia (2% 02) or hyperthermia (40 C) induced a rapid, significant increase in ATP release. In contrast, continuous culture at 2% 02, 34 C or 40 C caused marked impairment of osteoblast function and ATP release. Given the negative effects of extracellular nucleotides on bone cell function, locally increased concentrations following stress situations may contribute to the bone loss associated with hypoxia or inflammation in vivo. A bone densitometer was used to screen mice deficient in selected P2 receptors. Bone mineral content and density were increased up to 18% in P2X27 mice, decreased up to 10% in P2YfA and P2X2/3dbl '' mice but unaffected in P2X3"A animals. In summary, the work described here provides further evidence for the role of extracellular nucleotides and their receptors in the regulation of bone cell function in health and disease.
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Rossi, Lara <1979&gt. "Il nucleotide extracellulare UTP: induzione della migrazione di cellule staminali emopoietiche CD34+." Doctoral thesis, Alma Mater Studiorum - Università di Bologna, 2007. http://amsdottorato.unibo.it/183/.

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La letteratura scientifica degli ultimi anni si è arricchita di un numero sempre crescente di studi volti a chiarire i meccanismi che presiedono ai processi di homing di cellule staminali emopoietiche e del loro attecchimento a lungo termine nel midollo osseo. Tali fenomeni sembrano coinvolgere da un lato, l’interazione delle cellule staminali emopoietiche con la complessa architettura e componente cellulare midollare, e dall’altro la riposta ad un’ampia gamma di molecole regolatrici, tra le quali chemochine, citochine, molecole di adesione, enzimi proteolitici e mediatori non peptidici. Fanno parte di quest’ultimo gruppo anche i nucleotidi extracellulari, un gruppo di molecole-segnale recentemente caratterizzate come mediatori di numerose risposte biologiche, tra le quali l’allestimento di fenomeni flogistici e chemiotattici. Nel presente studio è stata investigata la capacità dei nucleotidi extracellulari ATP ed UTP di promuovere, in associazione alla chemochina CXCL12, la migrazione di cellule staminali umane CD34+. E’ così emerso che la stimolazione con UTP è in grado di incrementare significativamente la migrazione dei progenitori emopoietici in risposta al gradiente chemioattrattivo di CXCL12, nonché la loro capacità adesiva. Le analisi citofluorimetriche condotte su cellule migranti sembrano inoltre suggerire che l’UTP agisca interferendo con le dinamiche di internalizzazione del recettore CXCR4, rendendo così le cellule CD34+ maggiormente responsive, e per tempi più lunghi, al gradiente attrattivo del CXCL12. Saggi di homing competitivo in vivo hanno parallelamente mostrato, in topi NOD/SCID, che la stimolazione con UTP aumenta significativamente la capacità dei progenitori emopoeitci umani di localizzarsi a livello midollare. Sono state inoltre indagate alcune possibili vie di trasduzione del segnale attivate dalla stimolazione di recettori P2Y con UTP. Esperimenti di inibizione in presenza della tossina della Pertosse hanno evidenziato il coinvolgimento di proteine Gαi nella migrazione dipendente da CXCL12 ed UTP. Ulteriori indicazioni sono provenute dall’analisi del profilo trascrizionale di cellule staminali CD34+ stimolate con UTP, con CXCL12 o con entrambi i fattori contemporaneamente. Da questa analisi è emerso il ruolo di proteine della famiglia delle Rho GTPasi e di loro effettori a valle (ROCK 1 e ROCK 2) nel promuovere la migrazione UTP-dipendente. Questi dati sono stati confermati successivamente in vitro mediante esperimenti con Tossina B di C. Difficile (un inibitore delle Rho GTPasi) e con Y27632 (in grado di inibire specificatamente le cinasi ROCK). Nel complesso, i dati emersi in questo studio dimostrano la capacità del nucleotide extracellulare UTP di modulare la migrazione in vitro di progenitori emopoietici umani, nonché il loro homing midollare in vivo. L’effetto dell’UTP su questi fenomeni si esplica in concerto con la chemochina CXCL12, attraverso l’attivazione concertata di vie di trasduzione del segnale almeno parzialmente condivise da CXCR4 e recettori P2Y e attraverso il reclutamento comune di proteine ad attività GTPasica, tra le quali le proteine Gαi e i membri della famiglia delle Rho GTPasi.
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Hoebertz, Astrid. "Purinergic signalling in bone cells." Thesis, University College London (University of London), 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.249706.

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Vekaria, Renu. "The functional role of extracellular nucleotides in the renal tubule." Thesis, University College London (University of London), 2006. http://discovery.ucl.ac.uk/1446143/.

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There is increasing evidence that extracellular nucleotides (such as ATP, ADP, UTP and UDP), as well as the nucleoside adenosine, behave as autocrine or paracrine agents in most tissues including the kidney, acting on a group of receptors known as purinoceptors. Previous studies have shown that activation of these receptors by exogenous nucleotides can influence a variety of renal vascular and tubular functions. Purinoceptors of various subtypes are present on basolateral and apical membranes of renal tubules. However, the extent to which apical receptors are stimulated by endogenous nucleotides is unknown. Using micropuncture, the first part of this study quantified endogenous ATP in the lumen of proximal and distal tubules of the rat in vivo, both under control conditions and during pathophysiological manoeuvres. The results showed that ATP levels were sufficiently high to activate some purinoceptor subtypes. To assess whether the intraluminal ATP was being secreted or merely filtered at the glomerulus, the ATP content of fluid from Bowman's space (in Munich-Wistar rats) was compared with that in proximal tubules. The conclusion was that tubular epithelial cells secrete ATP. Using a proximal tubular epithelial cell line, the mechanism of ATP release was examined. Intracellular stores of ATP were visualised using a marker compound (quinacrine), and the fate of these stores was monitored following hypotonic stimulation of ATP release. The findings suggested that ATP is stored within the cytoplasm, possibly in vesicles, and is released by exocytosis. In the final part of the investigation, using immunohistochemistry, the distribution of five nucleotide-hydrolysing ectonucleotidases, namely NTPDases 1-3, NPP3 and ecto-5'- nucleotidase, was examined along the rat nephron. These enzymes (which differ in their hydrolysis pathways) were found to be differentially expressed along the major segments of the nephron, suggesting that they may be strategically located to influence the activity of the different purinoceptor subtypes.
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Cadassou, Octavia. "Cancer and microenvironment : the functional interplay between intra- and extracellular nucleotide metabolisms." Thesis, Lyon, 2018. http://www.theses.fr/2018LYSE1189/document.

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Les nucléotides jouent un rôle majeur dans une pléiade de processus biologiques comme la composition des acides nucléiques, la signalisation, ou la régulation de la balance énergétique. Les nucléotides extracellulaires exercent également des fonctions biologiques. Par conséquent, des dérégulations des pools de nucléotides impactent l’homéostasie de multiples façons, par exemple en promouvant l’instabilité génétique ou un environnement immunosuppresseur. Or, ces paramètres font partie des « Hallmarks du Cancer » décrits par Hanahan et Weinberg. Ces observations confirment l’éventualité d’un rôle clé des nucléotides dans le cadre du cancer.cN-II et CD73 sont des 5’-nucléotidases impliquées respectivement dans les métabolismes nucléotidiques intra- et extracellulaire. Elles sont de nouvelles cibles thérapeutiques en oncologie. Cependant, leurs rôles dans la biologie de la cellule cancéreuse, ou le possible impact de leur utilisation en tant que cible thérapeutique sur le comportement des cellules tumorales sont peu connus. Considérant l’implication de ces enzymes dans les métabolismes nucléotidiques, nous avons enquêté sur les modifications de l’agressivité de la cellule cancéreuse ou sur sa capacité à interagir avec son microenvironnement, dans le cas d’une invalidation ou une diminution d’expression de cN-II et/ou CD73. cN-II semble donc impliquée dans l’adaptabilité métabolique et la combinaison des invalidations de cN-II et CD73 est associée à une modification d’expression d’enzymes du métabolisme du glucose. CD73 peut aussi moduler l’expression de gènes de la migration cellulaire. cN-II est impliquée dans la migration cellulaire, via l’axe COX-2/PGE2, et dans la sensibilité à des agents modulant ce paramètre. Ces caractéristiques sont plus marquées en association avec une invalidation de CD73. Ici, cN-II et CD73 ne semblent pas jouer de rôle dans la prolifération ou le dialogue avec une sous-population de cellule de l’immunité innée
Nucleotides play a major role in nucleic acids constitution and are involved in various cell phenomena. Indeed, intracellular ATP, GTP, AMP, GMP and their cyclic forms are components of cell signaling and define the energetic balance. Extracellularly, they also play multiple roles. Thus, when nucleotide pools are deregulated various processes are impacted. For example, a low availability of nucleotides supports genetic instability and aberrant levels of extracellular adenosine can lead to an immunosuppressive microenvironment. Interestingly, the cited parameters are among the Cancer Hallmarks described by Hanahan and Weinberg. These observations confirm the possibility of a key role of these molecules in this pathology. cN-II and CD73 are 5’-nucleotidases, involved in intra- and extracellular nucleotide metabolism respectively and have been identified as possible targets for new anti-cancer therapies. Nevertheless, very little is known about their biological roles on cancer cells and what parameters of cell biology could be impacted by such strategies. Considering the involvement of these purines in cell metabolism, we wondered what changes a decrease in cN-II and/orCD73 expressions or their silencing could trigger in cancer cells as well as in the interplay with their microenvironment.We studied cancer cell aggressiveness and the interplay with innate immune cells under cN-II and CD73 modulations. We observed that cN-II is involved in metabolic adaptability. The association of cN-II and CD73 invalidations results in glucose-metabolism-related gene modifications. CD73 can regulate migration-related genes expression but does not affect the process. cN-II is also involved in cell migration, via the COX-2/PGE2 axis. Again, these characteristics are accentuated when associated with CD73 deficiency. Here, cN-II and CD73 do not seem to be involved in cancer cell proliferation or in their interplay with a subset of innate immune cells
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Books on the topic "Nucleotide extracellulaire"

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Luo, Laura Chun. Receptors for extracellular ATP and other nucleotides in osteoblastic cells. Faculty of Dentistry, University of Toronto], 1995.

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Kishore, Bellamkonda K., Robert John Unwin, Volker Vallon, and Helle Prætorius, eds. Extracellular Nucleotides in the Regulation of Kidney Functions. Frontiers Media SA, 2015. http://dx.doi.org/10.3389/978-2-88919-504-6.

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M, Schwiebert Erik, ed. Extracellular nucleotides and nucleosides: Release, receptors, and physiological and pathophysiological effects. Academic Press, 2003.

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Schwiebert, Erik Mills. Current Topics in Membranes: Extracellular Nucleotides and Nucleosides: Release, Receptors, and Physiological & Pathophysiological Effects (Current Topics in Membranes) (Current Topics in Membranes). Academic Press, 2003.

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Schwiebert, Erik Mills. Current Topics in Membranes: Extracellular Nucleotides and Nucleosides: Release, Receptors, and Physiological & Pathophysiological Effects (Current Topics in Membranes) (Current Topics in Membranes). Academic Press, 2003.

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(Editor), T. Kumazawa, L. Kruger (Editor), and K. Mizumura (Editor), eds. The Polymodal Receptor - A Gateway to Pathological Pain (Progress in Brain Research). Elsevier Science, 1996.

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Takao, Kumazawa, Kruger Lawrence, and Mizumura Kazue, eds. The polymodal receptor: A gateway to pathological pain. Elsevier, 1996.

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Book chapters on the topic "Nucleotide extracellulaire"

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Burnstock, Geoffrey. "History of Extracellular Nucleotides and Their Receptors." In The P2 Nucleotide Receptors. Humana Press, 1998. http://dx.doi.org/10.1007/978-1-4612-1800-5_1.

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Silinsky, Eugene M., Ivar von Kügelgen, Andrew Smith, and David P. Westfall. "Functions of Extracellular Nucleotides in Peripheral and Central Neuronal Tissues." In The P2 Nucleotide Receptors. Humana Press, 1998. http://dx.doi.org/10.1007/978-1-4612-1800-5_11.

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Pero, Ronald W., Anders Olsson, and Desmond Johnsonf. "Regulation of Extracellular Thymidine Pools in Human Blood Samples." In Genetic Consequences of Nucleotide Pool Imbalance. Springer US, 1985. http://dx.doi.org/10.1007/978-1-4613-2449-2_31.

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Slakey, L. L. "Extracellular Nucleotide Hydrolysis and Integration of Signalling." In Biochemistry of Arachidonic Acid Metabolism. Springer US, 1985. http://dx.doi.org/10.1007/978-1-4613-2597-0_20.

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Slakey, Linda L., and Ellen L. Gordon. "Extracellular Nucleotide Hydrolysis and the Integration of Signaling." In Cardiovascular Disease. Springer US, 1987. http://dx.doi.org/10.1007/978-1-4684-5296-9_36.

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MacManus, Christopher F., Holger K. Eltzschig, and Sean P. Colgan. "Regulated Extracellular Nucleotide Metabolism and Function at the Mucosa." In Extracellular ATP and Adenosine as Regulators of Endothelial Cell Function. Springer Netherlands, 2010. http://dx.doi.org/10.1007/978-90-481-3435-9_8.

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Seye, Cheikh I., and Gary A. Weisman. "The P2Y2 Nucleotide Receptor in Vascular Inflammation and Angiogenesis." In Extracellular ATP and Adenosine as Regulators of Endothelial Cell Function. Springer Netherlands, 2010. http://dx.doi.org/10.1007/978-90-481-3435-9_4.

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Barankiewicz, Jerzy, Hans-Michael Dosch, Roy Cheung, and Amos Cohen. "Relationship between Extracellular and Intracellular Nucleotide Metabolism in Human Lymphocytes." In Advances in Experimental Medicine and Biology. Springer US, 1989. http://dx.doi.org/10.1007/978-1-4684-5676-9_70.

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Pearson, D., and L. L. Slakey. "Intracellular and Extracellular Metabolism of Adenosine and Adenine Nucleotides." In Purines in Cellular Signaling. Springer New York, 1990. http://dx.doi.org/10.1007/978-1-4612-3400-5_2.

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Schrader, J., M. M. Borst, M. Kelm, B. Bading, and K. F. Bürrig. "Formation of Adenosine in the Heart from Extracellular Adenine Nucleotides." In Purines in Cellular Signaling. Springer New York, 1990. http://dx.doi.org/10.1007/978-1-4612-3400-5_5.

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Conference papers on the topic "Nucleotide extracellulaire"

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Müller, J., T. Hofbauer, T. Scherz, et al. "Arterial hypertension is associated with the DNase I single nucleotide polymorphism Q222R and enhanced neutrophil extracellular trap formation." In Late breaking Abstracts – Diabetes Kongress 2018 – 53. Jahrestagung der DDG. Georg Thieme Verlag KG, 2018. http://dx.doi.org/10.1055/s-0038-1657808.

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Zhang, Bailin, Guang Yang, Shujia Dai, et al. "Abstract 5468: SAR650984, a humanized anti-CD38 antibody potently modulates intracellular and extracellular nucleotide levels of cancer cells." In Proceedings: AACR Annual Meeting 2014; April 5-9, 2014; San Diego, CA. American Association for Cancer Research, 2014. http://dx.doi.org/10.1158/1538-7445.am2014-5468.

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Schneider, Sven, Sanja Cicko, Andreas Zech, Madelon Hoßfeld, and Marco Idzko. "Extracellular nucleotides contribute to the pathogenesis of viral-induced exacerbations in COPD via P2X4/P2X7-receptor activation." In ERS International Congress 2019 abstracts. European Respiratory Society, 2019. http://dx.doi.org/10.1183/13993003.congress-2019.pa5446.

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Gordon, J. L. "ADENINE NUCLEOTIDES AND THEREGULATION OF VASCULAR TONE." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643719.

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ATP, although known mainly as an intracellular energy source, is also capable of acting extracellularly as a vasoactive agent of great potency, at concentrations around lμM or less. ADP is approximately equipotent with ATP in its actions on extracellular receptors in the vasculature.ATP and ADP can arise extracellularly through release from the cytoplasm of cellsexposed to damaging stimuli or by degranulation of platelets. The concentration of the nucleotides in the cytoplasm of most cells (including vascular endothelial and smooth muscle cells) is more than ImM, and the concentration in the dense storage granules of platelets approaches 1M. Thus, there is potential for very high localised concentrations of ATP and ADP in the plasma following platelet degranulation or damageto cells of the vessel well. Release from vascular endothelial and smooth muscle cells can occur with no loss of cell viability or leakage of cytoplasmic proteins.The vasoactivity of ATP and ADP is mediated via P2 purinoceptors. Vasodilation can be induced through the release of EDRF from endothelial cells or through stimulation of PGI2 production (PGI2 is a vasodilator in many, althoughnot all, arterial beds). Purinoceptor-mediated prostacyclin production can be stimulated from perfused vascular beds (e.g. theheart andthe lung), from isolated blood vessels or from cultured endothelial cells.In some blood vessels, purinoceptor-mediated vasoconstriction can be induced by direct actionon the vascular smooth muscle cells. The receptors responsible are sub-classified as P2X (which induce vasoconstriction) and P2Y (whichinduce vasodilation). The P2Y purinoceptor that mediates EDRF production is very similar to that which is responsible for PGI2 production, although there are some intriguing differences inthe potency of ATP analogs at stimulating these two responses, even on the same cells. The intracellular mechanisms responsible have not yet been fully elucidated, but it appears that elevation of intracellular calcium is likely to play a causal role.Adenosine, which is the product of ATP and ADP metabolism by nucleotidases, can also induce vasodilation in many blood vessels, acting via P1] purinoceptors on the smooth muscle cells, but its potency is often less than that of ATP and ADP.The fate of adenine nucleotides released into the plasma is determined by ectonucleotidases on the luminal surface of the endothelial cells, not by enzymes in the blood itself (the half-life of ATP in samples of blood or plasma is many minutes, while in the microcirculation the half-life isless than one second). Endothelial ectonucleotidases have been detected in several vascular beds, and many of their characteristics are now known. These enzymes are distinct entities from the P2 purinoceptors on endothelium, as shown by the marked differences in potency of several ATP analogs as P2 receptor stimulants and as substrates for the nucleotidases.In summary, vascular endothelial and smooth muscle cells respond to extracellularATP and ADP, and can also metabolise thesenucleotides extracellularly by ectonucleotidases. In addition, ATP and ADP can be selectively released from the cells of the vessel wall and from activated platelets. Thus, the endothelial pericellular environment can be the site of complex interactions by which vascular tone is regulated through the release, actions and metabolism ofextracellular nucleotides.
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Schneider, Gabriela, Talita Glaser, Ahmed Abdelbaset Ismail, Henning Ulrich, and Mariusz Z. Ratajczak. "Abstract 4144: Extracellular nucleotides and purinergic signaling as novel, underappreciated, pro-metastatic factors for human lung cancer cells." In Proceedings: AACR 106th Annual Meeting 2015; April 18-22, 2015; Philadelphia, PA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1538-7445.am2015-4144.

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Ortega, M. P., C. Sunkel, and J. G. Priego. "INHIBITION OF HUMAN PLATELET FUNCTION BY PCA-4230." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643431.

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PCA-4230 (3-{2-(N-l,2-benzisothiazolyl-3(2H)one-1,1-dioxide) ethoxycarbonyl}-2,6-dimethyl-5-ethoxycarbonyl-4-methyl-l,4-dihy-dropyridine) is a new synthetic compound which has been selected after evaluation of .several series of molecules included in an ex tensive program of synthesis and biological screening.The purpose of this study was to investigate the In vUjiO effects of PCA-4230 on human platelet function.Platelet aggregation (PA) was measured, in platelet rich plasma (PRP) or washed platelets, according to Born’s technique. Release reaction (RR) was measured by the luminiscence method as adenosine triphosphate (ATP) release in response to stimulation. Aggregating agents were adenosine diphosphate (ADP), epinephrine (Epi), collagen (Col), thrombin (Thr), calcium ionophore (A23187) arachidonic acid (AA), thromboxane agonist (U46619) or platelet activating factor (PAF). Incubation with PCA-4230 (1 to 10 μM) we re carried out at 37°C for 15 minutes. PCA-4230 potentiation of Prostacyclin (PGI2) anti-aggregatory activity was also studied by addition to PRP of PGI2, PCA-4230 or both, and PA by ADP.PCA-4230 inhibited PA and RR in PRP in a concentration-dependent fashion when Col, Epi, U46619 or PAF were used as agonists. AA-and Thr-induced aggregation were only slightly impaired and no in hibition was shown on ADP or A23187-triggered activation. A23187-induced aggregation and RR were inhibited only in the absence of extracellular Ca++ in washed platelets. This effect was overcome by addition of Ca++ 1 mM. Additionally, the inhibitory effect of PGI2 on ADP-induced PA, was synergistically potentiated by PCA-4230, suggesting inhibitory activity of the compound on cjy clic nucleotide phosphodiesterase.Since PCA-4230 inhibited PA and RR induced by Epi, U46619 and PAF, mediated viareceptor-agonist binding, and Col-inducedactivation, it is reasonable to suspect that common process(es) may be involved. Recently, it has been suggested that intraplatelet Ca++ levels, actingas a second messenger, are directly linked to the d<2 gree of platelet activation.Therefore, the ability of PCA-4230 to modulate platelet function appears, at leastin part, to be due to regulation of cytosolic Ca++ levels. This hypothesis is confii: med by the results with A23187-induced aggregation in absence of extracellular Ca++.
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Beeler, D., L. Fritze, G. Soff, R. Jackman, and R. Rosenberg. "HUMAN THROMBOMODULIN cDNA:SEQUENCE AND TRANSLATED STRUCTURE." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643967.

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A 750 bp bovine Thrombomodulin (TM) cDNA fragment was used as an hybridization probe to screen an oligo-dT primed Lambda gtll. cDNA library prepared from human umbilical vein endothelial cell mRNA. A 2.4 kb positive human clone was isolated which showed an 80% nucleotide sequence homology with bovine TM cDNA. This clone and a 550 bp fragment from its 5' end were used to further screen the oligo-dT primed library as well as randomly primed library prepared from the same mRNA. The cDNA clones obtained allow us to describe the overall structure of human TM and reveal that it is extremely similar to the structure of bovine TM, especially as the bovine TM is organized like the receptor for low density lipoprotein (LDL R). Both TM and LDL R exhibit short cytoplasmic C-terminal tails which are either neutral or negatively charged. Other coated pit receptors such as the insulin receptor or the epidermal growth factor (EGF) receptor have very large cytoplasmic regions with a complex tyrosine kinase segment as well as multiple sites for phosphorylation. Both TM and LDL R possess a transmembrane region and an immediately adjacent extracellular serine/threonine rich region which in LDL R has been shown to bear 0-1inked sugars. Both TM and LDL R contain a more distal area of cysteine rich repeats, first noted in the EGF precursor and termed EGF type B. However, the TM EGF type B repeats appear to have been duplicated in TM resulting in their being 6 of them rather than the 3 found in LDL R. The N-terminal half of LDL R is thought to contain the ligand binding region of the receptor and is constructed from multiple cysteine rich repeats similar to those of Complement factor C9. The structure of this region of TM is quite different from that of LDL R, possessing few cysteines. We suspect that protein C and/or thrombin may bind to this unique domain of TM.
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Kruithof, E. KO, W. D. Schleuning, and F. Bachman. "PLASMINOGEN ACTIVATOR INHIBITOR BIOCHEMICAL AND CLINICAL ASPECTS." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644764.

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Plasminogen activator (PAs) are enzymes that convert the zymogen plasminogen into the trypsin-like protease plasmin, which degrades extracellular matrix proteins and fibrin in the course of fibrinolysis, embryogenesis, tissue remodeling and in tumor metastasis. Plasminogen activator inhibitors (PAIs) are important modulators of PA activity. Several proteins have been identified which inhibit at fast rates urokinase (u-PA) and tissue-type PA (t-PA). In the order of inhibition rate constants these are: a) PAI-1, present in human plasma and platelet extracts and purified from human endothelial cell, fibrosarcoma cell and melanoma cell conditioned media; b) PAI-2, first identified in extracts of human placenta and later also in extracts and conditioned media of human granulocytes and monocytes; and c) protease nexin, a broad specificity protease inhibitor that was first identified and purified from human fibroblasts. We have chosen to use phorbol myristate acetate (30 ng/ml) stimulated histiocytic lymphoma cells (U-937) for the purification of PAI-2. The concentration of PAI-2 in the conditioned media after three days culture in the absence of fetal calf serum is 5 mg/1 and PAI-2 represents 3% of total protein. PAI-2 was purified by a two step procedure consisting of isoelectric focusing and affinity chromatography on Cibacron-Blue agarose. Two forms of PAI-2 were identified: a 47 kDa, nonglycosylated, pi 5.0 form and a 60 kDa glycosylated, pi 4.4 form. Immunctolot analysis and in vivo protein labeling studies under culture conditions that assure 100% viability of the cells showed that the glycosylated Torn is secreted, whereas the 47 kDa, nonglycosylated form remains intracellular. The glycosylation does not affect the activity of the inhibitors since both forms of PAI-2 react with the same rate with u-PA. PAI-2 is a fast inhibitor of u-PA (kl=9×l05M−1s−1) and two-chain t-PA (kl=2×l05) and a rather slow inhibitor of one chain t-PA (kl=l×l02) and of plasmin (kl×l02), but does not inhibit glandular and plasma kallikrein or thrombin. The inhibition spectrum and the kinetics of inhibition clearly distinguish PAI-2 from PAI-1 (kl of reaction with u-PA and two and one chain t-PA above 107) and from protease nexin, that is an efficient inhibitor also of thrombin and plasmin.We have cloned a 1880 Ip fragment of PAI-2 cDNA and determined its nucleotide sequence. The derived acid sequence reveals that PAI-2 is like PAI-1 and protease nexin a member of the serpin family of proteins and contains arginine at its putative active site. In an attenpt to identify parts of the inhibitor proteins that are responsible for conferring PA specificity to PAI-1 and PAI-2 we have compared the primary structures of PAI-1 and PAI-2 with each other and with antithrombin III (AT III). Surprisingly, PAI-2 exhibits no homology with PAI-1 in the region close to the active site except for the active site arginine, whereas, in that region, AT III showed three and seven conserved aminoacids when compared to PAI-1 and PAI-2, respectively. This finding suggests that other regions than those close to the active site contribute to the specificity of PAIs.Plasma concentrations of PAI-2 were measured by a specific radioimmunoassay in over 50 healthy individuals, PAI-2 levels were below detection limit (15 ng/ml) in half of the saitples. Maximal concentrations encountered were in the 30 ng/ml range. PAI-2 measurements in over 300 hospitalized patients demonstrated significantly elevated PAI-2 concentrations only in pregnant women. Measurements in various stages of pregnancy showed a steady increase of PAI-2 from below detection limit in nonpregnant women to values of 250 ng/ml at term and of PAI-1 frcm 25 ng/ml to 150 ng/ml. Unlike to PAI-1 concentrations that normalize rapidly after delivery, PAI-2 concentrations remain significantly elevated for several days.
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Reports on the topic "Nucleotide extracellulaire"

1

Stacey, Gary. Extracellular nucleotide signaling in plants. Office of Scientific and Technical Information (OSTI), 2016. http://dx.doi.org/10.2172/1322413.

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