Journal articles: 'Adenosine-signalling'

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Fredholm, Bertil B., Giulia Arslan, Bj�rn Kull, Ewa Kontny, and Per Svenningsson. "Adenosine (P1) receptor signalling." Drug Development Research 39, no. 3-4 (November 1996): 262–68. http://dx.doi.org/10.1002/(sici)1098-2299(199611/12)39:3/4<262::aid-ddr5>3.0.co;2-p.

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CARUSO, M., S. HOLGATE, and R. POLOSA. "Adenosine signalling in airways." Current Opinion in Pharmacology 6, no. 3 (June 2006): 251–56. http://dx.doi.org/10.1016/j.coph.2006.02.002.

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Silva, Luis, Mario Subiabre, Joaquín Araos, Tamara Sáez, Rocío Salsoso, Fabián Pardo, Andrea Leiva, Rody San Martín, Fernando Toledo, and Luis Sobrevia. "Insulin/adenosine axis linked signalling." Molecular Aspects of Medicine 55 (June 2017): 45–61. http://dx.doi.org/10.1016/j.mam.2016.11.002.

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Burnstock, Geoffrey. "Purine and purinergic receptors." Brain and Neuroscience Advances 2 (January 2018): 239821281881749. http://dx.doi.org/10.1177/2398212818817494.

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Adenosine 5′-triphosphate acts as an extracellular signalling molecule (purinergic signalling), as well as an intracellular energy source. Adenosine 5′-triphosphate receptors have been cloned and characterised. P1 receptors are selective for adenosine, a breakdown product of adenosine 5′-triphosphate after degradation by ectonucleotidases. Four subtypes are recognised, A1, A2A, A2B and A3 receptors. P2 receptors are activated by purine and by pyrimidine nucleotides. P2X receptors are ligand-gated ion channel receptors (seven subunits (P2X1-7)), which form trimers as both homomultimers and heteromultimers. P2Y receptors are G protein-coupled receptors (eight subtypes (P2Y1/2/4/6/11/12/13/14)). There is both purinergic short-term signalling and long-term (trophic) signalling. The cloning of P2X-like receptors in primitive invertebrates suggests that adenosine 5′-triphosphate is an early evolutionary extracellular signalling molecule. Selective purinoceptor agonists and antagonists with therapeutic potential have been developed for a wide range of diseases, including thrombosis and stroke, dry eye, atherosclerosis, kidney failure, osteoporosis, bladder incontinence, colitis, neurodegenerative diseases and cancer.

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Liang, Bruce T., Tomasz A. Swierkosz, Howard C. Herrmann, Stephen Kimmel, and Kenneth A. Jacobson. "Adenosine and Ischemic Preconditioning." Current Pharmaceutical Design 5, no. 12 (December 1999): 1029–41. http://dx.doi.org/10.2174/1381612805666230112212126.

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Adenosine is released in large amounts during myocardial ischemia and is capable of exerting potent cardioprotective effects in the heart. Although these observations on adenosine have been known for a long time, how adenosine acts to achieve its anti-ischemic effect remains incompletely understood. However, recent advances on the chemistry and pharmacology of adenosine receptor ligands have provided important and novel information on the function of adenosine receptor subtypes in the cardiovascular system. The development of model systems for the cardiac actions of adenosine has yielded important insights into its mechanism of action and have begun to elucidate the sequence of signalling events from receptor activation to the actual exertion of its cardioprotective effect. The present review will focus on the adenosine receptors that mediate the potent anti-ischemic effect of adenosine, new ligands at the receptors, potential molecular signalling mechanisms downstream of the receptor, mediators for cardioprotection, and possible clinical applications in cardiovascular disorders.

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Vlajkovic, Srdjan M., and Peter R. Thorne. "Purinergic Signalling in the Cochlea." International Journal of Molecular Sciences 23, no. 23 (November 28, 2022): 14874. http://dx.doi.org/10.3390/ijms232314874.

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The mammalian cochlea is the sensory organ of hearing with a delicate, highly organised structure that supports unique operating mechanisms. ATP release from the secretory tissues of the cochlear lateral wall (stria vascularis) triggers numerous physiological responses by activating P2 receptors in sensory, supporting and neural tissues. Two families of P2 receptors, ATP-gated ion channels (P2X receptors) and G protein-coupled P2Y receptors, activate intracellular signalling pathways that regulate cochlear development, homeostasis, sensory transduction, auditory neurotransmission and response to stress. Of particular interest is a purinergic hearing adaptation, which reflects the critical role of the P2X2 receptor in adaptive cochlear response to elevated sound levels. Other P2 receptors are involved in the maturation of neural processes and frequency selectivity refinement in the developing cochlea. Extracellular ATP signalling is regulated by a family of surface-located enzymes collectively known as “ectonucleotidases” that hydrolyse ATP to adenosine. Adenosine is a constitutive cell metabolite with an established role in tissue protection and regeneration. The differential activation of A1 and A2A adenosine receptors defines the cochlear response to injury caused by oxidative stress, inflammation, and activation of apoptotic pathways. A1 receptor agonism, A2A receptor antagonism, and increasing adenosine levels in cochlear fluids all represent promising therapeutic tools for cochlear rescue from injury and prevention of hearing loss.

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Razak, Azlina A., Lopa Leach, and Vera Ralevic. "Impaired vasocontractile responses to adenosine in chorionic vessels of human term placenta from pregnant women with pre-existing and gestational diabetes." Diabetes and Vascular Disease Research 15, no. 6 (August 22, 2018): 528–40. http://dx.doi.org/10.1177/1479164118790904.

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Background: There is clinical and experimental evidence for altered adenosine signalling in the fetoplacental circulation in pregnancies complicated by diabetes, leading to adenosine accumulation in the placenta. However, the consequence for fetoplacental vasocontractility is unclear. This study examined contractility to adenosine of chorionic vessels from type 1 diabetes mellitus, gestational diabetes mellitus and normal pregnancies. Methods: Chorionic arteries and veins were isolated from human placenta from normal, gestational diabetes mellitus and type 1 diabetes mellitus pregnancies. Isometric tension recording measured responses to adenosine and the thromboxane A2 analogue U46619 (thromboxane A2 mediates fetoplacental vasoconstriction to adenosine). Adenosine and thromboxane prostanoid receptor protein expression was determined by immunoblotting. Results: Adenosine elicited contractions in chorionic arteries and veins which were impaired in both gestational diabetes mellitus and type 1 diabetes mellitus. Contractions to potassium chloride were unchanged. Adenosine A2A and A2B receptor protein levels were not different in gestational diabetes mellitus and normal pregnancies. Contractions to U46619 were unaltered in gestational diabetes mellitus arteries and increased in type 1 diabetes mellitus arteries. Overnight storage of vessels restored contractility to adenosine in gestational diabetes mellitus arteries and normalized contraction to U46619 in type 1 diabetes mellitus arteries. Conclusion: These data are consistent with the concept of aberrant adenosine signalling in diabetes; they show for the first time that this involves impaired adenosine contractility of the fetoplacental vasculature.

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DARCY, P. K., and P. R. FISHER. "Pharmacological evidence for a role for cyclic AMP signalling in Dictyostelium discoideum slug behaviour." Journal of Cell Science 96, no. 4 (August 1, 1990): 661–67. http://dx.doi.org/10.1242/jcs.96.4.661.

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Phototaxis and thermotaxis by Dictyostelium discoideum slugs on water agar were impaired by the presence in the agar of adenosine, which is a cyclic AMP receptor antagonist in aggregating amoebae. Caffeine, and presumably its analogue theophylline, inhibit cyclic AMP signalling in aggregating amoebae of D. discoideum. Both compounds perturbed slug behaviour in a similar manner to adenosine, as did both ammonium and sulphate ions. (NH4)3SO4 is known to perturb cyclic AMP binding to its receptor, and ammonia is an inhibitor of cyclic AMP signalling in aggregating amoebae. The receptor agonist, cyclic AMPS, disrupted slug organization and impaired phototaxis when present at concentrations high enough to saturate cyclic AMP receptors and compete effectively with endogenous cyclic AMP signals of similar magnitude to those observed during aggregation. Taken together with the considerable circumstantial evidence for cyclic AMP signalling in slugs, these results support a role for cyclic AMP signalling in slug behaviour.

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Przybyła, Tomasz, Monika Sakowicz-Burkiewicz, and Tadeusz Pawełczyk. "Purinergic signalling in B cells." Acta Biochimica Polonica 65, no. 1 (May 27, 2018): 1–7. http://dx.doi.org/10.18388/abp.2017_1588.

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Adenosine and adenosine triphosphate are involved in purinergic signalling which plays important role in control of immune system. Much data have been obtained regarding impact of purinergic signalling on dendritic cells, macrophages, monocytes and T lymphocytes, however less attention has been paid to purinergic regulation of B cells. This review summarizes present knowledge about ATP- and Ado-dependant signalling in B lymphocytes. Human B cells have been shown to express A2A-R and A3-R and each subtype of P2 receptors. Surface of B cells exhibits two antagonistic ectoenzymatic pathways, one relays on constitutive secretion and resynthesis of ATP while the second one depends on degradation of adenosine nucleotides to nucleosides and their subsequent degradation. Inactivated B cells remain under suppressive impact of autocrine and paracrine Ado however activated B lymphocytes increase ATP release and production. ATP protects B cells from suppressive impact of Ado and exerts pro-inflammatory impact on target tissues, it is also involved in IgM release. Ado synthesis however is related with optimal development, implantation and maintenance of plasmocyte population in bone marrow during primary immune response. Moreover Ado plays important role in immunoglobulin class switching which is a key mechanism of humoral immune response. Disruption of purinergic signalling is related with severe clinical implications. Impairment of Ado production in environment of B cells is one of the factors responsible for common variable immunodeficiency. List of evidence suggests also that dysfunction of immune system observed during diabetes may in part depend on disrupted ATP and Ado metabolism in B cells.

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Gracia, Eduard, Kamil Pérez-Capote, Estefanía Moreno, Jana Barkešová, Josefa Mallol, Carme Lluís, Rafael Franco, Antoni Cortés, Vicent Casadó, and Enric I. Canela. "A2A adenosine receptor ligand binding and signalling is allosterically modulated by adenosine deaminase." Biochemical Journal 435, no. 3 (April 13, 2011): 701–9. http://dx.doi.org/10.1042/bj20101749.

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A2ARs (adenosine A2A receptors) are highly enriched in the striatum, which is the main motor control CNS (central nervous system) area. BRET (bioluminescence resonance energy transfer) assays showed that A2AR homomers may act as cell-surface ADA (adenosine deaminase; EC 3.5.4.4)-binding proteins. ADA binding affected the quaternary structure of A2ARs present on the cell surface. ADA binding to adenosine A2ARs increased both agonist and antagonist affinity on ligand binding to striatal membranes where these proteins are co-expressed. ADA also increased receptor-mediated ERK1/2 (extracellular-signal-regulated kinase 1/2) phosphorylation. Collectively, the results of the present study show that ADA, apart from regulating the concentration of extracellular adenosine, may behave as an allosteric modulator that markedly enhances ligand affinity and receptor function. This powerful regulation may have implications for the physiology and pharmacology of neuronal A2ARs.

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Ciruela, Francisco, Carles Saura, Enric I. Canela, Josefa Mallol, Carmen Lluis, and Rafael Franco. "Adenosine deaminase affects ligand-induced signalling by interacting with cell surface adenosine receptors." FEBS Letters 380, no. 3 (February 19, 1996): 219–23. http://dx.doi.org/10.1016/0014-5793(96)00023-3.

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Aslam, Muhammad, Dursun Gündüz, Christian Troidl, Jacqueline Heger, Christian W. Hamm, and Rainer Schulz. "Purinergic Regulation of Endothelial Barrier Function." International Journal of Molecular Sciences 22, no. 3 (January 26, 2021): 1207. http://dx.doi.org/10.3390/ijms22031207.

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Increased vascular permeability is a hallmark of several cardiovascular anomalies, including ischaemia/reperfusion injury and inflammation. During both ischaemia/reperfusion and inflammation, massive amounts of various nucleotides, particularly adenosine 5′-triphosphate (ATP) and adenosine, are released that can induce a plethora of signalling pathways via activation of several purinergic receptors and may affect endothelial barrier properties. The nature of the effects on endothelial barrier function may depend on the prevalence and type of purinergic receptors activated in a particular tissue. In this review, we discuss the influence of the activation of various purinergic receptors and downstream signalling pathways on vascular permeability during pathological conditions.

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Spanoudakis, Chelsea, Rebecca Chapman, Simon Paine, Richard Grundy, Hester Franks, and Timothy Ritzmann. "EPEN-05. Adenosine receptor expression in paediatric ependymoma." Neuro-Oncology 24, Supplement_1 (June 1, 2022): i39. http://dx.doi.org/10.1093/neuonc/noac079.142.

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Abstract PURPOSE: Paediatric ependymoma is associated with dismal outcomes. Whilst understanding of its underlying biology has advanced, there has been little progress in treatment and clinical outcomes. Acting through four G protein-coupled receptors (encoded by ADORA1, ADORA2A, ADORA2B and ADORA3), adenosine is a signalling molecule often present at high levels in tumours. Adenosine signalling can aid tumour proliferation and invasiveness via mechanisms including suppression of tumour-infiltrating immune cells. Adenosine receptors therefore represent a potential therapeutic target in paediatric ependymoma, however neither levels nor patterns of expression have been previously reported. We hypothesised that adenosine receptors would be expressed in paediatric ependymoma and that this expression would vary between molecular subgroups. METHODS: Three publicly available gene expression datasets were analysed for adenosine receptor expression using Kruskal-Wallis, Mann-Whitney U and chi-square tests. RNAscope assays for adenosine receptors and CD68 were then performed on ten full-face ependymoma FFPE sections from posterior fossa A (PFA1 and PFA2) tumours to understand patterns of expression within ependymomas with the highest levels of expression identified by the gene expression datasets. RESULTS: Statistically significant differences were identified between adenosine-related genes across ependymoma subgroups of differing anatomical origin (supratentorial ZFTA-positive versus posterior fossa A and B (PFA/PFB)), with median adenosine-related gene levels generally higher in the PFA subgroup. Particularly, ADORA1, 2A, 2B and 3 gene expression was higher in PFA tumours than other subgroups. Analysis of the ten cases demonstrated measurable expression of all four adenosine receptors by RNAscope and patterns in the distribution and relative levels of expression of the adenosine receptors across PFA1 and PFA2 tumours were described. CONCLUSION: Using two different techniques we demonstrated that adenosine receptors are expressed in paediatric ependymomas. There are significant differences in level of expression between tumour subgroups. Adenosine receptors therefore represent a potential therapeutic target which should be explored further.

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Antonioli, Luca, Corrado Blandizzi, Balázs Csóka, Pál Pacher, and György Haskó. "Adenosine signalling in diabetes mellitus—pathophysiology and therapeutic considerations." Nature Reviews Endocrinology 11, no. 4 (February 17, 2015): 228–41. http://dx.doi.org/10.1038/nrendo.2015.10.

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Schulte, Gunnar, and Bertil B. Fredholm. "Signalling from adenosine receptors to mitogen-activated protein kinases." Cellular Signalling 15, no. 9 (September 2003): 813–27. http://dx.doi.org/10.1016/s0898-6568(03)00058-5.

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REES, D. Aled, Maurice F. SCANLON, and Jack HAM. "Novel insights into how purines regulate pituitary cell function." Clinical Science 104, no. 5 (May 1, 2003): 467–81. http://dx.doi.org/10.1042/cs20030053.

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Purine nucleosides and nucleotides are widely distributed substances that exhibit a diverse range of effects in a number of tissues, acting as important extracellular signalling molecules in addition to their more established roles in cellular metabolism. They mediate their effects via activation of distinct cell surface receptors, termed adenosine (or P1) and P2 purinergic receptors. Although roles for adenosine and adenine nucleotides have been described previously in the pituitary gland, the distribution of the receptor subtypes and the effects of their activation on pituitary function are not well defined. Recent evidence, however, has emerged to describe a complex signalling system for purines in the pituitary gland. Data from a variety of studies have shown that the expression pattern, number and affinity of adenosine and/or P2 receptors may be cell-type specific and that non-endocrine in addition to endocrine cells elaborate these receptors. These variations, along with the diverse range of signalling pathways activated, dictate the response of individual cell types to extracellular purines, with roles now emerging for these substances in the regulation of hormone release, pituitary cell proliferation and cytokine/growth factor expression. In this review, we discuss these advances and examine some implications for pituitary growth control and the response of the hypothalamic–pituitary–adrenal axis to stress and inflammation.

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Clark, Joanne C., Deirdre M. Kavanagh, Stephanie Watson, Jeremy A. Pike, Robert K. Andrews, Elizabeth E. Gardiner, Natalie S. Poulter, Stephen J. Hill, and Steve P. Watson. "Adenosine and Forskolin Inhibit Platelet Aggregation by Collagen but not the Proximal Signalling Events." Thrombosis and Haemostasis 119, no. 07 (May 26, 2019): 1124–37. http://dx.doi.org/10.1055/s-0039-1688788.

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Background The G protein-coupled receptor, adenosine A2A, signals through the stimulatory G protein, Gs, in platelets leading to activation of adenylyl cyclase and elevation of cyclic adenosine monophosphate (cAMP) and inhibition of platelet activation. Objective This article investigates the effect of A2A receptor activation on signalling by the collagen receptor glycoprotein (GP) VI in platelets. Methods Washed human platelets were stimulated by collagen or the GPVI-specific agonist collagen-related peptide (CRP) in the presence of the adenosine receptor agonist, 5′-N-ethylcarboxamidoadenosine (NECA) or the adenylyl cyclase activator, forskolin and analysed for aggregation, adenosine triphosphate secretion, protein phosphorylation, spreading, Ca2+ mobilisation, GPVI receptor clustering, cAMP, thromboxane B2 (TxB2) and P-selectin exposure. Results NECA, a bioactive adenosine analogue, partially inhibits aggregation and secretion to collagen or CRP in the absence or presence of the P2Y12 receptor antagonist, cangrelor and the cyclooxygenase inhibitor, indomethacin. The inhibitory effect in the presence of the three inhibitors is largely overcome at higher concentrations of collagen but not CRP. Neither NECA nor forskolin altered clustering of GPVI, elevation of Ca2+ or spreading of platelets on a collagen surface. Further, neither NECA nor forskolin, altered collagen-induced tyrosine phosphorylation of Syk, LAT nor PLCγ2. However, NECA and forskolin inhibited platelet activation by the TxA2 mimetic, U46619, but not the combination of adenosine diphosphate and collagen. Conclusion NECA and forskolin have no effect on the proximal signalling events by collagen. They inhibit platelet activation in a response-specific manner in part through inhibition of the feedback action of TxA2.

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Liu, Yi, Sonia Rebollo-Ramirez, and Gerald Larrouy-Maumus. "Metabolomics reveals that the cAMP receptor protein regulates nitrogen and peptidoglycan synthesis in Mycobacterium tuberculosis." RSC Advances 10, no. 44 (2020): 26212–19. http://dx.doi.org/10.1039/d0ra05153e.

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Mycobacterium tuberculosis requires extensive sensing and response to environment for its successful survival and pathogenesis, and signalling by cyclic adenosine 3′,5′-monophosphate (cAMP) is an important mechanism.

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Rees, DA, MF Scanlon, and J. Ham. "Adenosine signalling pathways in the pituitary gland: one ligand, multiple receptors." Journal of Endocrinology 177, no. 3 (June 1, 2003): 357–64. http://dx.doi.org/10.1677/joe.0.1770357.

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Adenosine receptors are widely distributed in most species and mediate a diverse range of physiological and pathological effects. Although adenosine receptors have been identified in the pituitary gland, the distribution of the individual subtypes (A(1), A(2A), A(2B), A(3)) has not been well defined. Furthermore, the effects of adenosine on pituitary trophic activity and function are not well established despite good evidence for growth- and immune-modulating properties of the nucleoside elsewhere. Recent advances have provided a more detailed description of adenosine receptor distribution and function in the anterior pituitary and this commentary reviews these observations and highlights some of the possible implications in relation to the control of the hypothalamic-pituitary-adrenal axis and the regulation of inflammation and pituitary cell growth.

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Schulte, Gunnar, and Bertil B. Fredholm. "Diverse inhibitors of intracellular signalling act as adenosine receptor antagonists." Cellular Signalling 14, no. 2 (February 2002): 109–13. http://dx.doi.org/10.1016/s0898-6568(01)00228-5.

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Andersson, Olov. "Role of adenosine signalling and metabolism in β-cell regeneration." Experimental Cell Research 321, no. 1 (February 2014): 3–10. http://dx.doi.org/10.1016/j.yexcr.2013.11.019.

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Ralevic, Vera. "Hypoxic vasodilatation: is an adenosine–prostaglandins–NO signalling cascade involved?" Journal of Physiology 544, no. 1 (October 2002): 2. http://dx.doi.org/10.1113/jphysiol.2002.028902.

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Bernascone, Silvia, Jessica Erriquez, Mario Ferraro, Armando A. Genazzani, and Carla Distasi. "Novel adenosine and cAMP signalling pathways in migrating glial cells." Cell Calcium 48, no. 1 (July 2010): 83–90. http://dx.doi.org/10.1016/j.ceca.2010.07.004.

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Matthews, Gareth DK, and Andrew A. Grace. "Unmasking Adenosine: The Purinergic Signalling Molecule Critical to Arrhythmia Pathophysiology and Management." Arrhythmia & Electrophysiology Review 8, no. 4 (February 11, 2020): 240–48. http://dx.doi.org/10.15420/aer.2019.05.

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Adenosine was identified in 1929 and immediately recognised as having a potential role in therapy for arrhythmia because of its negative chronotropic and dromotropic effects. Adenosine entered mainstream use in the 1980s as a highly effective agent for the termination of supraventricular tachycardia (SVT) involving the atrioventricular node, as well as for its ability to unmask the underlying rhythm in other SVTs. Adenosine has subsequently been found to have applications in interventional electrophysiology. While considered a safe agent because of its short half-life, adenosine may provoke arrhythmias in the form of AF, bradyarrhythmia and ventricular tachyarrhythmia. Adenosine is also associated with bronchospasm, although this may reflect irritant-induced dyspnoea rather than true obstruction. Adenosine is linked to numerous pathologies relevant to arrhythmia predisposition, including heart failure, obesity, ischaemia and the ageing process itself. This article examines 90 years of experience with adenosine in the light of new European Society of Cardiology guidelines for the management of SVT.

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Winder, Michael, Gunnar Tobin, Daša Zupančič, and Rok Romih. "Signalling Molecules in the Urothelium." BioMed Research International 2014 (2014): 1–14. http://dx.doi.org/10.1155/2014/297295.

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The urothelium was long considered to be a silent barrier protecting the body from the toxic effects of urine. However, today a number of dynamic abilities of the urothelium are well recognized, including its ability to act as a sensor of the intravesical environment. During recent years several pathways of these urothelial abilities have been proposed and a major part of these pathways includes release of signalling molecules. It is now evident that the urothelium represents only one part of the sensory web. Urinary bladder signalling is finely tuned machinery of signalling molecules, acting in autocrine and paracrine manner, and their receptors are specifically distributed among different types of cells in the urinary bladder. In the present review the current knowledge of the formation, release, and signalling effects of urothelial acetylcholine, ATP, adenosine, and nitric oxide in health and disease is discussed.

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Durham, Gillian A., and Timothy M. Palmer. "Is there a role for prostanoid-mediated inhibition of IL-6 trans-signalling in the management of pulmonary arterial hypertension?" Biochemical Society Transactions 47, no. 4 (July 24, 2019): 1143–56. http://dx.doi.org/10.1042/bst20190046.

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Abstract Inflammation has been highlighted as a key factor in pulmonary arterial hypertension (PAH) development, particularly interleukin-6 (IL-6). IL-6 activates JAK-STAT signalling to induce transcription of pro-inflammatory and pro-angiogenic genes, enabling PAH progression, as well as the transcription of suppressor of cytokine signalling 3 (SOCS3) which limits IL-6 signalling. Current PAH therapies include prostanoid drugs which induce vasodilation via stimulating intracellular 3′,5′-cyclic adenosine monophosphate (cAMP) levels. cAMP can also inhibit IL-6-mediated endothelial dysfunction via the induction of SOCS3. Thus, we propose that an important mechanism by which cAMP-mobilising prostanoid drugs limit PAH is by inhibiting IL-6-mediated pulmonary inflammation and remodelling via SOCS3 inhibition of IL-6 signalling. Further clarification may result in effective strategies with which to target the IL-6/JAK-STAT signalling pathway in PAH.

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Frezza, Christian. "Mitochondrial metabolites: undercover signalling molecules." Interface Focus 7, no. 2 (April 6, 2017): 20160100. http://dx.doi.org/10.1098/rsfs.2016.0100.

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Mitochondria are one of most characterized metabolic hubs of the cell. Here, crucial biochemical reactions occur and most of the cellular adenosine triphosphate (ATP) is produced. In addition, mitochondria act as signalling platforms and communicate with the rest of the cell by modulating calcium fluxes, by producing free radicals, and by releasing bioactive proteins. It is emerging that mitochondrial metabolites can also act as second messengers and can elicit profound (epi)genetic changes. This review describes the many signalling functions of mitochondrial metabolites under normal and stress conditions, focusing on metabolites of the tricarboxylic acid cycle. We provide a new framework for understanding the role of mitochondrial metabolism in cellular pathophysiology.

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Cabiati, Manuela, Raffaele Caruso, Alessandro Verde, Laura Sabatino, Maria-Aurora Morales, and Silvia Del Ry. "Transcriptomic Profiling of the Four Adenosine Receptors in Human Leukocytes of Heart Failure Patients." BioMed Research International 2013 (2013): 1–6. http://dx.doi.org/10.1155/2013/569438.

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In this study the transcriptomic profiling of adenosine receptors (ARs) in human leukocytes of heart failure (HF) patients as a function of clinical severity, assessing the possible changes with respect to healthy subjects (C), was evaluated. Total RNA was extracted from leukocytes ofC(n=8) and of HF patients (NYHA I-IIn=9; NYHA III-IVn=14) with a PAXgene Blood RNA Kit. An increase as a function of clinical severity was observed in each AR (A1R:C=0.02±0.009, NYHAI-II=0.21±0.09, NYHAIII-IV=3.6±1.3,P=0.03 Cversus NYHA III-IV,P=0.02NYHA I-II versus NYHA III-IV; A2aR:C=0.2±0.05, NYHAI-II=0.19±0.04, NYHAIII-IV=1.32±0.33,P=0.005 Cversus NYHA III-IV,P=0.003NYHA I-II versus NYHA III-IV; A2bR:C=1.78±0.36, NYHAI-II=1.35±0.29, NYHAIII-IV=4.07±1.21,P=0.03: NYHA I-II versus NYHA III-IV; A3R:C=0.76±0.21, NYHAI-II=0.94±0.19, NYHAIII-IV=3.14±0.77,P=0.01 Cversus NYHA III-IV and NYHA I-II versus NYHA III-IV, resp.). The mRNA expression of the ectonucleoside triphosphate diphosphohydrolase (CD39) and the ecto-5′-nucleotidase (CD73) were also evaluated. They resulted up-regulated. These findings show that components of adenosine metabolism and signalling are altered to promote adenosine production and signalling in HF patients. Thus, HF may benefit from adenosine-based drug therapy after confirmation by clinical trials.

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Htet, Myo, Jane E. Nally, Patricia E. Martin, and Yvonne Dempsie. "New Insights into Pulmonary Hypertension: A Role for Connexin-Mediated Signalling." International Journal of Molecular Sciences 23, no. 1 (December 29, 2021): 379. http://dx.doi.org/10.3390/ijms23010379.

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Pulmonary hypertension is a serious clinical condition characterised by increased pulmonary arterial pressure. This can lead to right ventricular failure which can be fatal. Connexins are gap junction-forming membrane proteins which serve to exchange small molecules of less than 1 kD between cells. Connexins can also form hemi-channels connecting the intracellular and extracellular environments. Hemi-channels can mediate adenosine triphosphate release and are involved in autocrine and paracrine signalling. Recently, our group and others have identified evidence that connexin-mediated signalling may be involved in the pathogenesis of pulmonary hypertension. In this review, we discuss the evidence that dysregulated connexin-mediated signalling is associated with pulmonary hypertension.

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Chernogorova, Petya, and Robert Zeiser. "Ectonucleotidases in Solid Organ and Allogeneic Hematopoietic Cell Transplantation." Journal of Biomedicine and Biotechnology 2012 (2012): 1–17. http://dx.doi.org/10.1155/2012/208204.

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Extracellular nucleotides are ubiquitous signalling molecules which modulate distinct physiological and pathological processes. Nucleotide concentrations in the extracellular space are strictly regulated by cell surface enzymes, called ectonucleotidases, which hydrolyze nucleotides to the respective nucleosides. Recent studies suggest that ectonucleotidases play a significant role in inflammation by adjusting the balance between ATP, a widely distributed proinflammatory danger signal, and the anti-inflammatory mediator adenosine. There is increasing evidence for a central role of adenosine in alloantigen-mediated diseases such as solid organ graft rejection and acute graft-versus-host disease (GvHD). Solid organ and hematopoietic cell transplantation are established treatment modalities for a broad spectrum of benign and malignant diseases. Immunological complications based on the recognition of nonself-antigens between donor and recipient like transplant rejection and GvHD are still major challenges which limit the long-term success of transplantation. Studies in the past two decades indicate that purinergic signalling influences the severity of alloimmune responses. This paper focuses on the impact of ectonucleotidases, in particular, NTPDase1/CD39 and ecto-5′-nucleotidase/CD73, on allograft rejection, acute GvHD, and graft-versus-leukemia effect, and on possible clinical implications for the modulation of purinergic signalling after transplantation.

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Czajkowski, Rafał, and Jolanta Barańska. "Cross-talk between the ATP and ADP nucleotide receptor signalling pathways in glioma C6 cells." Acta Biochimica Polonica 49, no. 4 (December 31, 2002): 877–89. http://dx.doi.org/10.18388/abp.2002_3747.

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In this review we summarize the present status of our knowledge on the enzymes involved in the extracellular metabolism of nucleotides and the receptors involved in nucleotide signalling. We focus on the mechanism of the ATP and ADP signalling pathways in glioma C6, representative of the type of nonexcitable cells. In these cells, ATP acts on the P2Y(2) receptor coupled to phospholipase C, whereas ADP on two distinct P2Y receptors: P2Y(1) and P2Y(12). The former is linked to phospholipase C and the latter is negatively coupled to adenylyl cyclase. The possible cross-talk between the ATP-, ADP- and adenosine-induced pathways, leading to simultaneous regulation of inositol 1,4,5-trisphosphate and cAMP mediated signalling, is discussed.

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Luchowska-Stańska, Urszula, David Morgan, Stephen J. Yarwood, and Graeme Barker. "Selective small-molecule EPAC activators." Biochemical Society Transactions 47, no. 5 (October 11, 2019): 1415–27. http://dx.doi.org/10.1042/bst20190254.

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Abstract The cellular signalling enzymes, EPAC1 and EPAC2, have emerged as key intracellular sensors of the secondary messenger cyclic 3′,5′-adenosine monophosphate (cyclic adenosine monophosphate) alongside protein kinase A. Interest has been galvanised in recent years thanks to the emergence of these species as potential targets for new cardiovascular disease therapies, including vascular inflammation and insulin resistance in vascular endothelial cells. We herein summarise the current state-of-the-art in small-molecule EPAC activity modulators, including cyclic nucleotides, sulphonylureas, and N-acylsulphonamides.

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Bhujbal, Swapnil P., and Jung-Mi Hah. "Generation of Non-Nucleotide CD73 Inhibitors Using a Molecular Docking and 3D-QSAR Approach." International Journal of Molecular Sciences 22, no. 23 (November 25, 2021): 12745. http://dx.doi.org/10.3390/ijms222312745.

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Radiotherapy and chemotherapy are conventional cancer treatments. Around 60% of all patients who are diagnosed with cancer receive radio- or chemotherapy in combination with surgery during their disease. Only a few patients respond to the blockage of immune checkpoints alone, or in combination therapy, because their tumours might not be immunogenic. Under these circumstances, an increasing level of extracellular adenosine via the activation of ecto-5’-nucleotidase (CD73) and consequent adenosine receptor signalling is a typical mechanism that tumours use to evade immune surveillance. CD73 is responsible for the conversion of adenosine monophosphate to adenosine. CD73 is overexpressed in various tumour types. Hence, targetting CD73’s signalling is important for the reversal of adenosine-facilitated immune suppression. In this study, we selected a potent series of the non-nucleotide small molecule inhibitors of CD73. Molecular docking studies were performed in order to examine the binding mode of the inhibitors inside the active site of CD73 and 3D-QSAR was used to study the structure–activity relationship. The obtained CoMFA (q2 = 0.844, ONC = 5, r2 = 0.947) and CoMSIA (q2 = 0.804, ONC = 4, r2 = 0.954) models showed reasonable statistical values. The 3D-QSAR contour map analysis revealed useful structural characteristics that were needed to modify non-nucleotide small molecule inhibitors. We used the structural information from the overall docking and 3D-QSAR results to design new, potent CD73 non-nucleotide inhibitors. The newly designed CD73 inhibitors exhibited higher activity (predicted pIC50) than the most active compound of all of the derivatives that were selected for this study. Further experimental studies are needed in order to validate the new CD73 inhibitors.

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Koshiba, Masahiro, Hidekazu Kosaka, Takashi Nakazawa, Nobuhide Hayashi, Ryuichi Saura, Noriko Kitamura, and Shunichi Kumagai. "2-Chloroadenosine but not adenosine induces apoptosis in rheumatoid fibroblasts independently of cell surface adenosine receptor signalling." British Journal of Pharmacology 135, no. 6 (March 2002): 1477–86. http://dx.doi.org/10.1038/sj.bjp.0704612.

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Tsiampali, Julia, Silke Neumann, Beatriz Giesen, Katharina Koch, Donata Maciaczyk, Christoph Janiak, Daniel Hänggi, and Jaroslaw Maciaczyk. "Enzymatic Activity of CD73 Modulates Invasion of Gliomas via Epithelial–Mesenchymal Transition-Like Reprogramming." Pharmaceuticals 13, no. 11 (November 11, 2020): 378. http://dx.doi.org/10.3390/ph13110378.

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Glioblastoma (GBM) is the most aggressive malignant primary brain tumour in adulthood. Despite strong research efforts current treatment options have a limited impact on glioma stem-like cells (GSCs) which contribute to GBM formation, progression and chemoresistance. Invasive growth of GSCs is in part associated with epithelial–mesenchymal-like transition (EMT), a mechanism associated with CD73 in several cancers. Here, we show that CD73 regulates the EMT activator SNAIL1 and further investigate the role of enzymatic and non-enzymatic CD73 activity in GBM progression. Reduction of CD73 protein resulted in significant suppression of GSC viability, proliferation and clonogenicity, whereas CD73 enzymatic activity exhibited negative effects only on GSC invasion involving impaired downstream adenosine (ADO) signalling. Furthermore, application of phosphodiesterase inhibitor pentoxifylline, a potent immunomodulator, effectively inhibited ZEB1 and CD73 expression and significantly decreased viability, clonogenicity, and invasion of GSC in vitro cultures. Given the involvement of adenosine and A3 adenosine receptor in GSC invasion, we investigated the effect of the pharmacological inhibition of A3AR on GSC maintenance. Direct A3AR inhibition promoted apoptotic cell death and impaired the clonogenicity of GSC cultures. Taken together, our data indicate that CD73 is an exciting novel target in GBM therapy. Moreover, pharmacological interference, resulting in disturbed ADO signalling, provides new opportunities to innovate GBM therapy.

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DORIS, ROSEMARIE, ELAINE KILGOUR, MILES D. HOUSLAY, GORDON E. THOMPSON, and RICHARD G. VERNON. "Modulation of adenosine signalling in sheep adipose tissue by growth hormone." Biochemical Society Transactions 23, no. 1 (February 1, 1995): 16S. http://dx.doi.org/10.1042/bst023016s.

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Meng, Fan, Zhige Guo, Yaling Hu, Weihao Mai, Zhenjie Zhang, Bin Zhang, Qianqian Ge, et al. "CD73-derived adenosine controls inflammation and neurodegeneration by modulating dopamine signalling." Brain 142, no. 3 (January 27, 2019): 700–718. http://dx.doi.org/10.1093/brain/awy351.

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Angioni, Roberta, Cristina Liboni, Stephanie Herkenne, Ricardo Sánchez‐Rodríguez, Giulia Borile, Elisabetta Marcuzzi, Bianca Calì, Maurizio Muraca, and Antonella Viola. "CD73 + extracellular vesicles inhibit angiogenesis through adenosine A 2B receptor signalling." Journal of Extracellular Vesicles 9, no. 1 (May 4, 2020): 1757900. http://dx.doi.org/10.1080/20013078.2020.1757900.

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Fulle, S. "Purinergic signalling during myogenesis: a role for adenosine and its receptors." Acta Physiologica 214, no. 4 (July 3, 2015): 436–39. http://dx.doi.org/10.1111/apha.12542.

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Kaplan, G. B., K. A. Leite-Morris, M. T. Sears, E. G. McClelland, and R. K. Sethi. "Regulation of adenosine- and G protein-mediated signalling in opiate dependence." Biological Psychiatry 39, no. 7 (April 1996): 505. http://dx.doi.org/10.1016/0006-3223(96)83969-2.

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Williams-Pritchard, Grant, Jason Peart, Peter Johnson, and John Headrick. "Signalling Cross-Talk Between Cardiomyocyte δ-Opioid and Adenosine A1 Receptors." Heart, Lung and Circulation 17 (2008): S229. http://dx.doi.org/10.1016/j.hlc.2008.05.573.

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Spormann, Luise, Christiane Rennert, Erik Kolbe, Fritzi Ott, Carolin Lossius, Robert Lehmann, Rolf Gebhardt, Thomas Berg, and Madlen Matz-Soja. "Cyclopamine and Rapamycin Synergistically Inhibit mTOR Signalling in Mouse Hepatocytes, Revealing an Interaction of Hedgehog and mTor Signalling in the Liver." Cells 9, no. 8 (July 31, 2020): 1817. http://dx.doi.org/10.3390/cells9081817.

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In the liver, energy homeostasis is mainly regulated by mechanistic target of rapamycin (mTOR) signalling, which influences relevant metabolic pathways, including lipid metabolism. However, the Hedgehog (Hh) pathway is one of the newly identified drivers of hepatic lipid metabolism. Although the link between mTOR and Hh signalling was previously demonstrated in cancer development and progression, knowledge of their molecular crosstalk in healthy liver is lacking. To close this information gap, we used a transgenic mouse model, which allows hepatocyte-specific deletion of the Hh pathway, and in vitro studies to reveal interactions between Hh and mTOR signalling. The study was conducted in male and female mice to investigate sexual differences in the crosstalk of these signalling pathways. Our results reveal that the conditional Hh knockout reduces mitochondrial adenosine triphosphate (ATP) production in primary hepatocytes from female mice and inhibits autophagy in hepatocytes from both sexes. Furthermore, in vitro studies show a synergistic effect of cyclopamine and rapamycin on the inhibition of mTor signalling and oxidative respiration in primary hepatocytes from male and female C57BL/6N mice. Overall, our results demonstrate that the impairment of Hh signalling influences mTOR signalling and therefore represses oxidative phosphorylation and autophagy.

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Menéndez Méndez, Aida, Jonathon Smith, and Tobias Engel. "Neonatal Seizures and Purinergic Signalling." International Journal of Molecular Sciences 21, no. 21 (October 22, 2020): 7832. http://dx.doi.org/10.3390/ijms21217832.

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Neonatal seizures are one of the most common comorbidities of neonatal encephalopathy, with seizures aggravating acute injury and clinical outcomes. Current treatment can control early life seizures; however, a high level of pharmacoresistance remains among infants, with increasing evidence suggesting current anti-seizure medication potentiating brain damage. This emphasises the need to develop safer therapeutic strategies with a different mechanism of action. The purinergic system, characterised by the use of adenosine triphosphate and its metabolites as signalling molecules, consists of the membrane-bound P1 and P2 purinoreceptors and proteins to modulate extracellular purine nucleotides and nucleoside levels. Targeting this system is proving successful at treating many disorders and diseases of the central nervous system, including epilepsy. Mounting evidence demonstrates that drugs targeting the purinergic system provide both convulsive and anticonvulsive effects. With components of the purinergic signalling system being widely expressed during brain development, emerging evidence suggests that purinergic signalling contributes to neonatal seizures. In this review, we first provide an overview on neonatal seizure pathology and purinergic signalling during brain development. We then describe in detail recent evidence demonstrating a role for purinergic signalling during neonatal seizures and discuss possible purine-based avenues for seizure suppression in neonates.

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Vieira, Cátia, Maria Teresa Magalhães-Cardoso, Fátima Ferreirinha, Isabel Silva, Ana Sofia Dias, Julie Pelletier, Jean Sévigny, and Paulo Correia-de-Sá. "Feed-Forward Inhibition of CD73 and Upregulation of Adenosine Deaminase Contribute to the Loss of Adenosine Neuromodulation in Postinflammatory Ileitis." Mediators of Inflammation 2014 (2014): 1–19. http://dx.doi.org/10.1155/2014/254640.

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Purinergic signalling is remarkably plastic during gastrointestinal inflammation. Thus, selective drugs targeting the “purinome” may be helpful for inflammatory gastrointestinal diseases. The myenteric neuromuscular transmission of healthy individuals is fine-tuned and controlled by adenosine acting onA2Aexcitatory receptors. Here, we investigated the neuromodulatory role of adenosine in TNBS-inflamed longitudinal muscle-myenteric plexus of the rat ileum. Seven-day postinflammation ileitis lacks adenosine neuromodulation, which may contribute to acceleration of gastrointestinal transit. The loss of adenosine neuromodulation results from deficient accumulation of the nucleoside at the myenteric synapse despite the fact that the increases in ATP release were observed. Disparity between ATP outflow and adenosine deficit in postinflammatory ileitis is ascribed to feed-forward inhibition of ecto-5′-nucleotidase/CD73 by high extracellular ATP and/or ADP. Redistribution of NTPDase2, but not of NTPDase3, from ganglion cell bodies to myenteric nerve terminals leads to preferential ADP accumulation from released ATP, thus contributing to the prolonged inhibition of muscle-bound ecto-5′-nucleotidase/CD73 and to the delay of adenosine formation at the inflamed neuromuscular synapse. On the other hand, depression of endogenous adenosine accumulation may also occur due to enhancement of adenosine deaminase activity. Both membrane-bound and soluble forms of ecto-5′-nucleotidase/CD73 and adenosine deaminase were detected in the inflamed myenteric plexus. These findings provide novel therapeutic targets for inflammatory gut motility disorders.

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Baker, David A., Laura G. Drought, Christian Flueck, Stephanie D. Nofal, Avnish Patel, Maria Penzo, and Eloise M. Walker. "Cyclic nucleotide signalling in malaria parasites." Open Biology 7, no. 12 (December 2017): 170213. http://dx.doi.org/10.1098/rsob.170213.

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The cyclic nucleotides 3′, 5′-cyclic adenosine monophosphate (cAMP) and 3′, 5′-cyclic guanosine monophosphate (cGMP) are intracellular messengers found in most animal cell types. They usually mediate an extracellular stimulus to drive a change in cell function through activation of their respective cyclic nucleotide-dependent protein kinases, PKA and PKG. The enzymatic components of the malaria parasite cyclic nucleotide signalling pathways have been identified, and the genetic and biochemical studies of these enzymes carried out to date are reviewed herein. What has become very clear is that cyclic nucleotides play vital roles in controlling every stage of the complex malaria parasite life cycle. Our understanding of the involvement of cyclic nucleotide signalling in orchestrating the complex biology of malaria parasites is still in its infancy, but the recent advances in our genetic tools and the increasing interest in signalling will deliver more rapid progress in the coming years.

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Monterisi, Stefania, and Manuela Zaccolo. "Components of the mitochondrial cAMP signalosome." Biochemical Society Transactions 45, no. 1 (February 8, 2017): 269–74. http://dx.doi.org/10.1042/bst20160394.

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3′-5′-Cyclic adenosine monophosphate/protein kinase A (cAMP/PKA) signalling is activated by different extracellular stimuli and mediates many diverse processes within the same cell. It is now well established that in order to translate into the appropriate cellular function multiple extracellular inputs, which may act simultaneously on the same cell, the cAMP/PKA signalling pathway is compartmentalised. Multimolecular complexes are organised at specific subcellular sites to generate spatially confined signalosomes, which include effectors, modulators and targets of the pathway. In recent years, it has become evident that mitochondria represent sites of compartmentalised cAMP signalling. However, the exact location and the molecular composition of distinct mitochondria signalosomes and their function remain largely unknown. In this review, we focus on individual components of the cAMP/PKA signalling pathway at distinct mitochondria subdomains represented by the outer and inner mitochondrial membranes, the intermembrane space and the matrix, highlighting some of the questions that remain unanswered.

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dos Anjos, Fernanda, Júlia Leão Batista Simões, Charles Elias Assmann, Fabiano Barbosa Carvalho, and Margarete Dulce Bagatini. "Potential Therapeutic Role of Purinergic Receptors in Cardiovascular Disease Mediated by SARS-CoV-2." Journal of Immunology Research 2020 (December 1, 2020): 1–14. http://dx.doi.org/10.1155/2020/8632048.

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Novel coronavirus disease 2019 (COVID-19) causes pulmonary and cardiovascular disorders and has become a worldwide emergency. Myocardial injury can be caused by direct or indirect damage, particularly mediated by a cytokine storm, a disordered immune response that can cause myocarditis, abnormal coagulation, arrhythmia, acute coronary syndrome, and myocardial infarction. The present review focuses on the mechanisms of this viral infection, cardiac biomarkers, consequences, and the possible therapeutic role of purinergic and adenosinergic signalling systems. In particular, we focus on the interaction of the extracellular nucleotide adenosine triphosphate (ATP) with its receptors P2X1, P2X4, P2X7, P2Y1, and P2Y2 and of adenosine (Ado) with A2A and A3 receptors, as well as their roles in host immune responses. We suggest that receptors of purinergic signalling could be ideal candidates for pharmacological targeting to protect against myocardial injury caused by a cytokine storm in COVID-19, in order to reduce systemic inflammatory damage to cells and tissues, preventing the progression of the disease by modulating the immune response and improving patient quality of life.

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Villalobos-Labra, Roberto, Luis Silva, Mario Subiabre, Joaquín Araos, Rocío Salsoso, Bárbara Fuenzalida, Tamara Sáez, et al. "Akt/mTOR Role in Human Foetoplacental Vascular Insulin Resistance in Diseases of Pregnancy." Journal of Diabetes Research 2017 (2017): 1–13. http://dx.doi.org/10.1155/2017/5947859.

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Insulin resistance is characteristic of pregnancies where the mother shows metabolic alterations, such as preeclampsia (PE) and gestational diabetes mellitus (GDM), or abnormal maternal conditions such as pregestational maternal obesity (PGMO). Insulin signalling includes activation of insulin receptor substrates 1 and 2 (IRS1/2) as well as Src homology 2 domain-containing transforming protein 1, leading to activation of 44 and 42 kDa mitogen-activated protein kinases and protein kinase B/Akt (Akt) signalling cascades in the human foetoplacental vasculature. PE, GDM, and PGMO are abnormal conditions coursing with reduced insulin signalling, but the possibility of the involvement of similar cell signalling mechanisms is not addressed. This review aimed to determine whether reduced insulin signalling in PE, GDM, and PGMO shares a common mechanism in the human foetoplacental vasculature. Insulin resistance in these pathological conditions results from reduced Akt activation mainly due to inhibition of IRS1/2, likely due to the increased activity of the mammalian target of rapamycin (mTOR) resulting from lower activity of adenosine monophosphate kinase. Thus, a defective signalling via Akt/mTOR in response to insulin is a central and common mechanism of insulin resistance in these diseases of pregnancy. In this review, we summarise the cell signalling mechanisms behind the insulin resistance state in PE, GDM, and PGMO focused in the Akt/mTOR signalling pathway in the human foetoplacental endothelium.

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Massimo Caruso, Giovanni Tringali, and Riccardo Polosa. "Evidence For A Functional Contribution of Adenosine Signalling in Inflammatory Airway Diseases." Immunology, Endocrine & Metabolic Agents in Medicinal Chemistry 7, no. 4 (August 1, 2007): 286–97. http://dx.doi.org/10.2174/187152207781369896.

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Atterbury, Alison, and Mark J. Wall. "Adenosine signalling at immature parallel fibre-Purkinje cell synapses in rat cerebellum." Journal of Physiology 587, no. 18 (September 14, 2009): 4497–508. http://dx.doi.org/10.1113/jphysiol.2009.176420.

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Journal articles on the topic 'Adenosine-signalling'

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