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[PMID]:28763502
[Au] Autor:Martín-Estebané M; Navascués J; Sierra-Martín A; Martín-Guerrero SM; Cuadros MA; Carrasco MC; Marín-Teva JL
[Ad] Endereço:Departamento de Biología Celular, Facultad de Ciencias, Universidad de Granada, Granada, Spain.
[Ti] Título:Onset of microglial entry into developing quail retina coincides with increased expression of active caspase-3 and is mediated by extracellular ATP and UDP.
[So] Source:PLoS One;12(8):e0182450, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Microglial cell precursors located in the area of the base of the pecten and the optic nerve head (BP/ONH) start to enter the retina of quail embryos at the 7th day of incubation (E7), subsequently colonizing the entire retina by central-to-peripheral tangential migration, as previously shown by our group. The present study demonstrates a precise chronological coincidence of the onset of microglial cell entry into the retina with a striking increase in death of retinal cells, as revealed by their active caspase-3 expression and TUNEL staining, in regions dorsal to the BP/ONH area, suggesting that dying retinal cells would contribute to the microglial cell inflow into the retina. However, the molecular mechanisms involved in this inflow are currently unclear. Extracellular nucleotides, such as ATP and UDP, have previously been shown to favor migration of microglia towards brain injuries because they are released by apoptotic cells and stimulate both chemotaxis and chemokinesis in microglial cells via signaling through purinergic receptors. Hence, we tested here the hypothesis that ATP and UDP play a role in the entry and migration of microglial precursors into the developing retina. For this purpose, we used an experimental model system based on organotypic cultures of E6.5 quail embryo retina explants, which mimics the entry and migration of microglial precursors in the in situ developing retina. Inhibition of purinergic signaling by treating retina explants with either apyrase, a nucleotide-hydrolyzing enzyme, or suramin, a broad spectrum antagonist of purinergic receptors, significantly prevents the entry of microglial cells into the retina. In addition, treatment of retina explants with either exogenous ATP or UDP results in significantly increased numbers of microglial cells entering the retina. In light of these findings, we conclude that purinergic signaling by extracellular ATP and UDP is necessary for the entry and migration of microglial cells into the embryonic retina by inducing chemokinesis in these cells.
[Mh] Termos MeSH primário: Trifosfato de Adenosina/metabolismo
Caspase 3/metabolismo
Regulação da Expressão Gênica no Desenvolvimento
Microglia/citologia
Retina/embriologia
Difosfato de Uridina/metabolismo
[Mh] Termos MeSH secundário: Animais
Sobrevivência Celular
Quimiotaxia
Ativação Enzimática
Microscopia Confocal
Nervo Óptico/patologia
Codorniz
Receptores Purinérgicos/metabolismo
Retina/fisiologia
Transdução de Sinais
Fatores de Tempo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Receptors, Purinergic); 58-98-0 (Uridine Diphosphate); 8L70Q75FXE (Adenosine Triphosphate); EC 3.4.22.- (Caspase 3)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171010
[Lr] Data última revisão:
171010
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170802
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0182450


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[PMID]:28667079
[Au] Autor:Kavvadas P; Abed A; Poulain C; Authier F; Labéjof LP; Calmont A; Afieri C; Prakoura N; Dussaule JC; Chatziantoniou C; Chadjichristos CE
[Ad] Endereço:National Institute for Health and Medical Research Unité Mixte de Recherche-S1155, Batiment Recherche, Tenon Hospital, Paris, France.
[Ti] Título:Decreased Expression of Connexin 43 Blunts the Progression of Experimental GN.
[So] Source:J Am Soc Nephrol;28(10):2915-2930, 2017 Oct.
[Is] ISSN:1533-3450
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:GN refers to a variety of renal pathologies that often progress to ESRD, but the molecular mechanisms underlying this progression remain incompletely characterized. Here, we determined whether dysregulated expression of the gap junction protein connexin 43, which has been observed in the progression of renal disease, contributes to GN progression. Immunostaining revealed expression of connexin 43 in damaged glomeruli in patients with glomerular diseases as well as in mice after induction of experimental GN. Notably, 2 weeks after the induction of GN with nephrotoxic serum, mice with a heterozygous deletion of the connexin 43 gene ( ) had proteinuria, BUN, and serum creatinine levels significantly lower than those of wild-type animals. Additionally, the connexin 43+/- mice showed less crescent formation, tubular dilation, monocyte infiltration, and interstitial renal fibrosis. Treatment of cultured podocytes with connexin 43-specific blocking peptides attenuated TGF- -induced cytoskeletal and morphologic changes and apoptosis as did treatment with the purinergic blocker suramin. Finally, therapeutic treatment of GN mice with connexin 43-specific antisense oligodeoxynucleotide improved functional and structural renal parameters. These findings suggest that crosstalk between connexin 43 and purinergic signaling contributes to podocyte damage in GN. Given that this protein is highly induced in individuals with glomerular diseases, connexin 43 may be a novel target for therapeutic treatment of GN.
[Mh] Termos MeSH primário: Conexina 43/metabolismo
Glomerulonefrite/metabolismo
[Mh] Termos MeSH secundário: Animais
Apoptose
Desdiferenciação Celular
Linhagem Celular
Modelos Animais de Doenças
Progressão da Doença
Feminino
Fibrose
Glomerulonefrite/patologia
Seres Humanos
Rim/patologia
Camundongos
Podócitos/metabolismo
Receptores Purinérgicos/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Connexin 43); 0 (GJA1 protein, mouse); 0 (Receptors, Purinergic)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171019
[Lr] Data última revisão:
171019
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170702
[St] Status:MEDLINE
[do] DOI:10.1681/ASN.2016111211


  3 / 3472 MEDLINE  
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[PMID]:28274860
[Au] Autor:Ye X; Shen T; Hu J; Zhang L; Zhang Y; Bao L; Cui C; Jin G; Zan K; Zhang Z; Yang X; Shi H; Zu J; Yu M; Song C; Wang Y; Qi S; Cui G
[Ad] Endereço:Department of Neurology, the Affiliated Hospital of Xuzhou Medical University, Xuzhou, Jiangsu Province, China.
[Ti] Título:Purinergic 2X7 receptor/NLRP3 pathway triggers neuronal apoptosis after ischemic stroke in the mouse.
[So] Source:Exp Neurol;292:46-55, 2017 Jun.
[Is] ISSN:1090-2430
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Previous research has shown that Purinergic 2X7 receptor (P2X7R) and NLRP3 inflammasome contribute to the inflammatory activation. In this study, we investigated whether P2X7R/NLRP3 pathway is involved in the caspase-3 dependent neuronal apoptosis after ischemic stroke by using a focal cortex ischemic stroke model. The expressions of P2X7R, NLRP3 inflammsome components, and cleaved caspase-3 were significantly enhanced in the ischemic brain tissue after stroke. However, the expression of cleaved caspase-3 was significantly attenuated after treatment of stroke with P2X7R antagonist (BBG) or NLRP3 inhibitor (MCC950). The treatment also significantly reduced the infarction volume, neuronal apoptosis, and neurological impairment. In addition, in vitro data also support the hypothesis that P2X7R/NLRP3 pathway plays a vital role in caspase-3 dependent neuronal apoptosis after ischemic stroke. Further investigation of effective regulation of P2X7R and NLRP3 in stroke is warranted.
[Mh] Termos MeSH primário: Apoptose/fisiologia
Isquemia/metabolismo
Proteína 3 que Contém Domínio de Pirina da Família NLR/metabolismo
Acidente Vascular Cerebral/metabolismo
[Mh] Termos MeSH secundário: Animais
Proteínas Reguladoras de Apoptose/metabolismo
Proteínas de Transporte/metabolismo
Células Cultivadas
Modelos Animais de Doenças
Inflamassomos/metabolismo
Masculino
Camundongos Endogâmicos C57BL
Receptores Purinérgicos/metabolismo
Transdução de Sinais/fisiologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Apoptosis Regulatory Proteins); 0 (Carrier Proteins); 0 (Inflammasomes); 0 (NLR Family, Pyrin Domain-Containing 3 Protein); 0 (Nlrp3 protein, mouse); 0 (Receptors, Purinergic)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:170728
[Lr] Data última revisão:
170728
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170310
[St] Status:MEDLINE


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[PMID]:28179298
[Au] Autor:Lertsuwan K; Peters W; Johnson L; Lertsuwan J; Marwa I; Sikes RA
[Ad] Endereço:Department of Biochemistry, Faculty of Science, Mahidol University, Bangkok, Thailand.
[Ti] Título:Purinergic Receptor Expression and Cellular Responses to Purinergic Agonists in Human Prostate Cancer Cells.
[So] Source:Anticancer Res;37(2):529-537, 2017 02.
[Is] ISSN:1791-7530
[Cp] País de publicação:Greece
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Anticancer activity of extracellular nucleotides has been investigated in many types of cancer. Herein, the effects of extracellular nucleotides and the receptor profile for these nucleotides on prostate cancer (PCa) were elaborated. MATERIALS AND METHODS: PCa cell lines representing different stages of PCa were used. The effects of ATP and adenosine on PCa growth and migration on different extracellular matrix proteins were examined by MTT and wound-healing assays. Purinergic receptor profiling was carried out by reverse transcription-polymerase chain reaction (RT-PCR). RESULTS: A growth-inhibitory effect of ATP and adenosine was observed on all PCa cell lines tested. Several ATP-recognized P2 receptors and adenosine receptors were commonly expressed in PCa cell lines. Neither ATP nor adenosine had any significant effect on PCa migration. CONCLUSION: ATP and adenosine had an antiproliferative effect on PCa cells without affecting their motility, indicating their potential as a novel therapy for PCa.
[Mh] Termos MeSH primário: Trifosfato de Adenosina/farmacologia
Adenosina/farmacologia
Neoplasias da Próstata/tratamento farmacológico
Neoplasias da Próstata/metabolismo
Agonistas Purinérgicos/farmacologia
Receptores Purinérgicos/biossíntese
[Mh] Termos MeSH secundário: Processos de Crescimento Celular/efeitos dos fármacos
Linhagem Celular Tumoral
Movimento Celular/efeitos dos fármacos
Relação Dose-Resposta a Droga
Seres Humanos
Masculino
Neoplasias da Próstata/patologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Purinergic Agonists); 0 (Receptors, Purinergic); 8L70Q75FXE (Adenosine Triphosphate); K72T3FS567 (Adenosine)
[Em] Mês de entrada:1702
[Cu] Atualização por classe:170213
[Lr] Data última revisão:
170213
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170210
[St] Status:MEDLINE


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[PMID]:28057794
[Au] Autor:Burnstock G
[Ad] Endereço:From the Autonomic Neuroscience Institute, Royal Free and University College Medical School, London, United Kingdom. g.burnstock@ucl.ac.uk.
[Ti] Título:Purinergic Signaling in the Cardiovascular System.
[So] Source:Circ Res;120(1):207-228, 2017 Jan 06.
[Is] ISSN:1524-4571
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:There is nervous control of the heart by ATP as a cotransmitter in sympathetic, parasympathetic, and sensory-motor nerves, as well as in intracardiac neurons. Centers in the brain control heart activities and vagal cardiovascular reflexes involve purines. Adenine nucleotides and nucleosides act on purinoceptors on cardiomyocytes, AV and SA nodes, cardiac fibroblasts, and coronary blood vessels. Vascular tone is controlled by a dual mechanism. ATP, released from perivascular sympathetic nerves, causes vasoconstriction largely via P2X1 receptors. Endothelial cells release ATP in response to changes in blood flow (via shear stress) or hypoxia, to act on P2 receptors on endothelial cells to produce nitric oxide, endothelium-derived hyperpolarizing factor, or prostaglandins to cause vasodilation. ATP is also released from sensory-motor nerves during antidromic reflex activity, to produce relaxation of some blood vessels. Purinergic signaling is involved in the physiology of erythrocytes, platelets, and leukocytes. ATP is released from erythrocytes and platelets, and purinoceptors and ectonucleotidases are expressed by these cells. P1, P2Y , P2Y , and P2X1 receptors are expressed on platelets, which mediate platelet aggregation and shape change. Long-term (trophic) actions of purine and pyrimidine nucleosides and nucleotides promote migration and proliferation of vascular smooth muscle and endothelial cells via P1 and P2Y receptors during angiogenesis, vessel remodeling during restenosis after angioplasty and atherosclerosis. The involvement of purinergic signaling in cardiovascular pathophysiology and its therapeutic potential are discussed, including heart failure, infarction, arrhythmias, syncope, cardiomyopathy, angina, heart transplantation and coronary bypass grafts, coronary artery disease, diabetic cardiomyopathy, hypertension, ischemia, thrombosis, diabetes mellitus, and migraine.
[Mh] Termos MeSH primário: Doenças Cardiovasculares/metabolismo
Sistema Cardiovascular/metabolismo
Receptores Purinérgicos/metabolismo
Transdução de Sinais/fisiologia
[Mh] Termos MeSH secundário: Animais
Doenças Cardiovasculares/fisiopatologia
Sistema Cardiovascular/fisiopatologia
Seres Humanos
Músculo Liso Vascular/metabolismo
Vasoconstrição/fisiologia
Vasodilatação/fisiologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Receptors, Purinergic)
[Em] Mês de entrada:1705
[Cu] Atualização por classe:170505
[Lr] Data última revisão:
170505
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170107
[St] Status:MEDLINE
[do] DOI:10.1161/CIRCRESAHA.116.309726


  6 / 3472 MEDLINE  
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[PMID]:28030754
[Au] Autor:Jovanovic S; Radulovic T; Coddou C; Dietz B; Nerlich J; Stojilkovic SS; Rübsamen R; Milenkovic I
[Ad] Endereço:Institute of Biology, Faculty of Biosciences, Pharmacy and Psychology, University of Leipzig, Leipzig, Germany.
[Ti] Título:Tonotopic action potential tuning of maturing auditory neurons through endogenous ATP.
[So] Source:J Physiol;595(4):1315-1337, 2017 Feb 15.
[Is] ISSN:1469-7793
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:KEY POINTS: Following the genetically controlled formation of neuronal circuits, early firing activity guides the development of sensory maps in the auditory, visual and somatosensory system. However, it is not clear whether the activity of central auditory neurons is specifically regulated depending on the position within the sensory map. In the ventral cochlear nucleus, the first central station along the auditory pathway, we describe a mechanism through which paracrine ATP signalling enhances firing in a cell-specific and tonotopically-determined manner. Developmental down-regulation of P2X2/3R currents along the tonotopic axis occurs simultaneously with an increase in AMPA receptor currents, suggesting a high-to-low frequency maturation pattern. Facilitated action potential (AP) generation, measured as higher firing rate, shorter EPSP-AP delay in vivo and shorter AP latency in slice experiments, is consistent with increased synaptic efficacy caused by ATP. The long lasting change in intrinsic neuronal excitability is mediated by the heteromeric P2X2/3 receptors. ABSTRACT: Synaptic refinement and strengthening are activity-dependent processes that establish orderly arranged cochleotopic maps throughout the central auditory system. The maturation of auditory brainstem circuits is guided by action potentials (APs) arising from the inner hair cells in the developing cochlea. The AP firing of developing central auditory neurons can be modulated by paracrine ATP signalling, as shown for the cochlear nucleus bushy cells and principal neurons in the medial nucleus of the trapezoid body. However, it is not clear whether neuronal activity may be specifically regulated with respect to the nuclear tonotopic position (i.e. sound frequency selectivity). Using slice recordings before hearing onset and in vivo recordings with iontophoretic drug applications after hearing onset, we show that cell-specific purinergic modulation follows a precise tonotopic pattern in the ventral cochlear nucleus of developing gerbils. In high-frequency regions, ATP responsiveness diminished before hearing onset. In low-to-mid frequency regions, ATP modulation persisted after hearing onset in a subset of low-frequency bushy cells (characteristic frequency< 10 kHz). Down-regulation of P2X2/3R currents along the tonotopic axis occurs simultaneously with an increase in AMPA receptor currents, thus suggesting a high-to-low frequency maturation pattern. Facilitated AP generation, measured as higher firing frequency, shorter EPSP-AP delay in vivo, and shorter AP latency in slice experiments, is consistent with increased synaptic efficacy caused by ATP. Finally, by combining recordings and pharmacology in vivo, in slices, and in human embryonic kidney 293 cells, it was shown that the long lasting change in intrinsic neuronal excitability is mediated by the P2X2/3R.
[Mh] Termos MeSH primário: Potenciais de Ação
Trifosfato de Adenosina/metabolismo
Núcleo Coclear/metabolismo
Potenciais Pós-Sinápticos Excitadores
Receptores Purinérgicos/metabolismo
[Mh] Termos MeSH secundário: Animais
Nervo Coclear/metabolismo
Nervo Coclear/fisiologia
Núcleo Coclear/citologia
Núcleo Coclear/crescimento & desenvolvimento
Núcleo Coclear/fisiologia
Feminino
Gerbillinae
Células HEK293
Células Ciliadas Auditivas Internas/metabolismo
Células Ciliadas Auditivas Internas/fisiologia
Seres Humanos
Masculino
Tempo de Reação
Receptores de AMPA/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Receptors, AMPA); 0 (Receptors, Purinergic); 8L70Q75FXE (Adenosine Triphosphate)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170901
[Lr] Data última revisão:
170901
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161229
[St] Status:MEDLINE
[do] DOI:10.1113/JP273272


  7 / 3472 MEDLINE  
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[PMID]:27993681
[Au] Autor:Takahashi K; Fukushima K; Onishi Y; Inui K; Node Y; Fukushima N; Honoki K; Tsujiuchi T
[Ad] Endereço:Division of Molecular Oncology, Department of Life Science, Faculty of Science and Engineering, Kindai University, 3-4-1, Kowakae, Higashiosaka, Osaka 577-8502, Japan.
[Ti] Título:Lysophosphatidic acid (LPA) signaling via LPA and LPA negatively regulates cell motile activities of colon cancer cells.
[So] Source:Biochem Biophys Res Commun;483(1):652-657, 2017 Jan 29.
[Is] ISSN:1090-2104
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Lysophosphatidic acid (LPA) is an extracellular biological lipid and interacts with six subtypes of G protein-coupled LPA receptors (LPA to LPA ). LPA receptors exhibit a variety of cellular functions, depending on types of cancer cells. In this study, to assess the roles of LPA and LPA in cell growth and motile activities of colon cancer cells, LPA and LPA knockdown cells were established from DLD1 and HCT116 cells. LPA treatment increased the cell growth activities of LPA and LPA knockdown cells, compared with control cells. The cell motile activities of LPA and LPA knockdown cells were significantly higher than those of control cells. To evaluate the effects of LPA and LPA on cell motile activity induced by anticancer drug, long-term fluorouracil (5-FU) treated (DLD-5FU) cells were generated. The expression levels of LPAR1, LPAR4 and LPAR6 genes were significantly increased in DLD-5FU cells. DLD-5FU cells showed the high cell motile activity, compared with DLD1 cells. The increased cell motile activity was markedly stimulated by LPA and LPA knockdown. In contrast, the cell motile activity enhanced by 5-FU treatment was suppressed by LPA knockdown. These results suggest that LPA signaling via LPA and LPA negatively regulates the cell motile activities of DLD1 and HCT116 cells as well as long-term 5-FU treated cells.
[Mh] Termos MeSH primário: Neoplasias do Colo/patologia
Lisofosfolipídeos/metabolismo
Receptores de Ácidos Lisofosfatídicos/metabolismo
Receptores Purinérgicos/metabolismo
[Mh] Termos MeSH secundário: Antimetabólitos Antineoplásicos/farmacologia
Linhagem Celular Tumoral
Movimento Celular/efeitos dos fármacos
Neoplasias do Colo/metabolismo
Fluoruracila/farmacologia
Células HCT116
Seres Humanos
Lisofosfolipídeos/farmacologia
Transdução de Sinais
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antimetabolites, Antineoplastic); 0 (Lysophospholipids); 0 (P2RY9 receptor, human); 0 (Receptors, Lysophosphatidic Acid); 0 (Receptors, Purinergic); PG6M3969SG (lysophosphatidic acid); U3P01618RT (Fluorouracil)
[Em] Mês de entrada:1705
[Cu] Atualização por classe:170529
[Lr] Data última revisão:
170529
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161221
[St] Status:MEDLINE


  8 / 3472 MEDLINE  
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[PMID]:27915186
[Au] Autor:Cieslak M; Wojtczak A; Komoszynski M
[Ad] Endereço:Neurology Clinic, Marek Cieslak, Torun, Poland.
[Ti] Título:Role of the purinergic signaling in epilepsy.
[So] Source:Pharmacol Rep;69(1):130-138, 2017 Feb.
[Is] ISSN:1734-1140
[Cp] País de publicação:Poland
[La] Idioma:eng
[Ab] Resumo:Adenine nucleotides and adenosine are signaling molecules that activate purinergic receptors P1 and P2. Activation of A1 adenosine receptors has an anticonvulsant action, whereas activation of A2A receptors might initiate seizures. Therefore, a significant limitation to the use of A1 receptor agonists as drugs in the CNS might be their peripheral side effects. The anti-epileptic activity of adenosine is related to its increased concentration outside the cell. This increase might result from the inhibition of the equilibrative nucleoside transporters (ENTs). Moreover, the implantation of implants or stem cells into the brain might cause slow and persistent increases in adenosine concentrations in the extracellular spaces of the brain. The role of adenosine in seizure inhibition has been confirmed by results demonstrating that in patients with epilepsy, the adenosine kinase (ADK) present in astrocytes is the only purine-metabolizing enzyme that exhibits increased expression. Increased ADK activity causes intensified phosphorylation of adenosine to 5'-AMP, which therefore lowers the adenosine level in the extracellular spaces. These changes might initiate astrogliosis and epileptogenesis, which are the manifestations of epilepsy. Seizures might induce inflammatory processes and vice versa. Activation of P2X7 receptors causes intensified release of pro-inflammatory cytokines (IL-1ß and TNF-α) and activates metabolic pathways that induce inflammatory processes in the CNS. Therefore, antagonists of P2X7 and the interleukin 1ß receptor might be efficient drugs for recurring seizures and prolonged status epilepticus. Inhibitors of ADK would simultaneously inhibit the seizures, prevent the astrogliosis and epileptogenesis processes and prevent the formation of new epileptogenic foci. Therefore, these drugs might become beneficial seizure-suppressing drugs.
[Mh] Termos MeSH primário: Epilepsia/metabolismo
Receptor A2A de Adenosina/metabolismo
Receptores Purinérgicos P2X7/metabolismo
Transdução de Sinais/fisiologia
[Mh] Termos MeSH secundário: Adenosina/metabolismo
Adenosina/farmacologia
Adenosina Quinase/antagonistas & inibidores
Adenosina Quinase/metabolismo
Animais
Epilepsia/tratamento farmacológico
Seres Humanos
Antagonistas do Receptor Purinérgico P2X/metabolismo
Antagonistas do Receptor Purinérgico P2X/farmacologia
Antagonistas do Receptor Purinérgico P2X/uso terapêutico
Receptores Purinérgicos/metabolismo
Transdução de Sinais/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Purinergic P2X Receptor Antagonists); 0 (Receptor, Adenosine A2A); 0 (Receptors, Purinergic); 0 (Receptors, Purinergic P2X7); EC 2.7.1.20 (Adenosine Kinase); K72T3FS567 (Adenosine)
[Em] Mês de entrada:1703
[Cu] Atualização por classe:170323
[Lr] Data última revisão:
170323
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161205
[St] Status:MEDLINE


  9 / 3472 MEDLINE  
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[PMID]:27885718
[Au] Autor:Gicquel T; Le Daré B; Boichot E; Lagente V
[Ad] Endereço:Laboratoire de toxicologie biologique et médico-légale, CHU Rennes, F-35033, Rennes, France.
[Ti] Título:Purinergic receptors: new targets for the treatment of gout and fibrosis.
[So] Source:Fundam Clin Pharmacol;31(2):136-146, 2017 Apr.
[Is] ISSN:1472-8206
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Adenosine triphosphate is involved in many metabolic reactions, but it has also a role as a cellular danger signal transmitted through purinergic receptors (PRs). Indeed, adenosine 5'-triphosphate (ATP) can bind to PRs which are found in the membrane of many cell types, although the relative proportions of the receptor subtypes differ. PRs are classified according to genetic and pharmacological criteria and especially their affinities for agonists and their transduction mechanism (i.e. as metabotropic P2YRs or ionotropic P2XRs). Extracellular ATP release by activated or necrotic cells may activate various PRs and especially P2X7R, the best-characterized PR, on immune cells. P2X7R is known to regulate the activation of the Nod-like receptor (NLR)-family protein, NLRP3 inflammasome, which permit the release of IL-1ß, a potent pro-inflammatory cytokine. The P2X7R/NLRP3 pathway is involved in many inflammatory diseases, such as gout, and in fibrosis diseases associated with inflammatory process, liver or lung fibrosis. Some authors imaging also a real promising therapeutic potential of P2X7R blockage. Thus, several pharmaceutical companies have developed P2X7R antagonists as novel anti-inflammatory drug candidates. Clinical trials of the efficacy of these antagonists are now underway. A better understanding of the P2X7R/NLRP3 signalling pathways permits the identification of targets and the development of a new class of drugs able to inhibit the fibrogenesis process and collagen deposition.
[Mh] Termos MeSH primário: Fibrose/tratamento farmacológico
Gota/tratamento farmacológico
Receptores Purinérgicos/efeitos dos fármacos
[Mh] Termos MeSH secundário: Trifosfato de Adenosina/metabolismo
Animais
Anti-Inflamatórios/farmacologia
Desenho de Drogas
Fibrose/patologia
Gota/patologia
Seres Humanos
Inflamassomos/metabolismo
Proteína 3 que Contém Domínio de Pirina da Família NLR/efeitos dos fármacos
Proteína 3 que Contém Domínio de Pirina da Família NLR/metabolismo
Antagonistas do Receptor Purinérgico P2X/farmacologia
Receptores Purinérgicos/metabolismo
Receptores Purinérgicos P2X7/efeitos dos fármacos
Receptores Purinérgicos P2X7/metabolismo
Transdução de Sinais/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Anti-Inflammatory Agents); 0 (Inflammasomes); 0 (NLR Family, Pyrin Domain-Containing 3 Protein); 0 (Purinergic P2X Receptor Antagonists); 0 (Receptors, Purinergic); 0 (Receptors, Purinergic P2X7); 8L70Q75FXE (Adenosine Triphosphate)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:170620
[Lr] Data última revisão:
170620
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161126
[St] Status:MEDLINE
[do] DOI:10.1111/fcp.12256


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[PMID]:27871906
[Au] Autor:Menezes CB; Frasson AP; Meirelles LC; Tasca T
[Ad] Endereço:Laboratório de Pesquisa em Parasitologia, Faculdade de Farmácia, Universidade Federal do Rio Grande do Sul, Av. Ipiranga 2752, 90610-000, Porto Alegre, RS, Brazil.
[Ti] Título:Adenosine, but not guanosine, protects vaginal epithelial cells from Trichomonas vaginalis cytotoxicity.
[So] Source:Microbes Infect;19(2):122-131, 2017 Feb.
[Is] ISSN:1769-714X
[Cp] País de publicação:France
[La] Idioma:eng
[Ab] Resumo:Trichomonas vaginalis causes the most common non-viral sexually transmitted disease worldwide. The cytoadherence and cytotoxicity upon the vaginal epithelial cells are crucial for the infection. Extracellular nucleotides are released during cell damage and, along with their nucleosides, can activate purinoceptors. The opposing effects of nucleotides versus nucleosides are regulated by ectonucleotidases. Herein we evaluated the hemolysis and cytolysis induced by T. vaginalis, as well as the extracellular nucleotide hydrolysis along with the effects mediated by nucleotides and nucleosides on cytotoxicity. In addition, the gene expression of purinoceptors in host cells was determined. The hemolysis and cytolysis exerted by all T. vaginalis isolates presented positive Pearson correlation. All T. vaginalis isolates were able to hydrolyze nucleotides, showing higher NTPDase than ecto-5'-nucleotidase activity. The most cytotoxic isolate, TV-LACM6, hydrolyzes ATP, GTP with more efficiency than AMP and GMP. The vaginal epithelial cell line (HMVII) expressed the genes for all subtypes of P1, P2X and P2Y receptors. Finally, when nucleotides and nucleosides were tested, the cytotoxic effect elicited by TV-LACM6 was increased with nucleotides. In contrast, the cytotoxicity was reversed by adenosine in presence of EHNA, but not by guanosine, contributing to the understanding of the purinergic signaling role on T. vaginalis cytotoxicity.
[Mh] Termos MeSH primário: Adenosina/metabolismo
Células Epiteliais/efeitos dos fármacos
Células Epiteliais/parasitologia
Guanosina/metabolismo
Trichomonas vaginalis/crescimento & desenvolvimento
[Mh] Termos MeSH secundário: Linhagem Celular
Sobrevivência Celular
Células Epiteliais/fisiologia
Feminino
Seres Humanos
Hidrólise
Nucleotídeos/metabolismo
Pirofosfatases/metabolismo
Receptores Purinérgicos/análise
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Nucleotides); 0 (Receptors, Purinergic); 12133JR80S (Guanosine); EC 3.6.1.- (Pyrophosphatases); K72T3FS567 (Adenosine)
[Em] Mês de entrada:1705
[Cu] Atualização por classe:170503
[Lr] Data última revisão:
170503
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161123
[St] Status:MEDLINE



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