The Experts below are selected from a list of 135 Experts worldwide ranked by ideXlab platform
Mutsumi Watanabe - One of the best experts on this subject based on the ideXlab platform.
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opposite fates of the Purine Metabolite allantoin under water and nitrogen limitations in bread wheat
Plant Molecular Biology, 2019Co-Authors: Alberto Casartelli, Vanessa Melino, Ute Baumann, Matteo Riboni, Radoslaw Suchecki, Nirupama S Jayasinghe, Himasha Mendis, Mutsumi WatanabeAbstract:Degradation of nitrogen-rich Purines is tightly and oppositely regulated under drought and low nitrogen supply in bread wheat. Allantoin is a key target Metabolite for improving nitrogen homeostasis under stress. The Metabolite allantoin is an intermediate of the catabolism of Purines (components of nucleotides) and is known for its housekeeping role in nitrogen (N) recycling and also for its function in N transport and storage in nodulated legumes. Allantoin was also shown to differentially accumulate upon abiotic stress in a range of plant species but little is known about its role in cereals. To address this, Purine catabolic pathway genes were identified in hexaploid bread wheat and their chromosomal location was experimentally validated. A comparative study of two Australian bread wheat genotypes revealed a highly significant increase of allantoin (up to 29-fold) under drought. In contrast, allantoin significantly decreased (up to 22-fold) in response to N deficiency. The observed changes were accompanied by transcriptional adjustment of key Purine catabolic genes, suggesting that the recycling of Purine-derived N is tightly regulated under stress. We propose opposite fates of allantoin in plants under stress: the accumulation of allantoin under drought circumvents its degradation to ammonium (NH4+) thereby preventing N losses. On the other hand, under N deficiency, increasing the NH4+ liberated via allantoin catabolism contributes towards the maintenance of N homeostasis.
Fayong Luo - One of the best experts on this subject based on the ideXlab platform.
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therapeutic effect of lactobacillus reuteri dsm 17938 on treg deficiency induced autoimmunity ipex syndrome via the inosine adenosine 2a receptors
Journal of Immunology, 2017Co-Authors: Yuying Liu, Thomas K Hoang, Ting Wang, Christopher M Taylor, Xiangjun Tian, Meng Luo, Dat Q Tran, Jain Zhou, Nina Tatevian, Fayong LuoAbstract:Regulatory T-cell (Treg) deficiency causes lethal, CD4 + T cell-driven autoimmune diseases. Stem cell transplantation is used to treat these diseases, but this procedure is limited by the availability of a suitable donor. The intestinal microbiota drives host immune homeostasis by regulating the development of Treg, Th1 and Th2 cells. It is currently unclear if Treg-deficiency autoimmune disorders can be treated by targeting the enteric microbiota. Our aims are to determine the autoimmunity, gut microbiota, and plasma metabolomics affected by probiotic Lactobacillus reuteri DSM 17938 (LR), and to further identify the mechanism of modulated Metabolite(s) in suppressing autoimmunity in Treg-deficient scurfy (SF) mice. We demonstrated that Foxp3 + Treg deficiency results in gut microbial dysbiosis and autoimmunity over the lifespan of SF mouse. Remodeling microbiota with LR prolonged survival and reduced multi-organ inflammation in SF mice. LR changed the metabolomics profile disrupted by Treg-deficiency with a major effect of restoring levels of the Purine Metabolite inosine. Feeding inosine itself prolonged life and inhibited multi-organ inflammation by reducing Th1/Th2 cells and their associated cytokines. Mechanistically, the inhibition of inosine on the differentiation of Th1 and Th2 cells in vitro depended on adenosine A 2A receptors. Both A 2A receptor specific antagonist or genetically knockout A 2A to SF mice reversed the anti-inflammatory effects of both inosine and LR in vivo. In conclusions, A 2A receptors mediate a substantial protective effect of inosine and LR. The LR-modulated-microbiota-inosine-A 2A axis might represent a potential avenue for combatting autoimmune diseases mediated by Treg dysfunction.
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resetting microbiota by lactobacillus reuteri inhibits t reg deficiency induced autoimmunity via adenosine a2a receptors
Journal of Experimental Medicine, 2017Co-Authors: Thomas K Hoang, Ting Wang, Michael J Ferris, Christopher M Taylor, Xiangjun Tian, Meng Luo, Dat Q Tran, Jain Zhou, Nina Tatevian, Fayong LuoAbstract:Regulatory T (T reg) cell deficiency causes lethal, CD4+ T cell-driven autoimmune diseases. Stem cell transplantation is used to treat these diseases, but this procedure is limited by the availability of a suitable donor. The intestinal microbiota drives host immune homeostasis by regulating the differentiation and expansion of T reg, Th1, and Th2 cells. It is currently unclear if T reg cell deficiency-mediated autoimmune disorders can be treated by targeting the enteric microbiota. Here, we demonstrate that Foxp3+ T reg cell deficiency results in gut microbial dysbiosis and autoimmunity over the lifespan of scurfy (SF) mouse. Remodeling microbiota with Lactobacillus reuteri prolonged survival and reduced multiorgan inflammation in SF mice. L. reuteri changed the metabolomic profile disrupted by T reg cell deficiency, and a major effect was to restore levels of the Purine Metabolite inosine. Feeding inosine itself prolonged life and inhibited multiorgan inflammation by reducing Th1/Th2 cells and their associated cytokines. Mechanistically, the inhibition of inosine on the differentiation of Th1 and Th2 cells in vitro depended on adenosine A2A receptors, which were also required for the efficacy of inosine and of L. reuteri in vivo. These results reveal that the microbiota-inosine-A2A receptor axis might represent a potential avenue for combatting autoimmune diseases mediated by T reg cell dysfunction.
Vanessa Melino - One of the best experts on this subject based on the ideXlab platform.
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opposite fates of the Purine Metabolite allantoin under water and nitrogen limitations in bread wheat
Plant Molecular Biology, 2019Co-Authors: Alberto Casartelli, Vanessa Melino, Ute Baumann, Matteo Riboni, Radoslaw Suchecki, Nirupama S Jayasinghe, Himasha Mendis, Mutsumi WatanabeAbstract:Degradation of nitrogen-rich Purines is tightly and oppositely regulated under drought and low nitrogen supply in bread wheat. Allantoin is a key target Metabolite for improving nitrogen homeostasis under stress. The Metabolite allantoin is an intermediate of the catabolism of Purines (components of nucleotides) and is known for its housekeeping role in nitrogen (N) recycling and also for its function in N transport and storage in nodulated legumes. Allantoin was also shown to differentially accumulate upon abiotic stress in a range of plant species but little is known about its role in cereals. To address this, Purine catabolic pathway genes were identified in hexaploid bread wheat and their chromosomal location was experimentally validated. A comparative study of two Australian bread wheat genotypes revealed a highly significant increase of allantoin (up to 29-fold) under drought. In contrast, allantoin significantly decreased (up to 22-fold) in response to N deficiency. The observed changes were accompanied by transcriptional adjustment of key Purine catabolic genes, suggesting that the recycling of Purine-derived N is tightly regulated under stress. We propose opposite fates of allantoin in plants under stress: the accumulation of allantoin under drought circumvents its degradation to ammonium (NH4+) thereby preventing N losses. On the other hand, under N deficiency, increasing the NH4+ liberated via allantoin catabolism contributes towards the maintenance of N homeostasis.
D G L Van Wylen - One of the best experts on this subject based on the ideXlab platform.
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Purine Metabolite accumulation during myocardial ischemia adenosine pretreatment versus brief ischemia
Basic Research in Cardiology, 1997Co-Authors: D G L Van Wylen, S A MantheiAbstract:Hearts preconditioned by brief ischemia are characterized by a reduced rate of cellular Purine Metabolite production during subsequent prolonged ischemia; the purpose of this study was to determine if transient exogenous adenosine pretreatment can mimic this phenomenon. The accumulation of interstitial fluid (ISF) Purine Metabolites during prolonged ischemia in untreated anesthetized dogs (n=7) was compared to that in a group pretreated with brief ischemia (ischemic preconditioned group; n=9), a group pretreated with 1.5 μmoles/min intracoronary adenosine (n=7). Ischemic preconditioning was achieved by a 5 min period of left anterior descending coronary artery (LAD) occulusion followed by 10 min of reperfusion. The adenosine-treated groups were subjected to 10 min of intracoronary adenosine followed by 10 min of recovery. All animals were exposed to 60 min LAD occlusion followed by 60 min reperfusion. The changes in ISF adenosine and adenosine Metabolites were assessed by cardiac microdialysis, using dialysate concentrations as indices of ISF levels. Ischemic preconditioning decreased the rate of dialysate adenosine and total Purine accumulation during the prolonged ischemia. Although the two doses of exogenous adenosine bracketed the increase in ISF adenosine seen with ischemic preconditioning, neither adenosine dose was able to attenuate the rate of Purine Metabolite accumulation during prolonged ischemia. We conclude that exogenous adenosine pretreatment is unable to mimic the reduced ischemia-induced Purine efflux that is characteristic of myocytes pretreated with brief ischemia.
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effect of ischemic preconditioning on interstitial Purine Metabolite and lactate accumulation during myocardial ischemia
Circulation, 1994Co-Authors: D G L Van WylenAbstract:The purpose of this study was to determine the effect of ischemic preconditioning on the changes in interstitial fluid (ISF) Purine Metabolites and lactate during prolonged regional myocardial ischemia. The study consisted of two groups of anesthetized dogs: a control group (n = 13) that was exposed to 60 minutes of regional myocardial ischemia and a preconditioned group (n = 10). In the preconditioned group, regional myocardial ischemia was induced for two 5-minute episodes, each followed by 10 minutes of reperfusion. These preconditioning episodes were followed by 60 minutes of sustained regional ischemia. Cardiac ISF was sampled by microdialysis probes implanted in the left ventricular myocardium; dialysate levels served as indices of ISF concentrations. In the preconditioned group, dialysate concentrations of adenosine, inosine, hypoxanthine, total Purines, and lactate increased during each of the 5-minute ischemia episodes, with further increases occurring during the first 5 minutes of reperfusion. However, the increases in dialysate Purine Metabolites during the first period of ischemia/reperfusion were greater than those that occurred during the second ischemia/reperfusion. In addition, preconditioning reduced the rate of ISF Purine Metabolite and lactate accumulation during the prolonged ischemia when compared with nonpreconditioned animals. These data suggest that preconditioning reduces the energy imbalance that occurs during subsequent myocardial ischemia and thereby diminishes the rate of net adenine nucleotide degradation and cellular production and release of Purine Metabolites and lactate. In addition, the increase in ISF adenosine seen during the preconditioning episode is consistent with the notion that preconditioning-induced cardioprotection is mediated in part by the action of adenosine at extracellular A1 adenosine receptors.
Shunsuke Watanabe - One of the best experts on this subject based on the ideXlab platform.
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allantoin a stress related Purine Metabolite can activate jasmonate signaling in a myc2 regulated and abscisic acid dependent manner
Journal of Experimental Botany, 2016Co-Authors: Hiroshi Takagi, Yasuhiro Ishiga, Shunsuke Watanabe, Tomokazu Konishi, Mayumi Egusa, Nobuhiro Akiyoshi, Takakazu Matsuura, Izumi C Mori, Takashi Hirayama, Hironori KaminakaAbstract:Allantoin is a metabolic intermediate of Purine catabolism that often accumulates in stressed plants. Recently, we used Arabidopsis knockout mutants (aln) of ALLANTOINASE to show that this Purine Metabolite activates abscisic acid (ABA) production, thereby stimulating stress-related gene expression and enhancing seedling tolerance to abiotic stress. A detailed re-examination of the microarray data of an aln mutant (aln-1) confirmed the increased expression of ABA-related genes and also revealed altered expression of genes involved in jasmonic acid (JA) responses, probably under the control of MYC2, a master switch in the JA signaling pathway. Consistent with the transcriptome profiles, the aln-1 mutant displayed increased JA levels and enhanced responses to mechanical wounding and exogenous JA. Moreover, aln mutants demonstrated modestly increased susceptibility to Pseudomonas syringae and Pectobacterium carotovorum, probably reflecting the antagonistic action of MYC2 on the defense against these bacterial phytopathogens. Exogenously administered allantoin elicited the expression of JA-responsive genes, including MYC2, in wild-type plants, supporting the idea that allantoin might be responsible for the observed JA-related phenotypes of aln mutants. However, mutants deficient in bioactive JA (jar1-1), insensitive to JA (myc2-3), or deficient in ABA (aba2-1 and bglu18) suppressed the effect of exogenous allantoin. The suppression was further confirmed in aln-1 jar1-1 and aln-1 bglu18 double mutants. These results indicate that allantoin can activate the MYC2-regulated JA signaling pathway through ABA production. Overall, this study suggests a possible connection of Purine catabolism with stress hormone homeostasis and signaling, and highlights the potential importance of allantoin in these interactions.
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the Purine Metabolite allantoin enhances abiotic stress tolerance through synergistic activation of abscisic acid metabolism
Plant Cell and Environment, 2014Co-Authors: Shunsuke Watanabe, Hiroshi Takagi, Mayumi Matsumoto, Yuki Hakomori, Hiroshi Shimada, Atsushi SakamotoAbstract:Purine catabolism is regarded as a housekeeping function that remobilizes nitrogen for plant growth and development. However, emerging evidence suggests that certain Purine Metabolites might contribute to stress protection of plants. Here, we show that in Arabidopsis, the intermediary Metabolite allantoin plays a role in abiotic stress tolerance via activation of abscisic acid (ABA) metabolism. The aln loss-of-function of ALN, encoding allantoinase, results in increased allantoin accumulation, genome-wide up-regulation of stress-related genes and enhanced tolerance to drought-shock and osmotic stress in aln mutant seedlings. This phenotype is not caused by a general response to Purine catabolism inhibition, but rather results from a specific effect of allantoin. Allantoin activates ABA production both through increased transcription of NCED3, encoding a key enzyme in ABA biosynthesis, and through post-translational activation via high-molecular-weight complex formation of BG1, a β-glucosidase hydrolysing glucose-conjugated ABA. Exogenous application of allantoin to wild-type plants also activates the two ABA-producing pathways that lead to ABA accumulation and stress-responsive gene expression, but this effect is abrogated in ABA-deficient and BG1-knockout mutants. We propose that Purine catabolism functions not only in nitrogen metabolism, but also in stress tolerance by influencing ABA production, which is mediated by the possible regulatory action of allantoin.
