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Pesquisa : D08.811.682.690.562 [Categoria DeCS]
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[PMID]:28208054
[Au] Autor:Sharma I; Dutta RK; Singh NK; Kanwar YS
[Ad] Endereço:Department of Pathology, Northwestern University, Chicago, Illinois.
[Ti] Título:High Glucose-Induced Hypomethylation Promotes Binding of Sp-1 to Myo-Inositol Oxygenase: Implication in the Pathobiology of Diabetic Tubulopathy.
[So] Source:Am J Pathol;187(4):724-739, 2017 Apr.
[Is] ISSN:1525-2191
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The catabolic enzyme myo-inositol oxygenase (MIOX) is expressed in proximal tubules and up-regulated in the diabetic state. Previously, we reported its transcriptional and translation regulation by high glucose (HG), osmolytes, and fatty acids. However, its epigenetic regulation is unknown. Bisulfite sequencing revealed that both human and mouse MIOX promoters, enriched with CpG sites, are hypomethylated and unmethylated under HG ambience and hyperglycemic states associated with increased MIOX expression. Eletrophoretic mobility shift assays revealed increased binding of unmethylated oligos with nucleoproteins of cells maintained under HG. In addition, a strong binding of specificity protein (Sp)-1 transcription factor with MIOX promoter was observed under HG, especially with unmethylated Sp-1 oligo. Specificity of binding was established by supershift assays and treatment with the Sp-1 inhibitor mithramycin. Promoter analysis revealed an increase in luciferase activity under HG, which was reduced after mutation of the Sp-1-binding site. Sp1 siRNA treatment reduced mRNA and protein expression of Sp-1 and MIOX and generation of reactive oxygen species derived from NADPH oxidase (NOX)-4 and mitochondrial sources. In addition, there was reduced expression of hypoxia-inducible factor-1α relevant in the pathogenesis of diabetic nephropathy. Sp1 siRNA treatment reduced fibronectin expression, an extracellular matrix protein that is increased in diabetic nephropathy and tubulopathy. HG-induced MIOX expression was also reduced with the treatment of apelin-13, which deacetylates histones. Overall, these findings highlight the epigenetic regulation of MIOX in the pathogenesis of diabetic tubulopathy.
[Mh] Termos MeSH primário: Metilação de DNA/genética
Nefropatias Diabéticas/enzimologia
Nefropatias Diabéticas/patologia
Glucose/toxicidade
Inositol Oxigenase/metabolismo
Fator de Transcrição Sp1/metabolismo
[Mh] Termos MeSH secundário: Animais
Sequência de Bases
Sítios de Ligação
Linhagem Celular
Ilhas de CpG/genética
Nefropatias Diabéticas/genética
Fibronectinas/metabolismo
Deleção de Genes
Seres Humanos
Subunidade alfa do Fator 1 Induzível por Hipóxia/metabolismo
Inositol Oxigenase/genética
Peptídeos e Proteínas de Sinalização Intercelular/farmacologia
Túbulos Renais/efeitos dos fármacos
Túbulos Renais/metabolismo
Túbulos Renais/patologia
Camundongos Endogâmicos C57BL
Mitocôndrias/efeitos dos fármacos
Mitocôndrias/metabolismo
Nucleoproteínas/metabolismo
Oxirredução/efeitos dos fármacos
Regiões Promotoras Genéticas
Ligação Proteica/efeitos dos fármacos
RNA Interferente Pequeno/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Fibronectins); 0 (Hypoxia-Inducible Factor 1, alpha Subunit); 0 (Intercellular Signaling Peptides and Proteins); 0 (Nucleoproteins); 0 (RNA, Small Interfering); 0 (Sp1 Transcription Factor); 0 (apelin-13 peptide); EC 1.13.99.1 (Inositol Oxygenase); IY9XDZ35W2 (Glucose)
[Em] Mês de entrada:1705
[Cu] Atualização por classe:170522
[Lr] Data última revisão:
170522
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170217
[St] Status:MEDLINE


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[PMID]:27895157
[Au] Autor:Dutta RK; Kondeti VK; Sharma I; Chandel NS; Quaggin SE; Kanwar YS
[Ad] Endereço:Departments of Pathology and.
[Ti] Título:Beneficial Effects of -Inositol Oxygenase Deficiency in Cisplatin-Induced AKI.
[So] Source:J Am Soc Nephrol;28(5):1421-1436, 2017 May.
[Is] ISSN:1533-3450
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Overexpression of the proximal tubular enzyme -inositol oxygenase (MIOX) induces oxidant stress However, the relevance of MIOX to tubular pathobiology remains enigmatic. To investigate the role of MIOX in cisplatin-induced tubular AKI, we generated conditional MIOX-overexpressing transgenic (MIOX-TG) mice and MIOX-knockout (MIOX ) mice with tubule-specific MIOX overexpression or knockout, respectively. Compared with cisplatin-treated wild-type (WT) mice, cisplatin-treated MIOX-TG mice had even greater increases in urea, creatinine, and KIM-1 levels and more tubular injury and apoptosis, but these effects were attenuated in cisplatin-treated MIOX mice. Similarly, MIOX-TG mice had the highest and MIOX mice had the lowest renal levels of Bax, cleaved caspase-3, and NADPH oxidase-4 expression and reactive oxygen species (ROS) generation after cisplatin treatment. , cisplatin dose-dependently increased ROS generation in LLC-PK1 cells. Furthermore, MIOX overexpression in these cells accentuated cisplatin-induced ROS generation and perturbations in the ratio of GSH to oxidized GSH, whereas MIOX-siRNA or -acetyl cysteine treatment attenuated these effects. Additionally, the cisplatin-induced enhancement of p53 activation, NF- B binding to DNA, and NF- B nuclear translocation in WT mice was exacerbated in MIOX-TG mice but absent in MIOX mice. , MIOX-siRNA or NAC treatment reduced the dose-dependent increase in p53 expression induced by cisplatin. We also observed a remarkable influx of inflammatory cells and upregulation of cytokines in kidneys of cisplatin-treated MIOX-TG mice. Finally, analysis of genomic DNA in WT mice revealed cisplatin-induced hypomethylation of the MIOX promoter. These data suggest that MIOX overexpression exacerbates, whereas MIOX gene disruption protects against, cisplatin-induced AKI.
[Mh] Termos MeSH primário: Lesão Renal Aguda/induzido quimicamente
Lesão Renal Aguda/enzimologia
Cisplatino/efeitos adversos
Inositol Oxigenase/deficiência
[Mh] Termos MeSH secundário: Animais
Inositol Oxigenase/fisiologia
Masculino
Camundongos
Camundongos Knockout
Camundongos Transgênicos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
EC 1.13.99.1 (Inositol Oxygenase); Q20Q21Q62J (Cisplatin)
[Em] Mês de entrada:1705
[Cu] Atualização por classe:170531
[Lr] Data última revisão:
170531
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161130
[St] Status:MEDLINE
[do] DOI:10.1681/ASN.2016070744


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[PMID]:27444324
[Au] Autor:Liu Y; Gong X; Wang C; Du G; Chen J; Kang Z
[Ad] Endereço:The Key Laboratory of Industrial Biotechnology, Ministry of Education, Jiangnan University, Wuxi 214122, China; Synergetic Innovation Center of Food Safety and Nutrition, 1800 Lihu Road, Wuxi, Jiangsu 214122, China.
[Ti] Título:Production of glucaric acid from myo-inositol in engineered Pichia pastoris.
[So] Source:Enzyme Microb Technol;91:8-16, 2016 Sep.
[Is] ISSN:1879-0909
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:A potential myo-inositol oxygenase (ppMIOX) was identified as a functional enzyme and a glucaric acid synthetic pathway was firstly constructed in Pichia pastoris. Coexpression of the native ppMIOX and the urinate dehydrogenase (Udh) from Pseudomonas putida KT2440 led to obvious accumulation of glucaric acid (90.46±0.04mg/L) from myo-inositol whereas no glucaric acid was detected from glucose. In comparison, coexpression of the heterologous mouse MIOX (mMIOX) and Udh resulted in higher titers of glucaric acid from glucose and myo-inositol, 107.19±11.91mg/L and 785.4±1.41mg/L, respectively. By applying a fusion expression strategy with flexible peptides, the mMIOX specific activity and the glucaric acid concentration were significantly increased. Using glucose and myo-inositol as carbon substrates, the production of glucaric acid was substantially enhanced to 6.61±0.30g/L in fed-batch cultures. To the best of our knowledge, this is the highest reported value to date.
[Mh] Termos MeSH primário: Ácido Glucárico/metabolismo
Inositol/metabolismo
Pichia/genética
Pichia/metabolismo
[Mh] Termos MeSH secundário: Aldeído Oxirredutases/genética
Aldeído Oxirredutases/metabolismo
Sequência de Aminoácidos
Animais
Vias Biossintéticas
Fermentação
Proteínas Fúngicas/genética
Proteínas Fúngicas/metabolismo
Genes Fúngicos
Inositol Oxigenase/genética
Inositol Oxigenase/metabolismo
Cinética
Camundongos
Engenharia de Proteínas
Proteínas Recombinantes de Fusão/genética
Proteínas Recombinantes de Fusão/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Fungal Proteins); 0 (Recombinant Fusion Proteins); 4L6452S749 (Inositol); EC 1.1.1.203 (uronate dehydrogenase); EC 1.13.99.1 (Inositol Oxygenase); EC 1.2.- (Aldehyde Oxidoreductases); QLZ991V4A2 (Glucaric Acid)
[Em] Mês de entrada:1704
[Cu] Atualização por classe:170424
[Lr] Data última revisão:
170424
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160723
[St] Status:MEDLINE


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[PMID]:27312887
[Au] Autor:Gupta A; Hicks MA; Manchester SP; Prather KL
[Ad] Endereço:Department of Chemical Engineering, Massachusetts Institute of Technology, Cambridge, MA, USA.
[Ti] Título:Porting the synthetic D-glucaric acid pathway from Escherichia coli to Saccharomyces cerevisiae.
[So] Source:Biotechnol J;11(9):1201-8, 2016 Sep.
[Is] ISSN:1860-7314
[Cp] País de publicação:Germany
[La] Idioma:eng
[Ab] Resumo:D-Glucaric acid can be produced as a value-added chemical from biomass through a de novo pathway in Escherichia coli. However, previous studies have identified pH-mediated toxicity at product concentrations of 5 g/L and have also found the eukaryotic myo-inositol oxygenase (MIOX) enzyme to be rate-limiting. We ported this pathway to Saccaromyces cerevisiae, which is naturally acid-tolerant and evaluate a codon-optimized MIOX homologue. We constructed two engineered yeast strains that were distinguished solely by their MIOX gene - either the previous version from Mus musculus or a homologue from Arabidopsis thaliana codon-optimized for expression in S. cerevisiae - in order to identify the rate-limiting steps for D-glucaric acid production both from a fermentative and non-fermentative carbon source. myo-Inositol availability was found to be rate-limiting from glucose in both strains and demonstrated to be dependent on growth rate, whereas the previously used M. musculus MIOX activity was found to be rate-limiting from glycerol. Maximum titers were 0.56 g/L from glucose in batch mode, 0.98 g/L from glucose in fed-batch mode, and 1.6 g/L from glucose supplemented with myo-inositol. Future work focusing on the MIOX enzyme, the interplay between growth and production modes, and promoting aerobic respiration should further improve this pathway.
[Mh] Termos MeSH primário: Escherichia coli/crescimento & desenvolvimento
Ácido Glucárico/metabolismo
Inositol Oxigenase/metabolismo
Saccharomyces cerevisiae/crescimento & desenvolvimento
[Mh] Termos MeSH secundário: Animais
Técnicas de Cultura Celular por Lotes/métodos
Vias Biossintéticas
Escherichia coli/genética
Escherichia coli/metabolismo
Fermentação
Engenharia Genética
Glucose/metabolismo
Inositol/metabolismo
Inositol Oxigenase/genética
Camundongos
Saccharomyces cerevisiae/genética
Saccharomyces cerevisiae/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
4L6452S749 (Inositol); EC 1.13.99.1 (Inositol Oxygenase); IY9XDZ35W2 (Glucose); QLZ991V4A2 (Glucaric Acid)
[Em] Mês de entrada:1701
[Cu] Atualização por classe:170117
[Lr] Data última revisão:
170117
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160618
[St] Status:MEDLINE
[do] DOI:10.1002/biot.201500563


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[PMID]:26792859
[Au] Autor:Sun L; Dutta RK; Xie P; Kanwar YS
[Ad] Endereço:From the Department of Nephrology and Renal Institute, 2nd Xiangya Hospital, Central South University, Changsha, Hunan 410011, China and.
[Ti] Título:myo-Inositol Oxygenase Overexpression Accentuates Generation of Reactive Oxygen Species and Exacerbates Cellular Injury following High Glucose Ambience: A NEW MECHANISM RELEVANT TO THE PATHOGENESIS OF DIABETIC NEPHROPATHY.
[So] Source:J Biol Chem;291(11):5688-707, 2016 Mar 11.
[Is] ISSN:1083-351X
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Diabetic nephropathy (DN) is characterized by perturbations in metabolic/cellular signaling pathways with generation of reactive oxygen species (ROS). The ROS are regarded as a common denominator of various pathways, and they inflict injury on renal glomerular cells. Recent studies indicate that tubular pathobiology also plays a role in the progression of DN. However, the mechanism(s) for how high (25 mm) glucose (HG) ambience induces tubular damage remains enigmatic. myo-Inositol oxygenase (MIOX) is a tubular enzyme that catabolizes myo-inositol to d-glucuronate via the glucuronate-xylulose (G-X) pathway. In this study, we demonstrated that G-X pathway enzymes are expressed in the kidney, and MIOX expression/bioactivity was up-regulated under HG ambience in LLC-PK1 cells, a tubular cell line. We further investigated whether MIOX overexpression leads to accentuation of tubulo-interstitial injury, as gauged by some of the parameters relevant to the progression of DN. Under HG ambience, MIOX overexpression accentuated redox imbalance, perturbed NAD(+)/NADH ratios, increased ROS generation, depleted reduced glutathione, reduced GSH/GSSG ratio, and enhanced adaptive changes in the profile of the antioxidant defense system. These changes were also accompanied by mitochondrial dysfunctions, DNA damage and induction of apoptosis, accentuated activity of profibrogenic cytokine, and expression of fibronectin, the latter two being the major hallmarks of DN. These perturbations were largely blocked by various ROS inhibitors (Mito Q, diphenyleneiodonium chloride, and N-acetylcysteine) and MIOX/NOX4 siRNA. In conclusion, this study highlights a novel mechanism where MIOX under HG ambience exacerbates renal injury during the progression of diabetic nephropathy following the generation of excessive ROS via an unexplored G-X pathway.
[Mh] Termos MeSH primário: Nefropatias Diabéticas/patologia
Glucose/metabolismo
Inositol Oxigenase/metabolismo
Rim/patologia
Espécies Reativas de Oxigênio/metabolismo
[Mh] Termos MeSH secundário: Animais
Nefropatias Diabéticas/genética
Nefropatias Diabéticas/metabolismo
Peróxido de Hidrogênio/metabolismo
Inositol Oxigenase/análise
Inositol Oxigenase/genética
Rim/metabolismo
Células LLC-PK1
Masculino
Camundongos
Mitocôndrias/genética
Mitocôndrias/metabolismo
Mitocôndrias/patologia
NAD/metabolismo
Estresse Oxidativo
Suínos
Regulação para Cima
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Reactive Oxygen Species); 0U46U6E8UK (NAD); BBX060AN9V (Hydrogen Peroxide); EC 1.13.99.1 (Inositol Oxygenase); IY9XDZ35W2 (Glucose)
[Em] Mês de entrada:1608
[Cu] Atualização por classe:170311
[Lr] Data última revisão:
170311
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160122
[St] Status:MEDLINE
[do] DOI:10.1074/jbc.M115.669952


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[PMID]:26578517
[Au] Autor:Tominaga T; Dutta RK; Joladarashi D; Doi T; Reddy JK; Kanwar YS
[Ad] Endereço:From the Department of Pathology, Feinberg School of Medicine, Northwestern University, Chicago, Illinois 60611 and.
[Ti] Título:Transcriptional and Translational Modulation of myo-Inositol Oxygenase (Miox) by Fatty Acids: IMPLICATIONS IN RENAL TUBULAR INJURY INDUCED IN OBESITY AND DIABETES.
[So] Source:J Biol Chem;291(3):1348-67, 2016 Jan 15.
[Is] ISSN:1083-351X
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The kidney is one of the target organs for various metabolic diseases, including diabetes, metabolic syndrome, and obesity. Most of the metabolic studies underscore glomerular pathobiology, although the tubulo-interstitial compartment has been underemphasized. This study highlights mechanisms concerning the pathobiology of tubular injury in the context of myo-inositol oxygenase (Miox), a tubular enzyme. The kidneys of mice fed a high fat diet (HFD) had increased Miox expression and activity, and the latter was related to phosphorylation of serine/threonine residues. Also, expression of sterol regulatory element-binding protein1 (Srebp1) and markers of cellular/nuclear damage was increased along with accentuated apoptosis and loss of tubular brush border. Similar results were observed in cells treated with palmitate/BSA. Multiple sterol-response elements and E-box motifs were found in the miox promoter, and its activity was modulated by palmitate/BSA. Electrophoretic mobility and ChIP assays confirmed binding of Srebp to consensus sequences of the miox promoter. Exposure of palmitate/BSA-treated cells to rapamycin normalized Miox expression and prevented Srebp1 nuclear translocation. In addition, rapamycin treatment reduced p53 expression and apoptosis. Like rapamycin, srebp siRNA reduced Miox expression. Increased expression of Miox was associated with the generation of reactive oxygen species (ROS) in kidney tubules of mice fed an HFD and cell exposed to palmitate/BSA. Both miox and srebp1 siRNAs reduced generation of ROS. Collectively, these findings suggest that HFD or fatty acids modulate transcriptional, translational, and post-translational regulation of Miox expression/activity and underscore Miox being a novel target of the transcription factor Srebp1. Conceivably, activation of the mTORC1/Srebp1/Miox pathway leads to the generation of ROS culminating into tubulo-interstitial injury in states of obesity.
[Mh] Termos MeSH primário: Nefropatias Diabéticas/metabolismo
Inositol Oxigenase/metabolismo
Túbulos Renais/enzimologia
Obesidade/metabolismo
Estresse Oxidativo
Processamento de Proteína Pós-Traducional
Regulação para Cima
[Mh] Termos MeSH secundário: Animais
Apoptose
Linhagem Celular
Nefropatias Diabéticas/etiologia
Nefropatias Diabéticas/patologia
Dieta Hiperlipídica/efeitos adversos
Seres Humanos
Inositol Oxigenase/antagonistas & inibidores
Inositol Oxigenase/genética
Túbulos Renais/metabolismo
Túbulos Renais/patologia
Masculino
Camundongos
Obesidade/etiologia
Obesidade/patologia
Oxigenases/antagonistas & inibidores
Oxigenases/genética
Oxigenases/metabolismo
Fosforilação
Regiões Promotoras Genéticas
Proteínas/antagonistas & inibidores
Proteínas/genética
Proteínas/metabolismo
Interferência de RNA
Ratos
Proteína de Ligação a Elemento Regulador de Esterol 1/antagonistas & inibidores
Proteína de Ligação a Elemento Regulador de Esterol 1/genética
Proteína de Ligação a Elemento Regulador de Esterol 1/metabolismo
Sus scrofa
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Proteins); 0 (Sterol Regulatory Element Binding Protein 1); EC 1.13.- (Oxygenases); EC 1.13.99.1 (Inositol Oxygenase); EC 1.13.99.1 (MIOX protein, human); EC 1.13.99.1 (Miox protein, rat)
[Em] Mês de entrada:1606
[Cu] Atualização por classe:170118
[Lr] Data última revisão:
170118
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:151119
[St] Status:MEDLINE
[do] DOI:10.1074/jbc.M115.698191


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[PMID]:26311112
[Au] Autor:Chang HH; Chao HN; Walker CS; Choong SY; Phillips A; Loomes KM
[Ad] Endereço:School of Biological Sciences and Maurice Wilkins Centre for Molecular Biodiscovery, University of Auckland, Auckland, New Zealand.
[Ti] Título:Renal depletion of myo-inositol is associated with its increased degradation in animal models of metabolic disease.
[So] Source:Am J Physiol Renal Physiol;309(9):F755-63, 2015 Nov 01.
[Is] ISSN:1522-1466
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Renal depletion of myo-inositol (MI) is associated with the pathogenesis of diabetic nephropathy in animal models, but the underlying mechanisms involved are unclear. We hypothesized that MI depletion was due to changes in inositol metabolism and therefore examined the expression of genes regulating de novo biosynthesis, reabsorption, and catabolism of MI. We also extended the analyses from diabetes mellitus to animal models of dietary-induced obesity and hypertension. We found that renal MI depletion was pervasive across these three distinct disease states in the relative order: hypertension (-51%)>diabetes mellitus (-35%)>dietary-induced obesity (-19%). In 4-wk diabetic kidneys and in kidneys derived from insulin-resistant and hypertensive rats, MI depletion was correlated with activity of the MI-degrading enzyme myo-inositol oxygenase (MIOX). By contrast, there was decreased MIOX expression in 8-wk diabetic kidneys. Immunohistochemistry localized the MI-degrading pathway comprising MIOX and the glucuronate-xylulose (GX) pathway to the proximal tubules within the renal cortex. These findings indicate that MI depletion could reflect increased catabolism through MIOX and the GX pathway and implicate a common pathological mechanism contributing to renal oxidative stress in metabolic disease.
[Mh] Termos MeSH primário: Diabetes Mellitus Experimental/metabolismo
Hipertensão/metabolismo
Inositol/metabolismo
Túbulos Renais Proximais/metabolismo
Obesidade/metabolismo
[Mh] Termos MeSH secundário: Animais
Diabetes Mellitus Experimental/complicações
Diabetes Mellitus Experimental/genética
Nefropatias Diabéticas/etiologia
Nefropatias Diabéticas/metabolismo
Hipertensão/complicações
Hipertensão/genética
Inositol/deficiência
Inositol Oxigenase/genética
Inositol Oxigenase/metabolismo
Resistência à Insulina
Túbulos Renais Proximais/enzimologia
Masculino
Camundongos Endogâmicos C57BL
Obesidade/complicações
Obesidade/genética
Proteínas/genética
Proteínas/metabolismo
Ratos Endogâmicos SHR
Ratos Endogâmicos WKY
Ratos Wistar
Xilulose/genética
Xilulose/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Proteins); 4L6452S749 (Inositol); 5962-29-8 (Xylulose); EC 1.13.99.1 (Inositol Oxygenase); EC 1.13.99.1 (Miox protein, rat)
[Em] Mês de entrada:1602
[Cu] Atualização por classe:151102
[Lr] Data última revisão:
151102
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:150828
[St] Status:MEDLINE
[do] DOI:10.1152/ajprenal.00164.2015


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[PMID]:26129988
[Au] Autor:Höller S; Ueda Y; Wu L; Wang Y; Hajirezaei MR; Ghaffari MR; von Wirén N; Frei M
[Ad] Endereço:Institute of Crop Science and Resource Conservation (INRES), Abiotic Stress Tolerance in Crops, University of Bonn, Karlrobert-Kreiten Strasse 13, 53115, Bonn, Germany.
[Ti] Título:Ascorbate biosynthesis and its involvement in stress tolerance and plant development in rice (Oryza sativa L.).
[So] Source:Plant Mol Biol;88(6):545-60, 2015 Aug.
[Is] ISSN:1573-5028
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Ascorbic acid (AsA) biosynthesis and its implications for stress tolerance and plant development were investigated in a set of rice knock-out (KO) mutants for AsA biosynthetic genes and their wild-types. KO of two isoforms of GDP-D-mannose epimerase (OsGME) reduced the foliar AsA level by 20-30%, and KO of GDP-L-galactose phosphorylase (OsGGP) by 80%, while KO of myo-inositol oxygenase (OsMIOX) did not affect foliar AsA levels. AsA concentration was negatively correlated with lipid peroxidation in foliar tissue under ozone stress and zinc deficiency, but did not affect the sensitivity to iron toxicity. Lack of AsA reduced the photosynthetic efficiency as represented by the maximum carboxylation rate of Rubisco (Vmax), the maximum electron transport rate (Jmax) and the chlorophyll fluorescence parameter ΦPSII. Mutants showed lower biomass production than their wild-types, especially when OsGGP was lacking (around 80% reductions). All plants except for KO mutants of OsGGP showed distinct peaks in foliar AsA concentrations during the growth, which were consistent with up-regulation of OsGGP, suggesting that OsGGP plays a pivotal role in regulating foliar AsA levels during different growth stages. In conclusion, our data demonstrate multiple roles of AsA in stress tolerance and development of rice.
[Mh] Termos MeSH primário: Ácido Ascórbico/biossíntese
Oryza/crescimento & desenvolvimento
Oryza/metabolismo
Desenvolvimento Vegetal/fisiologia
Estresse Fisiológico/fisiologia
[Mh] Termos MeSH secundário: Regulação Enzimológica da Expressão Gênica/fisiologia
Regulação da Expressão Gênica de Plantas/fisiologia
Inositol Oxigenase/genética
Inositol Oxigenase/metabolismo
Ferro
Ozônio
Monoéster Fosfórico Hidrolases/genética
Monoéster Fosfórico Hidrolases/metabolismo
Proteínas de Plantas/genética
Proteínas de Plantas/metabolismo
Zinco
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Plant Proteins); 66H7ZZK23N (Ozone); E1UOL152H7 (Iron); EC 1.13.99.1 (Inositol Oxygenase); EC 3.1.3.2 (Phosphoric Monoester Hydrolases); J41CSQ7QDS (Zinc); PQ6CK8PD0R (Ascorbic Acid)
[Em] Mês de entrada:1510
[Cu] Atualização por classe:171031
[Lr] Data última revisão:
171031
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:150702
[St] Status:MEDLINE
[do] DOI:10.1007/s11103-015-0341-y


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[PMID]:26091094
[Au] Autor:Chen C; Sun X; Duanmu H; Yu Y; Liu A; Xiao J; Zhu Y
[Ad] Endereço:Key Laboratory of Agricultural Biological Functional Genes, Northeast Agricultural University, Harbin, 150030, P.R. China.
[Ti] Título:Ectopic Expression of a Glycine soja myo-Inositol Oxygenase Gene (GsMIOX1a) in Arabidopsis Enhances Tolerance to Alkaline Stress.
[So] Source:PLoS One;10(6):e0129998, 2015.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Myo-inositol participates in various aspects of plant physiology, and myo-inositol oxygenase is the key enzyme of the myo-inositol oxygenation pathway. Previous studies indicated that myo-inositol oxygenase may play a role in plant responses to abiotic stresses. In this study, we focused on the functional characterization of GsMIOX1a, a remarkable alkaline stress-responsive gene of Glycine soja 07256, based on RNA-seq data. Using quantitative real-time PCR, we demonstrated that GsMIOX1a is rapidly induced by alkaline stress and expressed predominantly in flowers. We also elucidated the positive function of GsMIOX1a in the alkaline response in the wild type, atmiox1 mutant as well as GsMIOX1a-overexpressing Arabidopsis. We determined that atmiox1 mutant decreased Arabidopsis tolerance to alkaline stress, whereas GsMIOX1a overexpression increased tolerance. Moreover, the expression levels of some alkaline stress-responsive and inducible marker genes, including H+-Ppase, NADP-ME, KIN1 and RD29B, were also up-regulated in GsMIOX1a overexpression lines compared with the wild type and atmiox1 mutant. Together, these results suggest that the GsMIOX1a gene positively regulates plant tolerance to alkaline stress. This is the first report to demonstrate that ectopic expression of myo-inositol oxygenase improves alkaline tolerance in plants.
[Mh] Termos MeSH primário: Adaptação Biológica
Arabidopsis/genética
Arabidopsis/metabolismo
Expressão Ectópica do Gene
Inositol Oxigenase/genética
Estresse Fisiológico/genética
[Mh] Termos MeSH secundário: Clonagem Molecular
Expressão Gênica
Germinação
Mutação
Especificidade de Órgãos/genética
Fenótipo
Filogenia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
EC 1.13.99.1 (Inositol Oxygenase)
[Em] Mês de entrada:1604
[Cu] Atualização por classe:170220
[Lr] Data última revisão:
170220
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:150620
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0129998


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[PMID]:25270067
[Au] Autor:Zhan M; Usman IM; Sun L; Kanwar YS
[Ad] Endereço:Departments of Pathology and Medicine, Northwestern University, Chicago, Illinois.
[Ti] Título:Disruption of renal tubular mitochondrial quality control by Myo-inositol oxygenase in diabetic kidney disease.
[So] Source:J Am Soc Nephrol;26(6):1304-21, 2015 Jun.
[Is] ISSN:1533-3450
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Diabetic kidney disease (DKD) is associated with oxidative stress and mitochondrial injury. Myo-inositol oxygenase (MIOX), a tubular-specific enzyme, modulates redox imbalance and apoptosis in tubular cells in diabetes, but these mechanisms remain unclear. We investigated the role of MIOX in perturbation of mitochondrial quality control, including mitochondrial dynamics and autophagy/mitophagy, under high-glucose (HG) ambience or a diabetic state. HK-2 or LLC-PK1 cells subjected to HG exhibited an upregulation of MIOX accompanied by mitochondrial fragmentation and depolarization, inhibition of autophagy/mitophagy, and altered expression of mitochondrial dynamic and mitophagic proteins. Furthermore, dysfunctional mitochondria accumulated in the cytoplasm, which coincided with increased reactive oxygen species generation, Bax activation, cytochrome C release, and apoptosis. Overexpression of MIOX in LLC-PK1 cells enhanced the effects of HG, whereas MIOX siRNA or d-glucarate, an inhibitor of MIOX, partially reversed these perturbations. Moreover, decreasing the expression of MIOX under HG ambience increased PTEN-induced putative kinase 1 expression and the dependent mitofusin-2-Parkin interaction. In tubules of diabetic mice, increased MIOX expression and mitochondrial fragmentation and defective autophagy were observed. Dietary supplementation of d-glucarate in diabetic mice decreased MIOX expression, attenuated tubular damage, and improved renal functions. Notably, d-glucarate administration also partially attenuated mitochondrial fragmentation, oxidative stress, and apoptosis and restored autophagy/mitophagy in the tubular cells of these mice. These results suggest a novel mechanism linking MIOX to impaired mitochondrial quality control during tubular injury in the pathogenesis of DKD and suggest d-glucarate as a potential therapeutic agent for the amelioration of DKD.
[Mh] Termos MeSH primário: Diabetes Mellitus Experimental/tratamento farmacológico
Nefropatias Diabéticas/genética
Glucuronatos/farmacologia
Inositol Oxigenase/genética
Túbulos Renais/metabolismo
Mitocôndrias/metabolismo
[Mh] Termos MeSH secundário: Animais
Apoptose/efeitos dos fármacos
Western Blotting
Células Cultivadas
Diabetes Mellitus Experimental/genética
Diabetes Mellitus Experimental/patologia
Nefropatias Diabéticas/enzimologia
Nefropatias Diabéticas/patologia
Modelos Animais de Doenças
Regulação da Expressão Gênica
Imuno-Histoquímica
Inositol Oxigenase/metabolismo
Testes de Função Renal
Túbulos Renais/enzimologia
Células LLC-PK1/efeitos dos fármacos
Células LLC-PK1/metabolismo
Masculino
Camundongos
Camundongos Endogâmicos ICR
Mitocôndrias/efeitos dos fármacos
Distribuição Aleatória
Espécies Reativas de Oxigênio/metabolismo
Sensibilidade e Especificidade
Estreptozocina/farmacologia
Suínos
Regulação para Cima
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL
[Nm] Nome de substância:
0 (Glucuronates); 0 (Reactive Oxygen Species); 5W494URQ81 (Streptozocin); EC 1.13.99.1 (Inositol Oxygenase)
[Em] Mês de entrada:1508
[Cu] Atualização por classe:170220
[Lr] Data última revisão:
170220
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:141002
[St] Status:MEDLINE
[do] DOI:10.1681/ASN.2014050457



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