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[PMID]:29320819
[Au] Autor:Chaibangyang W; Geadkaew-Krenc A; Vichasri-Grams S; Tesana S; Grams R
[Ad] Endereço:Graduate Program in Biomedical Sciences, Faculty of Allied Health Sciences, Thammasat University, Pathumthani 12121, Thailand.
[Ti] Título:Molecular and Biochemical Characterization of Opisthorchis viverrini Calreticulin.
[So] Source:Korean J Parasitol;55(6):643-652, 2017 Dec.
[Is] ISSN:1738-0006
[Cp] País de publicação:Korea (South)
[La] Idioma:eng
[Ab] Resumo:Calreticulin (CALR), a multifunctional protein thoroughly researched in mammals, comprises N-, P-, and C-domain and has roles in calcium homeostasis, chaperoning, clearance of apoptotic cells, cell adhesion, and also angiogenesis. In this study, the spatial and temporal expression patterns of the Opisthorchis viverrini CALR gene were analyzed, and calcium-binding and chaperoning properties of recombinant O. viverrini CALR (OvCALR) investigated. OvCALR mRNA was detected from the newly excysted juvenile to the mature parasite by RT-PCR while specific antibodies showed a wide distribution of the protein. OvCALR was localized in tegumental cell bodies, testes, ovary, eggs, Mehlis' gland, prostate gland, and vitelline cells of the mature parasite. Recombinant OvCALR showed an in vitro suppressive effect on the thermal aggregation of citrate synthase. The recombinant OvCALR C-domain showed a mobility shift in native gel electrophoresis in the presence of calcium. The results imply that OvCALR has comparable function to the mammalian homolog as a calcium-binding molecular chaperone. Inferred from the observed strong immunostaining of the reproductive tissues, OvCALR should be important for reproduction and might be an interesting target to disrupt parasite fecundity. Transacetylase activity of OvCALR as reported for calreticulin of Haemonchus contortus could not be observed.
[Mh] Termos MeSH primário: Calreticulina/genética
Calreticulina/metabolismo
Expressão Gênica
Opisthorchis/genética
Opisthorchis/metabolismo
[Mh] Termos MeSH secundário: Animais
Cálcio/metabolismo
Calreticulina/fisiologia
Citrato (si)-Sintase/metabolismo
Fertilidade/genética
Técnicas In Vitro
Chaperonas Moleculares
Opisthorchis/fisiologia
Proteínas Recombinantes
Reprodução/genética
Distribuição Tecidual
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Calreticulin); 0 (Molecular Chaperones); 0 (Recombinant Proteins); EC 2.3.3.1 (Citrate (si)-Synthase); SY7Q814VUP (Calcium)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180309
[Lr] Data última revisão:
180309
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180112
[St] Status:MEDLINE
[do] DOI:10.3347/kjp.2017.55.6.643


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[PMID]:28465283
[Au] Autor:Pinto SK; Lamon S; Stephenson EJ; Kalanon M; Mikovic J; Koch LG; Britton SL; Hawley JA; Camera DM
[Ad] Endereço:Centre for Exercise and Nutrition, Mary MacKillop Institute for Health Research, Australian Catholic University, Melbourne, Victoria, Australia.
[Ti] Título:Expression of microRNAs and target proteins in skeletal muscle of rats selectively bred for high and low running capacity.
[So] Source:Am J Physiol Endocrinol Metab;313(3):E335-E343, 2017 09 01.
[Is] ISSN:1522-1555
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Impairments in mitochondrial function and substrate metabolism are implicated in the etiology of obesity and Type 2 diabetes. MicroRNAs (miRNAs) can degrade mRNA or repress protein translation and have been implicated in the development of such disorders. We used a contrasting rat model system of selectively bred high- (HCR) or low- (LCR) intrinsic running capacity with established differences in metabolic health to investigate the molecular mechanisms through which miRNAs regulate target proteins mediating mitochondrial function and substrate oxidation processes. Quantification of select miRNAs using the rat miFinder miRNA PCR array revealed differential expression of 15 skeletal muscles (musculus tibialis anterior) miRNAs between HCR and LCR rats (14 with higher expression in LCR; < 0.05). Ingenuity Pathway Analysis predicted these altered miRNAs to collectively target multiple proteins implicated in mitochondrial dysfunction and energy substrate metabolism. Total protein abundance of citrate synthase (CS; miR-19 target) and voltage-dependent anion channel 1 (miR-7a target) were higher in HCR compared with LCR cohorts (~57 and ~26%, respectively; < 0.05). A negative correlation was observed for miR-19a-3p and CS ( = 0.32, = 0.015) protein expression. To determine whether miR-19a-3p can regulate CS in vitro, we performed luciferase reporter and transfection assays in C2C12 myotubes. MiR-19a-3p binding to the CS untranslated region did not change luciferase reporter activity; however, miR-19a-3p transfection decreased CS protein expression (∼70%; < 0.05). The differential miRNA expression targeting proteins implicated in mitochondrial dysfunction and energy substrate metabolism may contribute to the molecular basis, mediating the divergent metabolic health profiles of LCR and HCR rats.
[Mh] Termos MeSH primário: Tolerância ao Exercício/genética
MicroRNAs/metabolismo
Mitocôndrias Musculares/metabolismo
Músculo Esquelético/metabolismo
Corrida
[Mh] Termos MeSH secundário: Animais
Western Blotting
Linhagem Celular
Citrato (si)-Sintase/metabolismo
Metabolismo Energético/genética
Técnicas In Vitro
Camundongos
Fibras Musculares Esqueléticas/metabolismo
RNA Mensageiro/metabolismo
Ratos
Ratos Endogâmicos
Reação em Cadeia da Polimerase em Tempo Real
Reação em Cadeia da Polimerase Via Transcriptase Reversa
Canal de Ânion 1 Dependente de Voltagem/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (MIRN103 microRNA, rat); 0 (MIRN181 microRNA, rat); 0 (MIRN19 microRNA, rat); 0 (MIRN194 microRNA, rat); 0 (MIRN223 microRNA, rat); 0 (MIRN24 microRNA, rat); 0 (MIRN26 microRNA, rat); 0 (MIRN30 microRNA, rat); 0 (MicroRNAs); 0 (RNA, Messenger); EC 1.6.- (Voltage-Dependent Anion Channel 1); EC 2.3.3.1 (Citrate (si)-Synthase)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:180222
[Lr] Data última revisão:
180222
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170504
[St] Status:MEDLINE
[do] DOI:10.1152/ajpendo.00043.2017


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[PMID]:28467904
[Au] Autor:MacPherson S; Horkoff M; Gravel C; Hoffmann T; Zuber J; Lum JJ
[Ad] Endereço:Trev and Joyce Deeley Research Centre, British Columbia Cancer Agency, Victoria, BC V8R 6V5, Canada; Department of Biochemistry and Microbiology, University of Victoria, Victoria, BC V8W 2Y2, Canada.
[Ti] Título:STAT3 Regulation of Citrate Synthase Is Essential during the Initiation of Lymphocyte Cell Growth.
[So] Source:Cell Rep;19(5):910-918, 2017 May 02.
[Is] ISSN:2211-1247
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Citrate is a required carbon precursor for de novo fatty acid and membrane lipid synthesis. However, the pathways regulating intracellular citrate, particularly during the initial transition from a resting state to cell growth, remain unclear. Here, we show that STAT3 is among the first signaling events activated in resting lymphocytes following growth factor stimulation. During this period, the inhibition of STAT3 blocks the expression of citrate synthase (CS) and reduces the levels of intracellular citrate. As a consequence of CS loss and the reduction in citrate, cells are unable to grow or proliferate in response to extracellular growth factors. These effects were due to STAT3-dependent transcriptional regulation of CS, as exogenous addition of citrate could restore fatty acid synthesis, cell growth, and proliferation. Taken together, our studies reveal that transcription-dependent control of CS is essential for regulating the initiation of cell growth.
[Mh] Termos MeSH primário: Proliferação Celular
Citrato (si)-Sintase/genética
Linfócitos/citologia
Fator de Transcrição STAT3/metabolismo
Ativação Transcricional
[Mh] Termos MeSH secundário: Animais
Células Cultivadas
Citrato (si)-Sintase/metabolismo
Feminino
Linfócitos/metabolismo
Camundongos
Camundongos Endogâmicos C57BL
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (STAT3 Transcription Factor); EC 2.3.3.1 (Citrate (si)-Synthase)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180213
[Lr] Data última revisão:
180213
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170504
[St] Status:MEDLINE


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[PMID]:29212325
[Au] Autor:Lu Z; He X; Ma B; Zhang L; Li J; Jiang Y; Zhou G; Gao F
[Ad] Endereço:College of Animal Science and Technology, Key Laboratory of Animal Origin Food Production and Safety Guarantee of Jiangsu Province, Jiangsu Collaborative Innovation Center of Meat Production and Processing, Quality and Safety Control, Nanjing Agricultural University , Nanjing 210095, P.R. China.
[Ti] Título:Chronic Heat Stress Impairs the Quality of Breast-Muscle Meat in Broilers by Affecting Redox Status and Energy-Substance Metabolism.
[So] Source:J Agric Food Chem;65(51):11251-11258, 2017 Dec 27.
[Is] ISSN:1520-5118
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:We investigated the molecular mechanisms by which chronic heat stress impairs the breast-meat quality of broilers. Broilers were assigned to three groups: the normal control (NC) group, heat-stress (HS) group, and pair-fed (PF) group. After 7 days of heat exposure (32 °C), the high temperature had caused oxidative stress; elevated the activity of citrate synthase (CS), the mRNA expression of M-CPT1, and the phosphorylation level of AMPKα; and reduced the mRNA expression of avUCP. After 14 days of heat exposure, the heat stress had increased the lightness and drip loss and decreased the pH and shear force of the breast meat. Additionally, the heat exposure had increased the mRNA expressions of FAS, ACC, and PDK4; the content of lipids; and the activities of lactic dehydrogenase and pyruvate kinase, and it had decreased the mRNA expression of M-CPT1 and the activity of CS. In conclusion, chronic heat stress impairs meat quality by causing mitochondria to malfunction and affecting energy-substance aerobic metabolism, resulting in increased glycolysis and intramuscular fat deposition.
[Mh] Termos MeSH primário: Galinhas/fisiologia
Metabolismo Energético
Transtornos de Estresse por Calor/veterinária
Temperatura Alta/efeitos adversos
Carne/análise
Músculo Esquelético/metabolismo
Doenças das Aves Domésticas/metabolismo
[Mh] Termos MeSH secundário: Animais
Galinhas/genética
Citrato (si)-Sintase/genética
Citrato (si)-Sintase/metabolismo
Ácidos Graxos/análise
Ácidos Graxos/metabolismo
Feminino
Glicólise
Transtornos de Estresse por Calor/genética
Transtornos de Estresse por Calor/metabolismo
Masculino
Músculo Esquelético/química
Oxirredução
Doenças das Aves Domésticas/genética
Proteínas Quinases/genética
Proteínas Quinases/metabolismo
Estresse Fisiológico
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Fatty Acids); EC 2.3.3.1 (Citrate (si)-Synthase); EC 2.7.- (Protein Kinases); EC 2.7.1.- (AMP-activated protein kinase kinase)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180108
[Lr] Data última revisão:
180108
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171208
[St] Status:MEDLINE
[do] DOI:10.1021/acs.jafc.7b04428


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[PMID]:29053833
[Au] Autor:Manole A; Jaunmuktane Z; Hargreaves I; Ludtmann MHR; Salpietro V; Bello OD; Pope S; Pandraud A; Horga A; Scalco RS; Li A; Ashokkumar B; Lourenço CM; Heales S; Horvath R; Chinnery PF; Toro C; Singleton AB; Jacques TS; Abramov AY; Muntoni F; Hanna MG; Reilly MM; Revesz T; Kullmann DM; Jepson JEC; Houlden H
[Ad] Endereço:Department of Molecular Neuroscience and Neurogenetics Laboratory, UCL Institute of Neurology, Queen Square, London, WC1N 3BG, UK.
[Ti] Título:Clinical, pathological and functional characterization of riboflavin-responsive neuropathy.
[So] Source:Brain;140(11):2820-2837, 2017 11 01.
[Is] ISSN:1460-2156
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Brown-Vialetto-Van Laere syndrome represents a phenotypic spectrum of motor, sensory, and cranial nerve neuropathy, often with ataxia, optic atrophy and respiratory problems leading to ventilator-dependence. Loss-of-function mutations in two riboflavin transporter genes, SLC52A2 and SLC52A3, have recently been linked to Brown-Vialetto-Van Laere syndrome. However, the genetic frequency, neuropathology and downstream consequences of riboflavin transporter mutations are unclear. By screening a large cohort of 132 patients with early-onset severe sensory, motor and cranial nerve neuropathy we confirmed the strong genetic link between riboflavin transporter mutations and Brown-Vialetto-Van Laere syndrome, identifying 22 pathogenic mutations in SLC52A2 and SLC52A3, 14 of which were novel. Brain and spinal cord neuropathological examination of two cases with SLC52A3 mutations showed classical symmetrical brainstem lesions resembling pathology seen in mitochondrial disease, including severe neuronal loss in the lower cranial nerve nuclei, anterior horns and corresponding nerves, atrophy of the spinothalamic and spinocerebellar tracts and posterior column-medial lemniscus pathways. Mitochondrial dysfunction has previously been implicated in an array of neurodegenerative disorders. Since riboflavin metabolites are critical components of the mitochondrial electron transport chain, we hypothesized that reduced riboflavin transport would result in impaired mitochondrial activity, and confirmed this using in vitro and in vivo models. Electron transport chain complex I and complex II activity were decreased in SLC52A2 patient fibroblasts, while global knockdown of the single Drosophila melanogaster riboflavin transporter homologue revealed reduced levels of riboflavin, downstream metabolites, and electron transport chain complex I activity. This in turn led to abnormal mitochondrial membrane potential, respiratory chain activity and morphology. Riboflavin transporter knockdown in Drosophila also resulted in severely impaired locomotor activity and reduced lifespan, mirroring patient pathology, and these phenotypes could be partially rescued using a novel esterified derivative of riboflavin. Our findings expand the genetic, clinical and neuropathological features of Brown-Vialetto-Van Laere syndrome, implicate mitochondrial dysfunction as a downstream consequence of riboflavin transporter gene defects, and validate riboflavin esters as a potential therapeutic strategy.
[Mh] Termos MeSH primário: Encéfalo/patologia
Paralisia Bulbar Progressiva/genética
Perda Auditiva Neurossensorial/genética
Proteínas de Membrana Transportadoras/genética
Receptores Acoplados a Proteínas-G/genética
Medula Espinal/patologia
[Mh] Termos MeSH secundário: Adolescente
Animais
Atrofia
Encéfalo/ultraestrutura
Paralisia Bulbar Progressiva/metabolismo
Paralisia Bulbar Progressiva/patologia
Criança
Pré-Escolar
Citrato (si)-Sintase/metabolismo
Drosophila melanogaster
Complexo I de Transporte de Elétrons/metabolismo
Complexo II de Transporte de Elétrons/metabolismo
Complexo III da Cadeia de Transporte de Elétrons/metabolismo
Feminino
Fibroblastos/metabolismo
Técnicas de Silenciamento de Genes
Perda Auditiva Neurossensorial/metabolismo
Perda Auditiva Neurossensorial/patologia
Seres Humanos
Técnicas In Vitro
Lactente
Locomoção/genética
Longevidade/genética
Masculino
Microscopia Eletrônica
Vias Neurais
Riboflavina
Tratos Espinocerebelares/patologia
Tratos Espinotalâmicos/patologia
Adulto Jovem
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Membrane Transport Proteins); 0 (Receptors, G-Protein-Coupled); 0 (SLC52A2 protein, human); 0 (SLC52A3 protein, human); EC 1.10.2.2 (Electron Transport Complex III); EC 1.3.5.1 (Electron Transport Complex II); EC 1.6.5.3 (Electron Transport Complex I); EC 2.3.3.1 (Citrate (si)-Synthase); TLM2976OFR (Riboflavin)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171113
[Lr] Data última revisão:
171113
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:171021
[St] Status:MEDLINE
[do] DOI:10.1093/brain/awx231


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[PMID]:28887308
[Au] Autor:Malecki J; Jakobsson ME; Ho AYY; Moen A; Rustan AC; Falnes PØ
[Ad] Endereço:From the Department of Biosciences and.
[Ti] Título:Uncovering human METTL12 as a mitochondrial methyltransferase that modulates citrate synthase activity through metabolite-sensitive lysine methylation.
[So] Source:J Biol Chem;292(43):17950-17962, 2017 Oct 27.
[Is] ISSN:1083-351X
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Lysine methylation is an important and much-studied posttranslational modification of nuclear and cytosolic proteins but is present also in mitochondria. However, the responsible mitochondrial lysine-specific methyltransferases (KMTs) remain largely elusive. Here, we investigated METTL12, a mitochondrial human -adenosylmethionine (AdoMet)-dependent methyltransferase and found it to methylate a single protein in mitochondrial extracts, identified as citrate synthase (CS). Using several and approaches, we demonstrated that METTL12 methylates CS on Lys-395, which is localized in the CS active site. Interestingly, the METTL12-mediated methylation inhibited CS activity and was blocked by the CS substrate oxaloacetate. Moreover, METTL12 was strongly inhibited by the reaction product -adenosylhomocysteine (AdoHcy). In summary, we have uncovered a novel human mitochondrial KMT that introduces a methyl modification into a metabolic enzyme and whose activity can be modulated by metabolic cues. Based on the established naming nomenclature for similar enzymes, we suggest that METTL12 be renamed CS-KMT (gene name ).
[Mh] Termos MeSH primário: Citrato (si)-Sintase/metabolismo
Metiltransferases/metabolismo
Proteínas Mitocondriais/metabolismo
Ácido Oxaloacético/metabolismo
S-Adenosil-Homocisteína/metabolismo
[Mh] Termos MeSH secundário: Citrato (si)-Sintase/genética
Células HeLa
Seres Humanos
Metilação
Metiltransferases/classificação
Metiltransferases/genética
Proteínas Mitocondriais/classificação
Proteínas Mitocondriais/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (METTL12 protein, human); 0 (Mitochondrial Proteins); 2F399MM81J (Oxaloacetic Acid); 979-92-0 (S-Adenosylhomocysteine); EC 2.1.1.- (Methyltransferases); EC 2.3.3.1 (Citrate (si)-Synthase)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171103
[Lr] Data última revisão:
171103
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170910
[St] Status:MEDLINE
[do] DOI:10.1074/jbc.M117.808451


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[PMID]:28727827
[Au] Autor:McKee CD; Kosoy MY; Bai Y; Osikowicz LM; Franka R; Gilbert AT; Boonmar S; Rupprecht CE; Peruski LF
[Ad] Endereço:Division of Vector-Borne Diseases, Centers for Disease Control and Prevention, Fort Collins, CO, United States of America.
[Ti] Título:Diversity and phylogenetic relationships among Bartonella strains from Thai bats.
[So] Source:PLoS One;12(7):e0181696, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Bartonellae are phylogenetically diverse, intracellular bacteria commonly found in mammals. Previous studies have demonstrated that bats have a high prevalence and diversity of Bartonella infections globally. Isolates (n = 42) were obtained from five bat species in four provinces of Thailand and analyzed using sequences of the citrate synthase gene (gltA). Sequences clustered into seven distinct genogroups; four of these genogroups displayed similarity with Bartonella spp. sequences from other bats in Southeast Asia, Africa, and Eastern Europe. Thirty of the isolates representing these seven genogroups were further characterized by sequencing four additional loci (ftsZ, nuoG, rpoB, and ITS) to clarify their evolutionary relationships with other Bartonella species and to assess patterns of diversity among strains. Among the seven genogroups, there were differences in the number of sequence variants, ranging from 1-5, and the amount of nucleotide divergence, ranging from 0.035-3.9%. Overall, these seven genogroups meet the criteria for distinction as novel Bartonella species, with sequence divergence among genogroups ranging from 6.4-15.8%. Evidence of intra- and intercontinental phylogenetic relationships and instances of homologous recombination among Bartonella genogroups in related bat species were found in Thai bats.
[Mh] Termos MeSH primário: Infecções por Bartonella/veterinária
Bartonella/genética
Quirópteros/microbiologia
[Mh] Termos MeSH secundário: Animais
Proteínas de Bactérias/genética
Biodiversidade
Citrato (si)-Sintase/genética
Filogenia
Polimorfismo Genético
Tailândia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Bacterial Proteins); EC 2.3.3.1 (Citrate (si)-Synthase)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170926
[Lr] Data última revisão:
170926
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170721
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0181696


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[PMID]:28712868
[Au] Autor:Yan Y; Yang X; Zhao T; Zou Y; Li R; Xu Y
[Ad] Endereço:Department of Endocrinology, Zhongnan Hospital of Wuhan University, Wuhan, 430071, Hubei Province, China.
[Ti] Título:Salicylates promote mitochondrial biogenesis by regulating the expression of PGC-1α in murine 3T3-L1 pre-adipocytes.
[So] Source:Biochem Biophys Res Commun;491(2):436-441, 2017 Sep 16.
[Is] ISSN:1090-2104
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Mitochondrial dysfunction has been associated with insulin resistance and diabetes. Decreased mitochondrial density and mitochondrial copy numbers have been found in insulin-resistant individuals. Restoration of the number of mitochondria and normal mitochondrial function has become an important therapeutic target of diabetes. Salicylate, the main active ingredient in aspirin, has been in medicinal use since ancient times. Little information regarding the effects of salicylate on mitochondrial function has been reported. In this study, we assessed the effects of salicylate on the peroxisome proliferator-activated receptor γ coactivator 1α (PGC-1α) signaling pathway and mitochondrial biogenesis in pre-adipocytes. Our findings demonstrate that treatment with salicylate promoted the expression of PGC-1α and its downstream targets nuclear respiratory factor 1 (NRF1) and mitochondrial transcription factor A (TFAM). Importantly, salicylate treatment significantly increased the number of mDNA, citrate synthase activity, expression of respiratory chain complex I, and mitochondrial mass, which were suppressed by the specific AMPK inhibitor Compound C. Indeed, salicylate treatment induced the phosphorylation of AMPK, which was involved in the induction of PGC-1α, NRF1, and TFAM. Importantly, inhibition of PGC-1α expression using PGC-1α small RNA interference abolished the effects of salicylate on mitochondrial biogenesis. These results suggest that salicylate has a potential therapeutic capacity against mitochondrial dysfunction in diabetes.
[Mh] Termos MeSH primário: Adipócitos/efeitos dos fármacos
Hipoglicemiantes/farmacologia
Mitocôndrias/efeitos dos fármacos
Biogênese de Organelas
Coativador 1-alfa do Receptor gama Ativado por Proliferador de Peroxissomo/genética
Ácido Salicílico/farmacologia
[Mh] Termos MeSH secundário: Células 3T3-L1
Proteínas Quinases Ativadas por AMP/antagonistas & inibidores
Proteínas Quinases Ativadas por AMP/genética
Proteínas Quinases Ativadas por AMP/metabolismo
Adipócitos/citologia
Adipócitos/metabolismo
Animais
Diferenciação Celular/efeitos dos fármacos
Citrato (si)-Sintase/genética
Citrato (si)-Sintase/metabolismo
DNA Mitocondrial/genética
DNA Mitocondrial/metabolismo
Proteínas de Ligação a DNA/agonistas
Proteínas de Ligação a DNA/genética
Proteínas de Ligação a DNA/metabolismo
Complexo I de Transporte de Elétrons/genética
Complexo I de Transporte de Elétrons/metabolismo
Regulação da Expressão Gênica
Proteínas de Grupo de Alta Mobilidade/agonistas
Proteínas de Grupo de Alta Mobilidade/genética
Proteínas de Grupo de Alta Mobilidade/metabolismo
Camundongos
Mitocôndrias/genética
Mitocôndrias/metabolismo
Fator 1 Nuclear Respiratório/agonistas
Fator 1 Nuclear Respiratório/genética
Fator 1 Nuclear Respiratório/metabolismo
Coativador 1-alfa do Receptor gama Ativado por Proliferador de Peroxissomo/agonistas
Coativador 1-alfa do Receptor gama Ativado por Proliferador de Peroxissomo/antagonistas & inibidores
Coativador 1-alfa do Receptor gama Ativado por Proliferador de Peroxissomo/metabolismo
Fosforilação/efeitos dos fármacos
Inibidores de Proteínas Quinases/farmacologia
Pirazóis/farmacologia
Pirimidinas/farmacologia
RNA Interferente Pequeno/genética
RNA Interferente Pequeno/metabolismo
Transdução de Sinais
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (DNA, Mitochondrial); 0 (DNA-Binding Proteins); 0 (High Mobility Group Proteins); 0 (Hypoglycemic Agents); 0 (Nrf1 protein, mouse); 0 (Nuclear Respiratory Factor 1); 0 (Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha); 0 (Ppargc1a protein, mouse); 0 (Protein Kinase Inhibitors); 0 (Pyrazoles); 0 (Pyrimidines); 0 (RNA, Small Interfering); 0 (Tfam protein, mouse); 10K52CIC1Z ((6-(4-(2-piperidin-1-ylethoxy)phenyl))-3-pyridin-4-ylpyrazolo(1,5-a)pyrimidine); EC 1.6.5.3 (Electron Transport Complex I); EC 2.3.3.1 (Citrate (si)-Synthase); EC 2.7.11.31 (AMP-Activated Protein Kinases); O414PZ4LPZ (Salicylic Acid)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170718
[St] Status:MEDLINE


  9 / 3333 MEDLINE  
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[PMID]:28700655
[Au] Autor:Crouch ML; Knowels G; Stuppard R; Ericson NG; Bielas JH; Marcinek DJ; Syrjala KL
[Ad] Endereço:Clinical Research Division, Fred Hutchinson Cancer Research Center, Seattle, Washington, United States of America.
[Ti] Título:Cyclophosphamide leads to persistent deficits in physical performance and in vivo mitochondria function in a mouse model of chemotherapy late effects.
[So] Source:PLoS One;12(7):e0181086, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Fatigue is the symptom most commonly reported by long-term cancer survivors and is increasingly recognized as related to skeletal muscle dysfunction. Traditional chemotherapeutic agents can cause acute toxicities including cardiac and skeletal myopathies. To investigate the mechanism by which chemotherapy may lead to persistent skeletal muscle dysfunction, mature adult mice were injected with a single cyclophosphamide dose and evaluated for 6 weeks. We found that exposed mice developed a persistent decrease in treadmill running time compared to baseline (25.7±10.6 vs. 49.0±16.8 min, P = 0.0012). Further, 6 weeks after drug exposure, in vivo parameters of mitochondrial function remained below baseline including maximum ATP production (482.1 ± 48.6 vs. 696.2 ± 76.6, P = 0.029) and phosphocreatine to ATP ratio (3.243 ± 0.1 vs. 3.878 ± 0.1, P = 0.004). Immunoblotting of homogenized muscles from treated animals demonstrated a transient increase in HNE adducts 1 week after exposure that resolved by 6 weeks. However, there was no evidence of an oxidative stress response as measured by quantitation of SOD1, SOD2, and catalase protein levels. Examination of mtDNA demonstrated that the mutation frequency remained comparable between control and treated groups. Interestingly, there was evidence of a transient increase in NF-ĸB p65 protein 1 day after drug exposure as compared to saline controls (0.091±0.017 vs. 0.053±0.022, P = 0.033). These data suggest that continued impairment in muscle and mitochondria function in cyclophosphamide-treated animals is not linked to persistent oxidative stress and that alternative mechanisms need to be considered.
[Mh] Termos MeSH primário: Ciclofosfamida/farmacologia
DNA Mitocondrial/genética
Mitocôndrias/efeitos dos fármacos
Mitocôndrias/metabolismo
[Mh] Termos MeSH secundário: Animais
Western Blotting
Citrato (si)-Sintase/metabolismo
Feminino
Camundongos
Camundongos Endogâmicos C57BL
Músculo Esquelético/efeitos dos fármacos
Músculo Esquelético/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (DNA, Mitochondrial); 8N3DW7272P (Cyclophosphamide); EC 2.3.3.1 (Citrate (si)-Synthase)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170927
[Lr] Data última revisão:
170927
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170713
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0181086


  10 / 3333 MEDLINE  
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[PMID]:28597977
[Au] Autor:Finkemeier I
[Ad] Endereço:Institute of Plant Biology and Biotechnology, University of Muenster, Germany.
[Ti] Título:Identification of the missing mitochondrial methyltransferase of citrate synthase.
[So] Source:FEBS Lett;591(12):1653-1656, 2017 06.
[Is] ISSN:1873-3468
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Read the Original article at doi: 10.1002/1873-3468.12649.
[Mh] Termos MeSH primário: Citrato (si)-Sintase
Mitocôndrias
[Mh] Termos MeSH secundário: Metiltransferases
[Pt] Tipo de publicação:JOURNAL ARTICLE; COMMENT
[Nm] Nome de substância:
EC 2.1.1.- (Methyltransferases); EC 2.3.3.1 (Citrate (si)-Synthase)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171030
[Lr] Data última revisão:
171030
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170610
[St] Status:MEDLINE
[do] DOI:10.1002/1873-3468.12692



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