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[PMID]:29381758
[Au] Autor:Song N; Lin A; Zhao X
[Ad] Endereço:College of Plant Protection, Henan Agricultural University, Zhengzhou, China.
[Ti] Título:Insight into higher-level phylogeny of Neuropterida: Evidence from secondary structures of mitochondrial rRNA genes and mitogenomic data.
[So] Source:PLoS One;13(1):e0191826, 2018.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:It is well known that the rRNA structure information is important to assist phylogenetic analysis through identifying homologous positions to improve alignment accuracy. In addition, the secondary structure of some conserved motifs is highly stable among distantly related taxa, which can provide potentially informative characters for estimating phylogeny. In this paper, we applied the high-throughput pooled sequencing approach to the determination of neuropteran mitogenomes. Four complete mitogenome sequences were obtained: Micromus angulatus (Hemerobiidae), Chrysoperla nipponensis (Chrysopidae), Rapisma sp. (Ithonidae), and Thaumatosmylus sp. (Osmylidae). This allowed us to sample more complete mitochondrial RNA gene sequences. Secondary structure diagrams for the complete mitochondrial small and large ribosomal subunit RNA genes of eleven neuropterid species were predicted. Comparative analysis of the secondary structures indicated a closer relationship of Megaloptera and Neuroptera. This result was congruent with the resulting phylogeny inferred from sequence alignments of all 37 mitochondrial genes, namely the hypothesis of (Raphidioptera + (Megaloptera + Neuroptera)).
[Mh] Termos MeSH primário: Genoma Mitocondrial
Mitocôndrias/genética
Neópteros/classificação
Filogenia
RNA Ribossômico/genética
[Mh] Termos MeSH secundário: Animais
Genes de Insetos
Neópteros/genética
Conformação de Ácido Nucleico
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (RNA, Ribosomal)
[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:180131
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0191826


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[PMID]:29238189
[Au] Autor:Zhang CY; Sun XY; Ouyang JM; Gui BS
[Ad] Endereço:Institute of Biomineralization and Lithiasis Research, Jinan University, Guangzhou.
[Ti] Título:Diethyl citrate and sodium citrate reduce the cytotoxic effects of nanosized hydroxyapatite crystals on mouse vascular smooth muscle cells.
[So] Source:Int J Nanomedicine;12:8511-8525, 2017.
[Is] ISSN:1178-2013
[Cp] País de publicação:New Zealand
[La] Idioma:eng
[Ab] Resumo:Objective: This study aimed to investigate the damage mechanism of nanosized hydroxyapatite (nano-HAp) on mouse aortic smooth muscle cells (MOVASs) and the injury-inhibiting effects of diethyl citrate (Et Cit) and sodium citrate (Na Cit) to develop new drugs that can simultaneously induce anticoagulation and inhibit vascular calcification. Methods: The change in cell viability was evaluated using a cell proliferation assay kit, and the amount of lactate dehydrogenase (LDH) released was measured using an LDH kit. Intracellular reactive oxygen species (ROS) and mitochondrial damage were detected by DCFH-DA staining and JC-1 staining. Cell apoptosis and necrosis were detected by Annexin V staining. Intracellular calcium concentration and lysosomal integrity were measured using Fluo-4/AM and acridine orange, respectively. Results: Nano-HAp decreased cell viability and damaged the cell membrane, resulting in the release of a large amount of LDH. Nano-HAp entered the cells and damaged the mitochondria, and then induced cell apoptosis by producing a large amount of ROS. In addition, nano-HAp increased the intracellular Ca concentration, leading to lysosomal rupture and cell necrosis. On addition of the anticoagulant Et Cit or Na Cit, cell viability and mitochondrial membrane potential increased, whereas the amount of LDH released, ROS, and apoptosis rate decreased. Et Cit and Na Cit could also chelate with Ca to inhibit the intracellular Ca elevations induced by nano-HAp, prevent lysosomal rupture, and reduce cell necrosis. High concentrations of Et Cit and Na Cit exhibited strong inhibitory effects. The inhibitory capacity of Na Cit was stronger than that of Et Cit at similar concentrations. Conclusion: Both Et Cit and Na Cit significantly reduced the cytotoxicity of nano-HAp on MOVASs and inhibited the apoptosis and necrosis induced by nano-HAp crystals. The chelating function of citrate resulted in both anticoagulation and binding to HAp. Et Cit and Na Cit may play a role as anticoagulants in reducing injury to the vascular wall caused by nano-HAp.
[Mh] Termos MeSH primário: Citratos/farmacologia
Durapatita/efeitos adversos
Músculo Liso Vascular/citologia
Nanopartículas/efeitos adversos
[Mh] Termos MeSH secundário: Animais
Anticoagulantes/farmacologia
Apoptose/efeitos dos fármacos
Calcinose/prevenção & controle
Cálcio/metabolismo
Sobrevivência Celular/efeitos dos fármacos
Células Cultivadas
Durapatita/química
Potencial da Membrana Mitocondrial/efeitos dos fármacos
Camundongos
Mitocôndrias/efeitos dos fármacos
Mitocôndrias/metabolismo
Músculo Liso Vascular/efeitos dos fármacos
Músculo Liso Vascular/metabolismo
Nanopartículas/química
Espécies Reativas de Oxigênio/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Anticoagulants); 0 (Citrates); 0 (Reactive Oxygen Species); 0 (diethyl citrate); 1Q73Q2JULR (sodium citrate); 91D9GV0Z28 (Durapatite); 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:171215
[St] Status:MEDLINE
[do] DOI:10.2147/IJN.S145386


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[PMID]:29202688
[Au] Autor:Abrahamian M; Kagda M; Ah-Fong AMV; Judelson HS
[Ad] Endereço:Department of Microbiology and Plant Pathology, University of California, Riverside, CA, 92521, USA.
[Ti] Título:Rethinking the evolution of eukaryotic metabolism: novel cellular partitioning of enzymes in stramenopiles links serine biosynthesis to glycolysis in mitochondria.
[So] Source:BMC Evol Biol;17(1):241, 2017 Dec 04.
[Is] ISSN:1471-2148
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: An important feature of eukaryotic evolution is metabolic compartmentalization, in which certain pathways are restricted to the cytosol or specific organelles. Glycolysis in eukaryotes is described as a cytosolic process. The universality of this canon has been challenged by recent genome data that suggest that some glycolytic enzymes made by stramenopiles bear mitochondrial targeting peptides. RESULTS: Mining of oomycete, diatom, and brown algal genomes indicates that stramenopiles encode two forms of enzymes for the second half of glycolysis, one with and the other without mitochondrial targeting peptides. The predicted mitochondrial targeting was confirmed by using fluorescent tags to localize phosphoglycerate kinase, phosphoglycerate mutase, and pyruvate kinase in Phytophthora infestans, the oomycete that causes potato blight. A genome-wide search for other enzymes with atypical mitochondrial locations identified phosphoglycerate dehydrogenase, phosphoserine aminotransferase, and phosphoserine phosphatase, which form a pathway for generating serine from the glycolytic intermediate 3-phosphoglycerate. Fluorescent tags confirmed the delivery of these serine biosynthetic enzymes to P. infestans mitochondria. A cytosolic form of this serine biosynthetic pathway, which occurs in most eukaryotes, is missing from oomycetes and most other stramenopiles. The glycolysis and serine metabolism pathways of oomycetes appear to be mosaics of enzymes with different ancestries. While some of the noncanonical oomycete mitochondrial enzymes have the closest affinity in phylogenetic analyses with proteins from other stramenopiles, others cluster with bacterial, plant, or animal proteins. The genes encoding the mitochondrial phosphoglycerate kinase and serine-forming enzymes are physically linked on oomycete chromosomes, which suggests a shared origin. CONCLUSIONS: Stramenopile metabolism appears to have been shaped through the acquisition of genes by descent and lateral or endosymbiotic gene transfer, along with the targeting of the proteins to locations that are novel compared to other eukaryotes. Colocalization of the glycolytic and serine biosynthesis enzymes in mitochondria is apparently necessary since they share a common intermediate. The results indicate that descriptions of metabolism in textbooks do not cover the full diversity of eukaryotic biology.
[Mh] Termos MeSH primário: Evolução Biológica
Células Eucarióticas/metabolismo
Glicólise
Mitocôndrias/metabolismo
Serina/biossíntese
Estramenópilas/enzimologia
Estramenópilas/metabolismo
[Mh] Termos MeSH secundário: Animais
Citosol
Genes
Mitocôndrias/genética
Oomicetos/metabolismo
Fosforilação
Filogenia
Phytophthora infestans/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
452VLY9402 (Serine)
[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:171206
[St] Status:MEDLINE
[do] DOI:10.1186/s12862-017-1087-8


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[PMID]:28456662
[Au] Autor:Kinkar L; Laurimäe T; Sharbatkhori M; Mirhendi H; Kia EB; Ponce-Gordo F; Andresiuk V; Simsek S; Lavikainen A; Irshadullah M; Umhang G; Oudni-M'rad M; Acosta-Jamett G; Rehbein S; Saarma U
[Ad] Endereço:Department of Zoology, Institute of Ecology and Earth Sciences, University of Tartu, Vanemuise 46, 50410 Tartu, Estonia.
[Ti] Título:New mitogenome and nuclear evidence on the phylogeny and taxonomy of the highly zoonotic tapeworm Echinococcus granulosus sensu stricto.
[So] Source:Infect Genet Evol;52:52-58, 2017 Aug.
[Is] ISSN:1567-7257
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Cystic echinococcosis, a zoonotic disease caused by Echinococcus granulosus sensu lato (s. l.), is a significant global public health concern. Echinococcus granulosus s. l. is currently divided into numerous genotypes (G1-G8 and G10) of which G1-G3 are the most frequently implicated genotypes in human infections. Although it has been suggested that G1-G3 could be regarded as a distinct species E. granulosus sensu stricto (s. s.), the evidence to support this is inconclusive. Most importantly, data from nuclear DNA that provide means to investigate the exchange of genetic material between G1-G3 is lacking as none of the published nuclear DNA studies have explicitly included G2 or G3. Moreover, the commonly used relatively short mtDNA sequences, including the complete cox1 gene, have not allowed unequivocal differentiation of genotypes G1-G3. Therefore, significantly longer mtDNA sequences are required to distinguish these genotypes with confidence. The main aim of this study was to evaluate the phylogenetic relations and taxonomy of genotypes G1-G3 using sequences of nearly complete mitogenomes (11,443bp) and three nuclear loci (2984bp). A total of 23 G1-G3 samples were analysed, originating from 5 intermediate host species in 10 countries. The mtDNA data demonstrate that genotypes G1 and G3 are distinct mitochondrial genotypes (separated by 37 mutations), whereas G2 is not a separate genotype or even a monophyletic cluster, but belongs to G3. Nuclear data revealed no genetic separation of G1 and G3, suggesting that these genotypes form a single species due to ongoing gene flow. We conclude that: (a) in the taxonomic sense, genotypes G1 and G3 can be treated as a single species E. granulosus s. s.; (b) genotypes G1 and G3 should be regarded as distinct genotypes only in the context of mitochondrial data; (c) we recommend excluding G2 from the genotype list.
[Mh] Termos MeSH primário: Núcleo Celular/genética
DNA de Helmintos/genética
Echinococcus granulosus/classificação
Mitocôndrias/genética
[Mh] Termos MeSH secundário: África do Norte
Animais
Ásia
Echinococcus granulosus/genética
Echinococcus granulosus/isolamento & purificação
Echinococcus granulosus/metabolismo
Europa (Continente)
Genoma Mitocondrial
Genótipo
Seres Humanos
Filogenia
Filogeografia
América do Sul
Zoonoses/parasitologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (DNA, Helminth)
[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:170501
[St] Status:MEDLINE


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[PMID]:29441913
[Ti] Título:Stimulation of bone regeneration with pigment epithelium-derived factor microparticles: evidence and .
[So] Source:Pharmazie;71(7):382-389, 2016 Jul 07.
[Is] ISSN:0031-7144
[Cp] País de publicação:Germany
[La] Idioma:eng
[Ab] Resumo:The occurrence of bone defects can be due to a variety of factors not limited to bone fractures and tumours. Most diseased bone is removed and the patient fitted with prosthetics, prior to use of certain factors such as bone morphogenetic proteins (BMPs) to aid healing. Recently, the protein pigment epithelium-derived factor (PEDF) and the polysaccharide chitosan have been found to have promising effects on the regeneration of bone, with the major advantage of these agents being their safety to date. A study was performed to determine whether the combination of both chitosan and PEDF would enhance greater bone regeneration effects. Post-formulation, in silico tests (particle sizing and surface charge determination) were followed by several cell-based assays (microparticle cellular uptake, cytotoxicity, mitochondrial abundance, bone mineral formation, colony formation in matrigel, and colony formation in collagen I matrix), and finally in vivo testing where microparticles were injected periosteally in the hindlimb. Collectively, these findings support the idea that PEDF microencapsulated within chitosan promotes bone regeneration, and has potential for bone trauma management. Future studies will examine the ability of this promising bone regeneration microparticle to heal bone in disease states such as fracture and tumour-mediated osteolysis.
[Mh] Termos MeSH primário: Regeneração Óssea/efeitos dos fármacos
Proteínas do Olho/farmacologia
Fatores de Crescimento Neural/farmacologia
Serpinas/farmacologia
[Mh] Termos MeSH secundário: Animais
Densidade Óssea/efeitos dos fármacos
Cápsulas
Sobrevivência Celular/efeitos dos fármacos
Quitosana/farmacologia
Colágeno Tipo I/farmacologia
Ensaio de Unidades Formadoras de Colônias
Simulação por Computador
Composição de Medicamentos
Proteínas do Olho/administração & dosagem
Proteínas do Olho/metabolismo
Membro Posterior
Seres Humanos
Injeções
Masculino
Camundongos
Camundongos Endogâmicos BALB C
Mitocôndrias/efeitos dos fármacos
Fatores de Crescimento Neural/administração & dosagem
Fatores de Crescimento Neural/metabolismo
Tamanho da Partícula
Serpinas/administração & dosagem
Serpinas/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Capsules); 0 (Collagen Type I); 0 (Eye Proteins); 0 (Nerve Growth Factors); 0 (Serpins); 0 (pigment epithelium-derived factor); 9012-76-4 (Chitosan)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180308
[Lr] Data última revisão:
180308
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180215
[St] Status:MEDLINE
[do] DOI:10.1691/ph.2016.6010


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[PMID]:29182013
[Au] Autor:Dickerson T; Jauregui CE; Teng Y
[Ad] Endereço:College of Science & Mathematics, Augusta University, Augusta, GA 30912, USA.
[Ti] Título:Friend or foe? Mitochondria as a pharmacological target in cancer treatment.
[So] Source:Future Med Chem;9(18):2197-2210, 2017 12.
[Is] ISSN:1756-8927
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Mitochondria have acquired numerous functions over the course of evolution, such as those involved in controlling energy production, cellular metabolism, cell survival, apoptosis and autophagy within host cells. Tumor cells can develop defects in mitochondrial function, presenting a potential strategy for designing selective anticancer therapies. Therefore, cancer has been the main focus of recent research to uncover possible mitochondrial targets for therapeutic benefit. This comprehensive review covers not only the recent discoveries of the roles of mitochondria in cancer development, progression and therapeutic implications but also the findings regarding emerging mitochondrial therapeutic targets and mitochondria-targeted agents. Current challenges and future directions for developments and applications of mitochondrial-targeted therapeutics are also discussed.
[Mh] Termos MeSH primário: Mitocôndrias/metabolismo
Neoplasias/tratamento farmacológico
[Mh] Termos MeSH secundário: ATPases Associadas a Diversas Atividades Celulares/metabolismo
Trifosfato de Adenosina/metabolismo
Animais
Antineoplásicos/farmacologia
Antineoplásicos/uso terapêutico
DNA Mitocondrial/efeitos dos fármacos
DNA Mitocondrial/metabolismo
Metabolismo Energético/efeitos dos fármacos
Seres Humanos
Proteínas de Membrana/metabolismo
Mitocôndrias/genética
Proteínas Mitocondriais/metabolismo
Neoplasias/metabolismo
Neoplasias/patologia
Espécies Reativas de Oxigênio/metabolismo
Transdução de Sinais/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (ATAD3A protein, human); 0 (Antineoplastic Agents); 0 (DNA, Mitochondrial); 0 (Membrane Proteins); 0 (Mitochondrial Proteins); 0 (Reactive Oxygen Species); 8L70Q75FXE (Adenosine Triphosphate); EC 3.6.4.- (ATPases Associated with Diverse Cellular Activities)
[Em] Mês de entrada:1712
[Cu] Atualização por classe:180308
[Lr] Data última revisão:
180308
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171129
[St] Status:MEDLINE
[do] DOI:10.4155/fmc-2017-0110


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[PMID]:28471062
[Au] Autor:Rao AN; Patil A; Brodnik ZD; Qiang L; España RA; Sullivan KA; Black MM; Baas PW
[Ad] Endereço:Department of Neurobiology and Anatomy, Drexel University College of Medicine, Philadelphia, Pennsylvania.
[Ti] Título:Pharmacologically increasing microtubule acetylation corrects stress-exacerbated effects of organophosphates on neurons.
[So] Source:Traffic;18(7):433-441, 2017 Jul.
[Is] ISSN:1600-0854
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Many veterans of the 1990-1991 Gulf War contracted Gulf War Illness (GWI), a multisymptom disease that primarily affects the nervous system. Here, we treated cultures of human or rat neurons with diisopropyl fluorophosphate (DFP), an analog of sarin, one of the organophosphate (OP) toxicants to which the military veterans were exposed. All observed cellular defects produced by DFP were exacerbated by pretreatment with corticosterone or cortisol, which, in rat and human neurons, respectively, serves in our experiments to mimic the physical stress endured by soldiers during the war. To best mimic the disease, DFP was used below the level needed to inhibit acetylcholinesterase. We observed a diminution in the ratio of acetylated to total tubulin that was correctable by treatment with tubacin, a drug that inhibits HDAC6, the tubulin deacetylase. The reduction in microtubule acetylation was coupled with deficits in microtubule dynamics, which were correctable by HDAC6 inhibition. Deficits in mitochondrial transport and dopamine release were also improved by tubacin. Thus, various negative effects of the toxicant/stress exposures were at least partially correctable by restoring microtubule acetylation to a more normal status. Such an approach may have therapeutic benefit for individuals suffering from GWI or other neurological disorders linked to OP exposure.
[Mh] Termos MeSH primário: Anilidas/farmacologia
Substâncias para a Guerra Química/toxicidade
Ácidos Hidroxâmicos/farmacologia
Isoflurofato/toxicidade
Microtúbulos/efeitos dos fármacos
Neurônios/efeitos dos fármacos
Estresse Fisiológico
[Mh] Termos MeSH secundário: Acetilação
Animais
Transporte Biológico
Células Cultivadas
Corticosterona/farmacologia
Dopamina/secreção
Relação Dose-Resposta a Droga
Seres Humanos
Hidrocortisona/farmacologia
Microtúbulos/metabolismo
Mitocôndrias/efeitos dos fármacos
Mitocôndrias/metabolismo
Síndrome do Golfo Pérsico
Ratos
Tubulina (Proteína)/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Anilides); 0 (Chemical Warfare Agents); 0 (Hydroxamic Acids); 0 (Tubulin); 02C2G1D30D (tubacin); 12UHW9R67N (Isoflurophate); VTD58H1Z2X (Dopamine); W980KJ009P (Corticosterone); WI4X0X7BPJ (Hydrocortisone)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180308
[Lr] Data última revisão:
180308
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170505
[St] Status:MEDLINE
[do] DOI:10.1111/tra.12489


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[PMID]:28462525
[Au] Autor:Tummers B; Green DR
[Ad] Endereço:Department of Immunology, St. Jude Children's Research Hospital, Memphis, TN, USA.
[Ti] Título:Caspase-8: regulating life and death.
[So] Source:Immunol Rev;277(1):76-89, 2017 05.
[Is] ISSN:1600-065X
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Roles for cell death in development, homeostasis, and the control of infections and cancer have long been recognized. Although excessive cell damage results in passive necrosis, cells can be triggered to engage molecular programs that result in cell death. Such triggers include cellular stress, oncogenic signals that engage tumor suppressor mechanisms, pathogen insults, and immune mechanisms. The best-known forms of programmed cell death are apoptosis and a recently recognized regulated necrosis termed necroptosis. Of the two best understood pathways of apoptosis, the extrinsic and intrinsic (mitochondrial) pathways, the former is induced by the ligation of death receptors, a subset of the TNF receptor (TNFR) superfamily. Ligation of these death receptors can also induce necroptosis. The extrinsic apoptosis and necroptosis pathways regulate each other and their balance determines whether cells live. Integral in the regulation and initiation of death receptor-mediated activation of programmed cell death is the aspartate-specific cysteine protease (caspase)-8. This review describes the role of caspase-8 in the initiation of extrinsic apoptosis execution and the mechanism by which caspase-8 inhibits necroptosis. The importance of caspase-8 in the development and homeostasis and the way that dysfunctional caspase-8 may contribute to the development of malignancies in mice and humans are also explored.
[Mh] Termos MeSH primário: Caspase 8/imunologia
Inflamassomos/metabolismo
Mitocôndrias/metabolismo
Fator de Necrose Tumoral alfa/metabolismo
[Mh] Termos MeSH secundário: Animais
Apoptose
Homeostase
Seres Humanos
Necrose
Receptores de Morte Celular/metabolismo
Receptores do Fator de Necrose Tumoral/metabolismo
Transdução de Sinais
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW; RESEARCH SUPPORT, NON-U.S. GOV'T; RESEARCH SUPPORT, N.I.H., EXTRAMURAL
[Nm] Nome de substância:
0 (Inflammasomes); 0 (Receptors, Death Domain); 0 (Receptors, Tumor Necrosis Factor); 0 (Tumor Necrosis Factor-alpha); EC 3.4.22.- (Caspase 8)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180309
[Lr] Data última revisão:
180309
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170503
[St] Status:MEDLINE
[do] DOI:10.1111/imr.12541


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[PMID]:28462393
[Au] Autor:Pathak D; Berthet A; Bendor JT; Yu K; Sellnow RC; Orr AL; Nguyen MK; Edwards RH; Manfredsson FP; Nakamura K
[Ad] Endereço:Gladstone Institute of Neurological Disease, San Francisco, CA 94158.
[Ti] Título:Loss of α-Synuclein Does Not Affect Mitochondrial Bioenergetics in Rodent Neurons.
[So] Source:eNeuro;4(2), 2017 Mar-Apr.
[Is] ISSN:2373-2822
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Increased α-synuclein (αsyn) and mitochondrial dysfunction play central roles in the pathogenesis of Parkinson's disease (PD), and lowering αsyn is under intensive investigation as a therapeutic strategy for PD. Increased αsyn levels disrupt mitochondria and impair respiration, while reduced αsyn protects against mitochondrial toxins, suggesting that interactions between αsyn and mitochondria influences the pathologic and physiologic functions of αsyn. However, we do not know if αsyn affects normal mitochondrial function or if lowering αsyn levels impacts bioenergetic function, especially at the nerve terminal where αsyn is enriched. To determine if αsyn is required for normal mitochondrial function in neurons, we comprehensively evaluated how lowering αsyn affects mitochondrial function. We found that αsyn knockout (KO) does not affect the respiration of cultured hippocampal neurons or cortical and dopaminergic synaptosomes, and that neither loss of αsyn nor all three (α, ß and γ) syn isoforms decreased mitochondria-derived ATP levels at the synapse. Similarly, neither αsyn KO nor knockdown altered the capacity of synaptic mitochondria to meet the energy requirements of synaptic vesicle cycling or influenced the localization of mitochondria to dopamine (DA) synapses . Finally, αsyn KO did not affect overall energy metabolism in mice assessed with a Comprehensive Lab Animal Monitoring System. These studies suggest either that αsyn has little or no significant physiological effect on mitochondrial bioenergetic function, or that any such functions are fully compensated for when lost. These results implicate that αsyn levels can be reduced in neurons without impairing (or improving) mitochondrial bioenergetics or distribution.
[Mh] Termos MeSH primário: Mitocôndrias/metabolismo
Neurônios/metabolismo
Sinapses/metabolismo
alfa-Sinucleína/metabolismo
[Mh] Termos MeSH secundário: Animais
Dopamina/metabolismo
Hipocampo/metabolismo
Camundongos Knockout
Doença de Parkinson/metabolismo
alfa-Sinucleína/deficiência
alfa-Sinucleína/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Snca protein, mouse); 0 (alpha-Synuclein); VTD58H1Z2X (Dopamine)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180308
[Lr] Data última revisão:
180308
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170503
[St] Status:MEDLINE


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[PMID]:29442032
[Au] Autor:Jiang JF; Zhai J; Liu ZR; Chao L; Zhao YF; Wu YJ; Cui MX
[Ti] Título:Ampelopsin sodium induces mitochondrial-mediated apoptosis in human lung adenocarcinoma SPC-A-1 cell line.
[So] Source:Pharmazie;71(8):455-459, 2016 08 01.
[Is] ISSN:0031-7144
[Cp] País de publicação:Germany
[La] Idioma:eng
[Ab] Resumo:Ampelopsin is a well-known flavonoid which has variety of biological and pharmacological actions including anticancer effects and induction of apoptosis on the several cancer cell lines. The present study aimed to evaluate the role of ampelopsin sodium (Amp-Na) in the mitochondrial-mediated apoptosis of human lung adenocarcionma SPC-A-1 cells. The analysis of cell proliferation and ultrastructure were performed. Furthermore, to clarify its action mechanism by determining the mitochondrial membrane potential (Δψm), intracellular calcium (Ca2+) concentration, mitochondrial nitric oxide (NO) level and total ATPase activity. The results showed that Amp-Na markedly inhibited the SPC-A-1 cell proliferation and caused ultrastructural apoptosis feature in SPC-A-1 cells in a dose-dependent manner. Amp-Na led to a rapid and sustained Ca2+ elevation and Δψm reduction, and induced the mitochondrial NO production and decreased the total ATPase activity in SPC-A-1 cells. The results enhance the potential of Amp-Na as a therapeutic drug for treating lung cancer, and provide new information for mechanism of Amp-Na which induces mitochondrial-mediated apoptosis in tumor cells.
[Mh] Termos MeSH primário: Adenocarcinoma/tratamento farmacológico
Antineoplásicos Fitogênicos/farmacologia
Apoptose/efeitos dos fármacos
Flavonoides/farmacologia
Neoplasias Pulmonares/tratamento farmacológico
Mitocôndrias/efeitos dos fármacos
[Mh] Termos MeSH secundário: Adenocarcinoma/patologia
Adenocarcinoma/ultraestrutura
Adenosina Trifosfatases/metabolismo
Cálcio/metabolismo
Linhagem Celular Tumoral
Proliferação Celular
Relação Dose-Resposta a Droga
Seres Humanos
Neoplasias Pulmonares/patologia
Neoplasias Pulmonares/ultraestrutura
Potencial da Membrana Mitocondrial/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Antineoplastic Agents, Phytogenic); 0 (Flavonoids); 27200-12-0 (ampelopsin); EC 3.6.1.- (Adenosine Triphosphatases); SY7Q814VUP (Calcium)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180307
[Lr] Data última revisão:
180307
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180215
[St] Status:MEDLINE
[do] DOI:10.1691/ph.2016.6571



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