Base de dados : MEDLINE
Pesquisa : G04.599 [Categoria DeCS]
Referências encontradas : 290 [refinar]
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[PMID]:28596381
[Au] Autor:Wang XX; Luo Y; Wang D; Adorini L; Pruzanski M; Dobrinskikh E; Levi M
[Ad] Endereço:From the Division of Renal Diseases and Hypertension, Department of Medicine, Denver Veterans Affairs Medical Center and University of Colorado Anschutz Medical Campus, Aurora, Colorado 80045 and.
[Ti] Título:A dual agonist of farnesoid X receptor (FXR) and the G protein-coupled receptor TGR5, INT-767, reverses age-related kidney disease in mice.
[So] Source:J Biol Chem;292(29):12018-12024, 2017 Jul 21.
[Is] ISSN:1083-351X
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Even in healthy individuals, renal function gradually declines during aging. However, an observed variation in the rate of this decline has raised the possibility of slowing or delaying age-related kidney disease. One of the most successful interventional measures that slows down and delays age-related kidney disease is caloric restriction. We undertook the present studies to search for potential factors that are regulated by caloric restriction and act as caloric restriction mimetics. Based on our prior studies with the bile acid-activated nuclear hormone receptor farnesoid X receptor (FXR) and G protein-coupled membrane receptor TGR5 that demonstrated beneficial effects of FXR and TGR5 activation in the kidney, we reasoned that FXR and TGR5 could be excellent candidates. We therefore determined the effects of aging and caloric restriction on the expression of FXR and TGR5 in the kidney. We found that FXR and TGR5 expression levels are decreased in the aging kidney and that caloric restriction prevents these age-related decreases. Interestingly, in long-lived Ames dwarf mice, renal FXR and TGR5 expression levels were also increased. A 2-month treatment of 22-month-old C57BL/6J mice with the FXR-TGR5 dual agonist INT-767 induced caloric restriction-like effects and reversed age-related increases in proteinuria, podocyte injury, fibronectin accumulation, TGF-ß expression, and, most notably, age-related impairments in mitochondrial biogenesis and mitochondrial function. Furthermore, in podocytes cultured in serum obtained from old mice, INT-767 prevented the increases in the proinflammatory markers TNF-α, toll-like receptor 2 (TLR2), and TLR4. In summary, our results indicate that FXR and TGR5 may play an important role in modulation of age-related kidney disease.
[Mh] Termos MeSH primário: Envelhecimento
Anti-Inflamatórios não Esteroides/uso terapêutico
Ácidos e Sais Biliares/uso terapêutico
Rim/efeitos dos fármacos
Receptores Citoplasmáticos e Nucleares/agonistas
Receptores Acoplados a Proteínas-G/agonistas
Insuficiência Renal/tratamento farmacológico
[Mh] Termos MeSH secundário: Animais
Anti-Inflamatórios não Esteroides/farmacologia
Ácidos e Sais Biliares/farmacologia
Restrição Calórica
Células Cultivadas
Regulação da Expressão Gênica no Desenvolvimento
Seres Humanos
Hipolipemiantes/farmacologia
Hipolipemiantes/uso terapêutico
Mediadores da Inflamação/antagonistas & inibidores
Mediadores da Inflamação/metabolismo
Rim/imunologia
Rim/metabolismo
Rim/patologia
Longevidade
Camundongos Endogâmicos C57BL
Camundongos Mutantes
Mitocôndrias/enzimologia
Mitocôndrias/imunologia
Mitocôndrias/metabolismo
Mitocôndrias/patologia
Renovação Mitocondrial
Podócitos/efeitos dos fármacos
Podócitos/imunologia
Podócitos/metabolismo
Podócitos/patologia
Receptores Citoplasmáticos e Nucleares/genética
Receptores Citoplasmáticos e Nucleares/metabolismo
Receptores Acoplados a Proteínas-G/genética
Receptores Acoplados a Proteínas-G/metabolismo
Insuficiência Renal/metabolismo
Insuficiência Renal/patologia
Insuficiência Renal/prevenção & controle
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (6-ethyl-24-norcholane-3,7,23-triol-23 sulfate); 0 (Anti-Inflammatory Agents, Non-Steroidal); 0 (Bile Acids and Salts); 0 (GPBAR1 protein, human); 0 (Gpbar1 protein, mouse); 0 (Hypolipidemic Agents); 0 (Inflammation Mediators); 0 (Receptors, Cytoplasmic and Nuclear); 0 (Receptors, G-Protein-Coupled); 0 (farnesoid X-activated receptor)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170808
[Lr] Data última revisão:
170808
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170610
[St] Status:MEDLINE
[do] DOI:10.1074/jbc.C117.794982


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[PMID]:28432125
[Au] Autor:Dolezal JM; Wang H; Kulkarni S; Jackson L; Lu J; Ranganathan S; Goetzman ES; Bharathi SS; Beezhold K; Byersdorfer CA; Prochownik EV
[Ad] Endereço:From the Divisions of Hematology/Oncology and.
[Ti] Título:Sequential adaptive changes in a c-Myc-driven model of hepatocellular carcinoma.
[So] Source:J Biol Chem;292(24):10068-10086, 2017 Jun 16.
[Is] ISSN:1083-351X
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Hepatocellular carcinoma (HCC) is a common cancer that frequently overexpresses the c-Myc (Myc) oncoprotein. Using a mouse model of Myc-induced HCC, we studied the metabolic, biochemical, and molecular changes accompanying HCC progression, regression, and recurrence. These involved altered rates of pyruvate and fatty acid ß-oxidation and the likely re-directing of glutamine into biosynthetic rather than energy-generating pathways. Initial tumors also showed reduced mitochondrial mass and differential contributions of electron transport chain complexes I and II to respiration. The uncoupling of complex II's electron transport function from its succinate dehydrogenase activity also suggested a mechanism by which Myc generates reactive oxygen species. RNA sequence studies revealed an orderly progression of transcriptional changes involving pathways pertinent to DNA damage repair, cell cycle progression, insulin-like growth factor signaling, innate immunity, and further metabolic re-programming. Only a subset of functions deregulated in initial tumors was similarly deregulated in recurrent tumors thereby indicating that the latter can "normalize" some behaviors to suit their needs. An interactive and freely available software tool was developed to allow continued analyses of these and other transcriptional profiles. Collectively, these studies define the metabolic, biochemical, and molecular events accompanyingHCCevolution, regression, and recurrence in the absence of any potentially confounding therapies.
[Mh] Termos MeSH primário: Carcinoma Hepatocelular/metabolismo
Regulação Neoplásica da Expressão Gênica
Neoplasias Hepáticas/metabolismo
Fígado/metabolismo
Neoplasias Experimentais/metabolismo
Proteínas Proto-Oncogênicas c-myc/metabolismo
Regulação para Cima
[Mh] Termos MeSH secundário: Animais
Carcinogênese
Carcinoma Hepatocelular/patologia
Carcinoma Hepatocelular/prevenção & controle
Reparo do DNA
Complexo I de Transporte de Elétrons/genética
Complexo I de Transporte de Elétrons/metabolismo
Complexo II de Transporte de Elétrons/genética
Complexo II de Transporte de Elétrons/metabolismo
Feminino
Perfilação da Expressão Gênica
Inativação Gênica
Seres Humanos
Fígado/patologia
Masculino
Camundongos Transgênicos
Renovação Mitocondrial
Recidiva Local de Neoplasia/metabolismo
Recidiva Local de Neoplasia/patologia
Recidiva Local de Neoplasia/fisiopatologia
Recidiva Local de Neoplasia/prevenção & controle
Neoplasias Experimentais/patologia
Neoplasias Experimentais/prevenção & controle
Proteínas Proto-Oncogênicas c-myc/genética
Espécies Reativas de Oxigênio/metabolismo
Carga Tumoral
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Myc protein, mouse); 0 (Proto-Oncogene Proteins c-myc); 0 (Reactive Oxygen Species); EC 1.3.5.1 (Electron Transport Complex II); EC 1.6.5.3 (Electron Transport Complex I)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:170714
[Lr] Data última revisão:
170714
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170423
[St] Status:MEDLINE
[do] DOI:10.1074/jbc.M117.782052


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[PMID]:27847330
[Au] Autor:Marzetti E; Lorenzi M; Landi F; Picca A; Rosa F; Tanganelli F; Galli M; Doglietto GB; Pacelli F; Cesari M; Bernabei R; Calvani R; Bossola M
[Ad] Endereço:Department of Geriatrics, Neurosciences and Orthopedics, Catholic University of the Sacred Heart School of Medicine, Teaching Hospital "Agostino Gemelli", Rome 00168, Italy.
[Ti] Título:Altered mitochondrial quality control signaling in muscle of old gastric cancer patients with cachexia.
[So] Source:Exp Gerontol;87(Pt A):92-99, 2017 Jan.
[Is] ISSN:1873-6815
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Mitochondrial dysfunction is involved in the loss of muscle featuring both aging and cancer cachexia (CC). Whether mitochondrial quality control (MQC) is altered in skeletal myocytes of old patients with CC is unclear. The present investigation therefore sought to preliminarily characterize MQC pathways in muscle of old gastric cancer patients with cachexia. The study followed a case-control cross-sectional design. Intraoperative biopsies of the rectus abdominis muscle were obtained from 18 patients with gastric adenocarcinoma (nine with CC and nine non-cachectic) and nine controls, and assayed for the expression of a set of MQC mediators. The mitofusin 2 expression was reduced in cancer patients compared with controls, independent of CC. Fission protein 1 was instead up-regulated in CC patients relative to the other groups. The mitophagy regulators PTEN-induced putative kinase 1 and Parkin were both down-regulated in cancer patients compared with controls. The ratio between the protein content of the lipidated and non-lipidated forms of microtubule-associated protein 1 light chain 3B was lower in CC patients relative to controls and non-cachectic cancer patients. Finally, the expression of autophagy-associated protein 7, lysosome-associated membrane protein 2, peroxisome proliferator-activated receptor-γ coactivator-1α, and mitochondrial transcription factor A was unvarying among groups. Collectively, our findings indicate that, in old patients with gastric cancer, cachexia is associated with derangements of the muscular MQC axis at several checkpoints: mitochondrial dynamics, mitochondrial tagging for disposal, and mitophagy signaling. Further investigations are needed to corroborate these preliminary findings and determine whether MQC pathways may become target for future interventions.
[Mh] Termos MeSH primário: Adenocarcinoma/fisiopatologia
Caquexia/fisiopatologia
Mitocôndrias Musculares/metabolismo
Renovação Mitocondrial
Músculo Esquelético/patologia
Neoplasias Gástricas/fisiopatologia
[Mh] Termos MeSH secundário: Adulto
Idoso
Envelhecimento/patologia
Caquexia/etiologia
Estudos de Casos e Controles
Estudos Transversais
Metabolismo Energético
Feminino
Seres Humanos
Itália
Masculino
Meia-Idade
Degradação Mitocondrial
Estresse Oxidativo
Receptores Ativados por Proliferador de Peroxissomo/metabolismo
Transdução de Sinais
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Peroxisome Proliferator-Activated Receptors)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171016
[Lr] Data última revisão:
171016
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161117
[St] Status:MEDLINE


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[PMID]:27181353
[Au] Autor:Roy M; Itoh K; Iijima M; Sesaki H
[Ad] Endereço:Department of Cell Biology, Johns Hopkins University School of Medicine, Baltimore, MD, USA. Electronic address: mroy17@jhmi.edu.
[Ti] Título:Parkin suppresses Drp1-independent mitochondrial division.
[So] Source:Biochem Biophys Res Commun;475(3):283-8, 2016 07 01.
[Is] ISSN:1090-2104
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The cycle of mitochondrial division and fusion disconnect and reconnect individual mitochondria in cells to remodel this energy-producing organelle. Although dynamin-related protein 1 (Drp1) plays a major role in mitochondrial division in cells, a reduced level of mitochondrial division still persists even in the absence of Drp1. It is unknown how much Drp1-mediated mitochondrial division accounts for the connectivity of mitochondria. The role of a Parkinson's disease-associated protein-parkin, which biochemically and genetically interacts with Drp1-in mitochondrial connectivity also remains poorly understood. Here, we quantified the number and connectivity of mitochondria using mitochondria-targeted photoactivatable GFP in cells. We show that the loss of Drp1 increases the connectivity of mitochondria by 15-fold in mouse embryonic fibroblasts (MEFs). While a single loss of parkin does not affect the connectivity of mitochondria, the connectivity of mitochondria significantly decreased compared with a single loss of Drp1 when parkin was lost in the absence of Drp1. Furthermore, the loss of parkin decreased the frequency of depolarization of the mitochondrial inner membrane that is caused by increased mitochondrial connectivity in Drp1-knockout MEFs. Therefore, our data suggest that parkin negatively regulates Drp1-indendent mitochondrial division.
[Mh] Termos MeSH primário: Dinaminas/metabolismo
Mitocôndrias/metabolismo
Renovação Mitocondrial
Ubiquitina-Proteína Ligases/metabolismo
[Mh] Termos MeSH secundário: Animais
Sinalização do Cálcio
Linhagem Celular
Fibroblastos/citologia
Fibroblastos/metabolismo
Fibroblastos/ultraestrutura
Camundongos
Microscopia de Fluorescência
Mitocôndrias/ultraestrutura
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL
[Nm] Nome de substância:
EC 2.3.2.27 (Ubiquitin-Protein Ligases); EC 2.3.2.27 (parkin protein); EC 3.6.5.5 (Dnm1l protein, mouse); EC 3.6.5.5 (Dynamins)
[Em] Mês de entrada:1705
[Cu] Atualização por classe:171125
[Lr] Data última revisão:
171125
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160517
[St] Status:MEDLINE


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[PMID]:27146012
[Au] Autor:Koliaki C; Roden M
[Ad] Endereço:Department of Endocrinology and Diabetology, Medical Faculty, Heinrich Heine University, Düsseldorf 40225, Germany.
[Ti] Título:Alterations of Mitochondrial Function and Insulin Sensitivity in Human Obesity and Diabetes Mellitus.
[So] Source:Annu Rev Nutr;36:337-67, 2016 Jul 17.
[Is] ISSN:1545-4312
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Mitochondrial function refers to a broad spectrum of features such as resting mitochondrial activity, (sub)maximal oxidative phosphorylation capacity (OXPHOS), and mitochondrial dynamics, turnover, and plasticity. The interaction between mitochondria and insulin sensitivity is bidirectional and varies depending on tissue, experimental model, methodological approach, and features of mitochondrial function tested. In human skeletal muscle, mitochondrial abnormalities may be inherited (e.g., lower mitochondrial content) or acquired (e.g., impaired OXPHOS capacity and plasticity). Abnormalities ultimately lead to lower mitochondrial functionality due to or resulting in insulin resistance and type 2 diabetes mellitus. Similar mechanisms can also operate in adipose tissue and heart muscle. In contrast, mitochondrial oxidative capacity is transiently upregulated in the liver of obese insulin-resistant humans with or without fatty liver, giving rise to oxidative stress and declines in advanced fatty liver disease. These data suggest a highly tissue-specific interaction between insulin sensitivity and oxidative metabolism during the course of metabolic diseases in humans.
[Mh] Termos MeSH primário: Diabetes Mellitus Tipo 2/metabolismo
Medicina Baseada em Evidências
Resistência à Insulina
Mitocôndrias/metabolismo
Modelos Biológicos
Obesidade/metabolismo
Estresse Oxidativo
[Mh] Termos MeSH secundário: Animais
Diabetes Mellitus Tipo 1/metabolismo
Diabetes Mellitus Tipo 2/fisiopatologia
Seres Humanos
Mitocôndrias/enzimologia
Mitocôndrias Hepáticas/enzimologia
Mitocôndrias Hepáticas/metabolismo
Renovação Mitocondrial
Hepatopatia Gordurosa não Alcoólica/etiologia
Obesidade/fisiopatologia
Especificidade de Órgãos
Fosforilação Oxidativa
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Em] Mês de entrada:1707
[Cu] Atualização por classe:170720
[Lr] Data última revisão:
170720
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160506
[St] Status:MEDLINE
[do] DOI:10.1146/annurev-nutr-071715-050656


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[PMID]:27086599
[Au] Autor:Wang J; Wen X; Liu J; Sun H
[Ti] Título:Mitochondrial Biogenesis Inhibitors for Anticancer Therapy: A Review of Recent Patents.
[So] Source:Recent Pat Anticancer Drug Discov;11(3):332-41, 2016.
[Is] ISSN:2212-3970
[Cp] País de publicação:United Arab Emirates
[La] Idioma:eng
[Ab] Resumo:Recent studies show that enhanced mitochondrial biogenesis can "fuel" the cancer cells to grow and migrate. It is therefore proposed that inhibiting the mitochondrial biogenesis could be a new approach to cancer therapy. This review summarizes recent patents and papers in the development of small molecule inhibitors of key regulators responsible for tumor mitochondrial biogenesis, including PPARγcoactivator-1α(PGC-1α), PPARγcoactivator-1ß, estrogen-related receptor family (ERRs), estrogen receptor α(ERα), mammalian target of rapamycin, c-Myc and PPARs.
[Mh] Termos MeSH primário: Antineoplásicos/uso terapêutico
Mitocôndrias/efeitos dos fármacos
Renovação Mitocondrial/efeitos dos fármacos
Neoplasias/tratamento farmacológico
Biogênese de Organelas
[Mh] Termos MeSH secundário: Animais
Antineoplásicos/química
Descoberta de Drogas
Seres Humanos
Mitocôndrias/metabolismo
Mitocôndrias/patologia
Estrutura Molecular
Terapia de Alvo Molecular
Neoplasias/metabolismo
Neoplasias/patologia
Patentes como Assunto
Transdução de Sinais/efeitos dos fármacos
Relação Estrutura-Atividade
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Antineoplastic Agents)
[Em] Mês de entrada:1703
[Cu] Atualização por classe:170313
[Lr] Data última revisão:
170313
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160419
[St] Status:MEDLINE


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[PMID]:26977249
[Au] Autor:Gumeni S; Trougakos IP
[Ad] Endereço:Department of Cell Biology and Biophysics, Faculty of Biology, National & Kapodistrian University of Athens, 157 84 Athens, Greece.
[Ti] Título:Cross Talk of Proteostasis and Mitostasis in Cellular Homeodynamics, Ageing, and Disease.
[So] Source:Oxid Med Cell Longev;2016:4587691, 2016.
[Is] ISSN:1942-0994
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Mitochondria are highly dynamic organelles that provide essential metabolic functions and represent the major bioenergetic hub of eukaryotic cell. Therefore, maintenance of mitochondria activity is necessary for the proper cellular function and survival. To this end, several mechanisms that act at different levels and time points have been developed to ensure mitochondria quality control. An interconnected highly integrated system of mitochondrial and cytosolic chaperones and proteases along with the fission/fusion machinery represents the surveillance scaffold of mitostasis. Moreover, nonreversible mitochondrial damage targets the organelle to a specific autophagic removal, namely, mitophagy. Beyond the organelle dynamics, the constant interaction with the ubiquitin-proteasome-system (UPS) has become an emerging aspect of healthy mitochondria. Dysfunction of mitochondria and UPS increases with age and correlates with many age-related diseases including cancer and neurodegeneration. In this review, we discuss the functional cross talk of proteostasis and mitostasis in cellular homeodynamics and the impairment of mitochondrial quality control during ageing, cancer, and neurodegeneration.
[Mh] Termos MeSH primário: Fenômenos Fisiológicos Celulares
Senescência Celular/fisiologia
Doença/etiologia
Homeostase/fisiologia
Mitocôndrias/fisiologia
Renovação Mitocondrial/fisiologia
Proteínas/metabolismo
[Mh] Termos MeSH secundário: Animais
Seres Humanos
Degradação Mitocondrial/fisiologia
Dobramento de Proteína
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T; REVIEW
[Nm] Nome de substância:
0 (Proteins)
[Em] Mês de entrada:1703
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160316
[St] Status:MEDLINE
[do] DOI:10.1155/2016/4587691


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[PMID]:26739215
[Au] Autor:Liang Q; Kobayashi S
[Ad] Endereço:Department of Biomedical Sciences, New York Institute of Technology College of Osteopathic Medicine, Old Westbury, NY, USA. Electronic address: qliang03@nyit.edu.
[Ti] Título:Mitochondrial quality control in the diabetic heart.
[So] Source:J Mol Cell Cardiol;95:57-69, 2016 Jun.
[Is] ISSN:1095-8584
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Diabetes is a well-known risk factor for heart failure. Diabetic heart damage is closely related to mitochondrial dysfunction and increased ROS generation. However, clinical trials have shown no effects of antioxidant therapies on heart failure in diabetic patients, suggesting that simply antagonizing existing ROS by antioxidants is not sufficient to reduce diabetic cardiac injury. A potentially more effective treatment strategy may be to enhance the overall capacity of mitochondrial quality control to maintain a pool of healthy mitochondria that are needed for supporting cardiac contractile function in diabetic patients. Mitochondrial quality is controlled by a number of coordinated mechanisms including mitochondrial fission and fusion, mitophagy and biogenesis. The mitochondrial damage consistently observed in the diabetic hearts indicates a failure of the mitochondrial quality control mechanisms. Recent studies have demonstrated a crucial role for each of these mechanisms in cardiac homeostasis and have begun to interrogate the relative contribution of insufficient mitochondrial quality control to diabetic cardiac injury. In this review, we will present currently available literature that links diabetic heart disease to the dysregulation of major mitochondrial quality control mechanisms. We will discuss the functional roles of these mechanisms in the pathogenesis of diabetic heart disease and their potentials for targeted therapeutical manipulation.
[Mh] Termos MeSH primário: Complicações do Diabetes
Cardiopatias/etiologia
Cardiopatias/metabolismo
Mitocôndrias Cardíacas/metabolismo
Miocárdio/metabolismo
[Mh] Termos MeSH secundário: Animais
Autofagia
Cardiopatias/patologia
Seres Humanos
Degradação Mitocondrial
Renovação Mitocondrial
Transdução de Sinais
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[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:160108
[St] Status:MEDLINE


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[PMID]:26654779
[Au] Autor:Stotland A; Gottlieb RA
[Ad] Endereço:The Cedars-Sinai Heart Institute, Barbra Streisand Women's Heart Center, Cedars-Sinai Medical Center, Los Angeles, CA, United States.
[Ti] Título:α-MHC MitoTimer mouse: In vivo mitochondrial turnover model reveals remarkable mitochondrial heterogeneity in the heart.
[So] Source:J Mol Cell Cardiol;90:53-8, 2016 Jan.
[Is] ISSN:1095-8584
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:In order to maintain an efficient, energy-producing network in the heart, dysfunctional mitochondria are cleared through the mechanism of autophagy, which is closely linked with mitochondrial biogenesis; these, together with fusion and fission comprise a crucial process known as mitochondrial turnover. Until recently, the lack of molecular tools and methods available to researchers has impeded in vivo investigations of turnover. To investigate the process at the level of a single mitochondrion, our laboratory has developed the MitoTimer protein. Timer is a mutant of DsRed fluorescent protein characterized by transition from green fluorescence to a more stable red conformation over 48 h, and its rate of maturation is stable under physiological conditions. We fused the Timer cDNA with the inner mitochondrial membrane signal sequence and placed it under the control of a cardiac-restricted promoter. This construct was used to create the alpha-MHC-MitoTimer mice. Surprisingly, initial analysis of the hearts from these mice demonstrated a high degree of heterogeneity in the ratio of red-to-green fluorescence of MitoTimer in cardiac tissue. Further, scattered solitary mitochondria within cardiomyocytes display a much higher red-to-green fluorescence (red-shifted) relative to other mitochondria in the cell, implying a block in import of newly synthesized MitoTimer likely due to lower membrane potential. These red-shifted mitochondria may represent older, senescent mitochondria. Concurrently, the cardiomyocytes also contain a subpopulation of mitochondria that display a lower red-to-green fluorescence (green-shifted) relative to other mitochondria, indicative of germinal mitochondria that are actively engaged in import of newly-synthesized mito-targeted proteins. These mitochondria can be isolated and sorted from the heart by flow cytometry for further analysis. Initial studies suggest that these mice represent an elegant tool for the investigation of mitochondrial turnover in the heart.
[Mh] Termos MeSH primário: Efeito Fundador
Proteínas Luminescentes/genética
Camundongos Transgênicos
Mitocôndrias Cardíacas/metabolismo
Renovação Mitocondrial
Proteínas Recombinantes de Fusão/genética
[Mh] Termos MeSH secundário: Animais
Linhagem Celular
Citometria de Fluxo
Expressão Gênica
Coração
Proteínas Luminescentes/metabolismo
Potencial da Membrana Mitocondrial
Camundongos
Mitocôndrias Cardíacas/ultraestrutura
Mioblastos/metabolismo
Mioblastos/ultraestrutura
Miocárdio/metabolismo
Miocárdio/ultraestrutura
Miócitos Cardíacos/metabolismo
Miócitos Cardíacos/ultraestrutura
Regiões Promotoras Genéticas
Sinais Direcionadores de Proteínas
Proteínas Recombinantes de Fusão/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL
[Nm] Nome de substância:
0 (Luminescent Proteins); 0 (Protein Sorting Signals); 0 (Recombinant Fusion Proteins); 0 (fluorescent protein 583)
[Em] Mês de entrada:1610
[Cu] Atualização por classe:171010
[Lr] Data última revisão:
171010
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:151215
[St] Status:MEDLINE


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[PMID]:26209316
[Au] Autor:Giordano C; Carelli V
[Ad] Endereço:1 Department of Radiology, Oncology and Pathology, Sapienza, University of Rome, Rome, Italy carla.giordano@uniroma1.it valerio.carelli@unibo.it.
[Ti] Título:Reply: Mitochondrial DNA copy number differentiates the Leber's hereditary optic neuropathy affected individuals from the unaffected mutation carriers.
[So] Source:Brain;139(Pt 1):e2, 2016 Jan.
[Is] ISSN:1460-2156
[Cp] País de publicação:England
[La] Idioma:eng
[Mh] Termos MeSH primário: DNA Mitocondrial/genética
Renovação Mitocondrial/genética
Atrofia Óptica Hereditária de Leber/diagnóstico
Atrofia Óptica Hereditária de Leber/genética
Penetrância
[Mh] Termos MeSH secundário: Feminino
Seres Humanos
Masculino
[Pt] Tipo de publicação:COMMENT; LETTER; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (DNA, Mitochondrial)
[Em] Mês de entrada:1605
[Cu] Atualização por classe:170220
[Lr] Data última revisão:
170220
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:150726
[St] Status:MEDLINE
[do] DOI:10.1093/brain/awv217



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