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Pesquisa : D08.811.682.690.708.410.500 [Categoria DeCS]
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[PMID]:28747460
[Au] Autor:Schallner N; Lieberum JL; Gallo D; LeBlanc RH; Fuller PM; Hanafy KA; Otterbein LE
[Ad] Endereço:From the Department of Surgery (N.S., J.-L.L., D.G., L.E.O.) and Department of Neurology (R.H.L., P.M.F., K.A.H.), Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA; Department of Anesthesiology and Critical Care, Medical Center-University Freiburg, Faculty of Medicine, German
[Ti] Título:Carbon Monoxide Preserves Circadian Rhythm to Reduce the Severity of Subarachnoid Hemorrhage in Mice.
[So] Source:Stroke;48(9):2565-2573, 2017 09.
[Is] ISSN:1524-4628
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND AND PURPOSE: Subarachnoid hemorrhage (SAH) is associated with a temporal pattern of stroke incidence. We hypothesized that natural oscillations in gene expression controlling circadian rhythm affect the severity of neuronal injury. We moreover predict that heme oxygenase-1 (HO-1/ ) and its product carbon monoxide (CO) contribute to the restoration of rhythm and neuroprotection. METHODS: Murine SAH model was used where blood was injected at various time points of the circadian cycle. Readouts included circadian clock gene expression, locomotor activity, vasospasm, neuroinflammatory markers, and apoptosis. In addition, cerebrospinal fluid and peripheral blood leukocytes from SAH patients and controls were analyzed for clock gene expression. RESULTS: Significant elevations in the clock genes , , and were observed in the hippocampus, cortex, and suprachiasmatic nucleus in mice subjected to SAH at zeitgeber time (ZT) 12 when compared with ZT2. Clock gene expression amplitude correlated with basal expression of HO-1, which was also significantly greater at ZT12. SAH animals showed a significant reduction in cerebral vasospasm, neuronal apoptosis, and microglial activation at ZT12 compared with ZT2. In animals with myeloid-specific HO-1 deletion ( ), , and expression was reduced in the suprachiasmatic nucleus, which correlated with increased injury. Treatment with low-dose CO rescued mice, restored , expression, and reduced neuronal apoptosis. CONCLUSIONS: Clock gene expression regulates, in part, the severity of SAH and requires myeloid HO-1 activity to clear the erythrocyte burden and inhibit neuronal apoptosis. Exposure to CO rescues the loss of HO-1 and thus merits further investigation in patients with SAH.
[Mh] Termos MeSH primário: Monóxido de Carbono/metabolismo
Ritmo Circadiano/genética
Expressão Gênica/efeitos dos fármacos
Heme Oxigenase-1/genética
Proteínas de Membrana/genética
Hemorragia Subaracnóidea/genética
[Mh] Termos MeSH secundário: Fatores de Transcrição ARNTL/genética
Animais
Apoptose
Fatores de Transcrição Hélice-Alça-Hélice Básicos/genética
Proteínas CLOCK/genética
Líquido Cefalorraquidiano/metabolismo
Heme Oxigenase-1/metabolismo
Seres Humanos
Imuno-Histoquímica
Inflamação
Leucócitos/metabolismo
Locomoção
Proteínas de Membrana/metabolismo
Camundongos
Proteínas do Tecido Nervoso/genética
Proteínas Circadianas Period/genética
Reação em Cadeia da Polimerase em Tempo Real
Reação em Cadeia da Polimerase Via Transcriptase Reversa
Índice de Gravidade de Doença
Núcleo Supraquiasmático/metabolismo
Vasoespasmo Intracraniano
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, U.S. GOV'T, NON-P.H.S.; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (ARNTL Transcription Factors); 0 (Arntl protein, mouse); 0 (Basic Helix-Loop-Helix Transcription Factors); 0 (Membrane Proteins); 0 (Nerve Tissue Proteins); 0 (Npas2 protein, mouse); 0 (PER2 protein, human); 0 (Per1 protein, mouse); 0 (Per2 protein, mouse); 0 (Period Circadian Proteins); 7U1EE4V452 (Carbon Monoxide); EC 1.14.14.18 (Heme Oxygenase-1); EC 1.14.14.18 (Hmox1 protein, mouse); EC 2.3.1.48 (CLOCK Proteins); EC 2.3.1.48 (Clock protein, mouse)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:180307
[Lr] Data última revisão:
180307
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170728
[St] Status:MEDLINE
[do] DOI:10.1161/STROKEAHA.116.016165


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[PMID]:29378209
[Au] Autor:Zhu M; Tian Y; Zhang H; Ma X; Shang B; Zhang J; Jiao Y; Zhang Y; Hu J; Wang Y
[Ad] Endereço:Department of Psychiatry and Psychology, The Second Affiliated Hospital of Xi'an Jiaotong University, Xi'an 710004, China.
[Ti] Título:Methylphenidate ameliorates hypoxia-induced mitochondrial damage in human neuroblastoma SH-SY5Y cells through inhibition of oxidative stress.
[So] Source:Life Sci;197:40-45, 2018 Mar 15.
[Is] ISSN:1879-0631
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:AIMS: Methylphenidate (MPH) is a dopamine-reuptake inhibitor approved for the treatment of attention-deficit/hyperactivity disorder (ADHD). Nonetheless, the cellular and molecular mechanisms of MPH are still unknown. We attempt to determine whether MPH protect neuron cells against oxidative stress by using human neuroblastoma SH-SY5Y cells. MAIN METHODS: The SH-SY5Y cells were cultured in normoxic and hypoxic conditions in the presence of different doses of MPH. Then, reactive oxygen species (ROS), malondialdehyde (MDA), glutathione (GSH), superoxide dismutase (SOD) and adenosine triphosphate (ATP) production were quantitatively measured by using flow cytometry or spectrophotometry. The mitochondrial ultrastructure of the cells was observed by electron microscope, and the function of mitochondrial was evaluated by measuring mitochondrial membrane potential (MMP) using flow cytometry. The levels of SOD and heme oxygenase-1 (HO-1) proteins were detected by Western blot. KEY FINDINGS: We found that low doses of MPH treatment (50-500 ng/mL) led to decreased ROS and MDA production (P<0.05), increased GSH and SOD as well as ATP concentration (P<0.05) in hypoxic SH-SY5Y cells. Additionally, low doses of MPH significantly inhibited mitochondrial swelling and decreased the percentage of JC-1 monomer positive cells. However, we did not observe the same effects of MPH in normoxia. SIGNIFICANCE: Our results show that low doses of MPH play protective roles in maintaining mitochondrial homeostasis in response to hypoxia-induced oxidative stress. Our findings may provide novel insight into the mechanisms of MPH in the treatment of ADHD, and shed light on the disease mechanisms of ADHD.
[Mh] Termos MeSH primário: Metilfenidato/farmacologia
Mitocôndrias/metabolismo
Neuroblastoma/metabolismo
Estresse Oxidativo/efeitos dos fármacos
[Mh] Termos MeSH secundário: Trifosfato de Adenosina/metabolismo
Hipóxia Celular/efeitos dos fármacos
Linhagem Celular Tumoral
Heme Oxigenase-1/metabolismo
Seres Humanos
Mitocôndrias/patologia
Proteínas de Neoplasias/metabolismo
Neuroblastoma/tratamento farmacológico
Neuroblastoma/patologia
Espécies Reativas de Oxigênio/metabolismo
Superóxido Dismutase/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Neoplasm Proteins); 0 (Reactive Oxygen Species); 207ZZ9QZ49 (Methylphenidate); 8L70Q75FXE (Adenosine Triphosphate); EC 1.14.14.18 (HMOX1 protein, human); EC 1.14.14.18 (Heme Oxygenase-1); EC 1.15.1.1 (Superoxide Dismutase)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180301
[Lr] Data última revisão:
180301
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180130
[St] Status:MEDLINE


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[PMID]:29222050
[Au] Autor:Li N; Cao M; Yi S; Cheng J; Wang L; Tao Y; Wu D; Peng J; Zhang M; Qi P; Zhao J
[Ad] Endereço:Key Laboratory of Bio-Resource and Eco-Environment of Ministry of Education, College of Life Sciences, Sichuan University, Chengdu 610065, Sichuan, PR China.
[Ti] Título:Effects of the RNA-binding protein, KSRP, on innate immune response against Helicobacter pylori infection in mice.
[So] Source:Biochem Biophys Res Commun;495(2):1573-1579, 2018 01 08.
[Is] ISSN:1090-2104
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Helicobacter pylori (H. pylori) contributes to various gastric diseases such as chronic gastritis, gastric ulcer, and gastric carcinoma. Host innate immune response against the pathogen plays a significant role in elimination of pathogen infection. Importantly, pathogen elimination is closely related to numerous inflammatory-related genes that participate in complex biological response of cells to harmful stimuli. Here we studied effects of the KH-type splicing regulatory protein (KSRP), a RNA-binding protein, on innate immune response against H. pylori infection. We found that H. pylori infection downregulated KSRP expression directly, and that KSRP overexpression repressed upregulation of CXCL-2 expression induced by H. pylori and facilitated H. pylori proliferation in vitro. Similarly, KSRP overexpression in H. pylori mice also facilitated H. pylori proliferation and colonization, and induced more severe gastric mucosal damage. Intriguingly, CXCL-2 and HMOX-1 were upregulated in H. pylori infected mice after KSRP overexpression. This difference in expression of these genes implicated that KSRP was closely associated with and directly participated in the innate immune response against H. pylori. These results were beneficial for understanding the in vivo function of KSRP on innate immune response against pathogen infection.
[Mh] Termos MeSH primário: Infecções por Helicobacter/imunologia
Helicobacter pylori
Proteínas de Ligação a RNA/imunologia
Transativadores/imunologia
[Mh] Termos MeSH secundário: Animais
Linhagem Celular
Quimiocina CXCL2/genética
Regulação para Baixo
Feminino
Gastrite/genética
Gastrite/imunologia
Gastrite/patologia
Infecções por Helicobacter/genética
Infecções por Helicobacter/patologia
Helicobacter pylori/genética
Helicobacter pylori/imunologia
Helicobacter pylori/patogenicidade
Heme Oxigenase-1/genética
Seres Humanos
Imunidade Inata/genética
Masculino
Proteínas de Membrana/genética
Camundongos
Camundongos Endogâmicos BALB C
Proteínas de Ligação a RNA/genética
Receptor 2 Toll-Like/genética
Transativadores/genética
Regulação para Cima
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (CXCL2 protein, human); 0 (Chemokine CXCL2); 0 (Cxcl2 protein, mouse); 0 (KHSRP protein, human); 0 (KSRP protein, mouse); 0 (Membrane Proteins); 0 (RNA-Binding Proteins); 0 (TLR2 protein, human); 0 (Tlr2 protein, mouse); 0 (Toll-Like Receptor 2); 0 (Trans-Activators); EC 1.14.14.18 (HMOX1 protein, human); EC 1.14.14.18 (Heme Oxygenase-1); EC 1.14.14.18 (Hmox1 protein, mouse)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180220
[Lr] Data última revisão:
180220
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171210
[St] Status:MEDLINE


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[PMID]:29305861
[Au] Autor:Jeong B; Kim HR; Choi NS; Park BS; Eom H; Park JW; Kim JG; Lee BJ
[Ad] Endereço:Department of Biological Sciences, College of Natural Sciences, University of Ulsan, Ulsan 44610, South Korea.
[Ti] Título:Role of thyroid transcription factor-1 in transcriptional regulation of heme oxygenase-1.
[So] Source:Biochem Biophys Res Commun;496(1):147-152, 2018 01 29.
[Is] ISSN:1090-2104
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Here, we report thyroid transcription factor 1 (TTF-1) as an important transcription factor for the expression of heme oxygenase-1 (HO-1). HO-1 is a well-known cytoprotective enzyme against inflammation. We observed that HO-1 co-expressed with TTF-1 in mouse hypothalamic cells. Results from luciferase and chromatin immunoprecipitation assays revealed that TTF-1 directly activated HO-1 transcription by binding to binding domains in the 5'-flanking region of the HO-1 gene. A proinflammatory cytokine, tumor necrosis factor-alpha (TNF-α), induced nuclear translocation of TTF-1 and increased binding affinity of TTF-1 to its binding sites on the HO-1 gene. HO-1 mRNA increased with TTF-1 overexpression but decreased with RNA interference of TTF-1 expression in rat astroglial C6 cells. Together with results showing involvement of TTF-1 in the TNF-α-induced increase in interleukin 1 beta and monocyte chemotactic protein 1 production, this study suggests that TTF-1 plays an important role in the mouse hypothalamus TNF-α-induced inflammatory response for regulating HO-1 gene expression.
[Mh] Termos MeSH primário: Regulação da Expressão Gênica/fisiologia
Heme Oxigenase-1/metabolismo
Hipotálamo/metabolismo
Proteínas de Membrana/metabolismo
Fator Nuclear 1 de Tireoide/metabolismo
Ativação Transcricional/fisiologia
[Mh] Termos MeSH secundário: Animais
Linhagem Celular
Masculino
Camundongos
Camundongos Endogâmicos C57BL
Ratos
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Membrane Proteins); 0 (Thyroid Nuclear Factor 1); EC 1.14.14.18 (Heme Oxygenase-1); EC 1.14.14.18 (Hmox1 protein, mouse)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180215
[Lr] Data última revisão:
180215
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180107
[St] Status:MEDLINE


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[PMID]:29277609
[Au] Autor:An X; Shang F
[Ad] Endereço:Intensive Care Unit, Huai'an First People's Hospital, Nanjing Medical University, 6 Beijing Road West, Huai'an, Jiangsu 223300, PR China.
[Ti] Título:RA-XII exerts anti-oxidant and anti-inflammatory activities on lipopolysaccharide-induced acute renal injury by suppressing NF-κB and MAPKs regulated by HO-1/Nrf2 pathway.
[So] Source:Biochem Biophys Res Commun;495(3):2317-2323, 2018 01 15.
[Is] ISSN:1090-2104
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Acute kidney injury (AKI) is an abrupt loss of kidney function and severe AKI needs renal replacement therapeutic strategy and has high mortality. RA-XII is a natural cyclopeptide, isolated from the traditional Chinese medicine Rubia yunnanensis, exerting anti-inflammatory and anti-tumor activities. The present study aimed to explore the effects of RA-XII on LPS-induced ACI and the underlying molecular mechanism in TCMK-1 cells in vitro. The results indicated that RA-XII delayed the animal death caused by LPS in mice. The kidney histological changes were markedly attenuated by RA-XII. RA-XII also reduced the serum uric acid, creatinine, BUN and renal 8-OHdG. In addition, RA-XII suppressed LPS-induced oxidative stress in kidney, as evidenced by the up-regulation of superoxide dismutase (SOD), catalase (CAT) and glutathione (GSH) levels, and the down-regulation of malondialdehyde (MDA) levels. Additionally, RA-XII enhanced heme oxygenase (HO)-1 and nuclear factor erythroid 2-related factor 2 (Nrf2) expressions in renal tissue sections. Further, RA-XII reduced the release of pro-inflammatory cytokines, including tumor necrosis factor-alpha (TNF-α), interleukin-1ß (IL-1ß), IL-6 and IL-18, in renal, which was linked to the inhibition of inhibitor of alpha/nuclear factor kappa B (IκBα/NF-κB) and mitogen-activated protein kinases (MAPKs) pathways. The in vitro study illustrated that the anti-inflammatory effects of RA-XII were partially reversed following Nrf2 and HO-1 inhibition. Together, these findings strongly suggested that RA-XII is a potential agent against acute kidney injury.
[Mh] Termos MeSH primário: Lesão Renal Aguda/tratamento farmacológico
Lesão Renal Aguda/imunologia
Heme Oxigenase-1/imunologia
Sistema de Sinalização das MAP Quinases/imunologia
Proteínas de Membrana/imunologia
Fator 2 Relacionado a NF-E2/imunologia
NF-kappa B/imunologia
Peptídeos Cíclicos/administração & dosagem
[Mh] Termos MeSH secundário: Lesão Renal Aguda/induzido quimicamente
Animais
Anti-Inflamatórios/administração & dosagem
Antioxidantes/administração & dosagem
Relação Dose-Resposta a Droga
Lipopolissacarídeos
Sistema de Sinalização das MAP Quinases/efeitos dos fármacos
Camundongos
Camundongos Endogâmicos C57BL
Resultado do Tratamento
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Anti-Inflammatory Agents); 0 (Antioxidants); 0 (Lipopolysaccharides); 0 (Membrane Proteins); 0 (NF-E2-Related Factor 2); 0 (NF-kappa B); 0 (Nfe2l2 protein, mouse); 0 (Peptides, Cyclic); 143343-98-0 (RA XII); EC 1.14.14.18 (Heme Oxygenase-1); EC 1.14.14.18 (Hmox1 protein, mouse)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180214
[Lr] Data última revisão:
180214
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171227
[St] Status:MEDLINE


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[PMID]:28746897
[Au] Autor:Song W; Cressatti M; Zukor H; Liberman A; Galindez C; Schipper HM
[Ad] Endereço:Bloomfield Centre for Research in Aging, Lady Davis Institute, Jewish General Hospital, Montreal, Quebec, Canada.
[Ti] Título:Parkinsonian features in aging GFAP.HMOX1 transgenic mice overexpressing human HO-1 in the astroglial compartment.
[So] Source:Neurobiol Aging;58:163-179, 2017 Oct.
[Is] ISSN:1558-1497
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Epigenetic influences mediating brain iron deposition, oxidative mitochondrial injury, and macroautophagy in Parkinson disease and related conditions remain enigmatic. Here, we show that selective overexpression of the stress protein, heme oxygenase-1 (HO-1) in astrocytes of GFAP.HMOX1 transgenic mice between 8.5 and 19 months of age results in nigrostriatal hypodopaminergia associated with locomotor incoordination and stereotypy; downregulation of tyrosine hydroxylase, DAT, LMX1B, Nurr1, Pitx3 and DJ-1 mRNA and/or protein; overproduction of α-synuclein and ubiquitin; oxidative stress; basal ganglia siderosis; mitochondrial damage/mitophagy; and augmented GABAergic systems (increased GABA, GAD67 and reelin). The neurophenotype of these GFAP.HMOX1 mice is highly consistent with parkinsonism and differs dramatically from the schizophrenia-like features previously documented in younger GFAP.HMOX1 mice. Common stressors may elicit either early-onset developmental (schizophrenia) or later-life degenerative (PD) brain disorders depending on whether the glial HO-1 response is engaged prior to or following the maturation of dopaminergic circuitry. Curtailment of glial HO-1 transduction at strategic points of the life course may confer neuroprotection in human degenerative and developmental central nervous system disorders.
[Mh] Termos MeSH primário: Astrócitos/enzimologia
Expressão Gênica/genética
Proteína Glial Fibrilar Ácida/genética
Heme Oxigenase-1/genética
Heme Oxigenase-1/metabolismo
Proteínas de Membrana/genética
Doença de Parkinson/genética
[Mh] Termos MeSH secundário: Animais
Autofagia
Células Cultivadas
Dopamina/metabolismo
Seres Humanos
Camundongos Transgênicos
Mitocôndrias/patologia
Estresse Oxidativo
Doença de Parkinson/metabolismo
Doença de Parkinson/patologia
alfa-Sinucleína/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Glial Fibrillary Acidic Protein); 0 (Membrane Proteins); 0 (alpha-Synuclein); EC 1.14.14.18 (HMOX1 protein, human); EC 1.14.14.18 (Heme Oxygenase-1); EC 1.14.14.18 (Hmox1 protein, mouse); VTD58H1Z2X (Dopamine)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180214
[Lr] Data última revisão:
180214
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170727
[St] Status:MEDLINE


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[PMID]:28466968
[Au] Autor:Geard A; Pule GD; Chetcha Chemegni B; Ngo Bitoungui VJ; Kengne AP; Chimusa ER; Wonkam A
[Ad] Endereço:Division of Human Genetics, Department of Pathology, Faculty of Health Sciences, University of Cape Town, Cape Town, South Africa.
[Ti] Título:Clinical and genetic predictors of renal dysfunctions in sickle cell anaemia in Cameroon.
[So] Source:Br J Haematol;178(4):629-639, 2017 08.
[Is] ISSN:1365-2141
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Micro-albuminuria and glomerular hyperfiltration are primary indicators of renal dysfunctions in Sickle Cell Disease (SCD), with more severe manifestations previously associated with variants in APOL1 and HMOX1 among African Americans. We have investigated 413 SCD patients from Cameroon. Anthropometric variables, haematological indices, crude albuminuria, albumin-to-creatinine ratio (ACR) and estimated glomerular filtration rate (eGFR) were measured. Patients were genotyped for 3·7 kb alpha-globin gene (HBA1/HBA2) deletion, and for variants in APOL1 (G1/G2; rs60910145, rs73885319, rs71785313) and HMOX1 (rs3074372, rs743811). The median age was 15 years; the majority presented with micro-albuminuria (60·9%; n = 248), and approximately half with glomerular hyperfiltration (49·5%; n = 200). Age, male sex, haemoglobin level, leucocyte count, mean corpuscular volume, blood pressure, body mass index and creatinine levels significantly affected albuminuria and/or eGFR. Co-inheritance of alpha-thalassaemia was protective against macro-albuminuria (P = 0·03). APOL1 G1/G2 risk variants were significantly associated with the ACR (P = 0·01) and borderline with eGFR (P = 0·07). HMOX1 - rs743811 was borderline associated with micro-albuminuria (P = 0·07) and macro-albuminuria (P = 0·06). The results revealed a high proportion of micro-albuminuria and glomerular hyperfiltration among Cameroonian SCD patients, and support the possible use of targeted genetic biomarkers for risks assessment.
[Mh] Termos MeSH primário: Anemia Falciforme/complicações
Insuficiência Renal/etiologia
[Mh] Termos MeSH secundário: Adolescente
Adulto
Albuminúria/epidemiologia
Albuminúria/etiologia
Albuminúria/genética
Anemia Falciforme/epidemiologia
Anemia Falciforme/genética
Antropometria/métodos
Apolipoproteína L1
Apolipoproteínas/genética
Camarões/epidemiologia
Criança
Pré-Escolar
Feminino
Deleção de Genes
Predisposição Genética para Doença
Variação Genética
Taxa de Filtração Glomerular/genética
Hemoglobina A Glicada/genética
Heme Oxigenase-1/genética
Seres Humanos
Lipoproteínas HDL/genética
Masculino
Meia-Idade
Estudos Prospectivos
Insuficiência Renal/epidemiologia
Insuficiência Renal/genética
Fatores de Risco
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (APOL1 protein, human); 0 (Apolipoprotein L1); 0 (Apolipoproteins); 0 (Glycated Hemoglobin A); 0 (Lipoproteins, HDL); EC 1.14.14.18 (HMOX1 protein, human); EC 1.14.14.18 (Heme Oxygenase-1)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:180209
[Lr] Data última revisão:
180209
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170504
[St] Status:MEDLINE
[do] DOI:10.1111/bjh.14724


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[PMID]:29216642
[Au] Autor:Yang W; Huang J; Xiao B; Liu Y; Zhu Y; Wang F; Sun S
[Ti] Título:Taurine Protects Mouse Spermatocytes from Ionizing Radiation-Induced Damage Through Activation of Nrf2/HO-1 Signaling.
[So] Source:Cell Physiol Biochem;44(4):1629-1639, 2017.
[Is] ISSN:1421-9778
[Cp] País de publicação:Switzerland
[La] Idioma:eng
[Ab] Resumo:BACKGROUND/AIMS: The increasing prevalence of ionizing radiation exposure has inevitably raised public concern over the potential detrimental effects of ionizing radiation on male reproductive system function. The detection of drug candidates to prevent reproductive system from damage caused by ionizing radiation is urgent. We aimed to investigate the protective role of taurine on the injury of mouse spermatocyte-derived cells (GC-2) subjected to ionizing radiation. METHODS: mouse spermatocytes (GC-2 cells) were exposed to ionizing radiation with or without treatment of Taurine. The effect of ionizing radiation and Taurine treatment on GC-2 cells were evaluated by cell viability assay (CCK8), cell cycle and apoptosis. The relative protein abundance change was determined by Western blotting. The siRNA was used to explore whether Nrf2 signaling was involved in the cytoprotection of Taurine. RESULTS: Taurine significantly inhibited the decrease of cell viability, percentage of apoptotic cells and cell cycle arrest induced by ionizing radiation. Western blot analysis showed that taurine significantly limited the ionizing radiation-induced down-regulation of CyclinB1 and CDK1, and suppressed activation of Fas/FasL system pathway. In addition, taurine treatment significantly increased the expression of Nrf2 and HO-1 in GC-2 cells exposed to ionizing radiation, two components in antioxidant pathway. The above cytoprotection of Taurine was blocked by siNrf2. CONCLUSION: Our results demonstrate that taurine has the potential to effectively protect GC-2 cells from ionizing radiation- triggered damage via upregulation of Nrf2/HO-1 signaling.
[Mh] Termos MeSH primário: Heme Oxigenase-1/metabolismo
Fator 2 Relacionado a NF-E2/metabolismo
Substâncias Protetoras/farmacologia
Radiação Ionizante
Transdução de Sinais/efeitos dos fármacos
Taurina/farmacologia
[Mh] Termos MeSH secundário: Animais
Apoptose/efeitos dos fármacos
Apoptose/efeitos da radiação
Proteína Quinase CDC2/metabolismo
Pontos de Checagem do Ciclo Celular/efeitos dos fármacos
Pontos de Checagem do Ciclo Celular/efeitos da radiação
Linhagem Celular
Ciclina B1/metabolismo
Regulação para Baixo/efeitos dos fármacos
Proteína Ligante Fas/metabolismo
Masculino
Camundongos
Fator 2 Relacionado a NF-E2/antagonistas & inibidores
Fator 2 Relacionado a NF-E2/genética
Estresse Oxidativo/efeitos dos fármacos
Estresse Oxidativo/efeitos da radiação
Interferência de RNA
RNA Interferente Pequeno/metabolismo
Transdução de Sinais/efeitos da radiação
Espermatócitos/citologia
Espermatócitos/efeitos dos fármacos
Espermatócitos/metabolismo
Receptor fas/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Cyclin B1); 0 (Fas Ligand Protein); 0 (Fas protein, mouse); 0 (Fasl protein, mouse); 0 (NF-E2-Related Factor 2); 0 (Protective Agents); 0 (RNA, Small Interfering); 0 (fas Receptor); 1EQV5MLY3D (Taurine); EC 1.14.14.18 (Heme Oxygenase-1); EC 2.7.11.22 (CDC2 Protein Kinase)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180118
[Lr] Data última revisão:
180118
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171208
[St] Status:MEDLINE
[do] DOI:10.1159/000485762


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[PMID]:27778153
[Au] Autor:Atsaves V; Detsika MG; Poulaki E; Gakiopoulou H; Lianos EA
[Ad] Endereço:1st Division of Critical Care Medicine and Pulmonary Services, 'Evangelismos' Hospital, Department of Medicine, National and Kapodistrian University of Athens, School of Health Sciences, Athens, Greece.
[Ti] Título:Phenotypic characterization of a novel HO-1 depletion model in the rat.
[So] Source:Transgenic Res;26(1):51-64, 2017 02.
[Is] ISSN:1573-9368
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Although the protective role of HO-1 induction in various forms of kidney disease is well established, mechanisms other than heme catabolism to biliverdin, bilirubin and carbon monoxide have recently been identified. Unraveling these mechanisms requires the generation of appropriate animal models. The present study describes the generation of a HO-1 deficient Hmox1 rat model and characterizes its renal and extrarenal phenotype. Hmox1 rats had growth retardation and splenomegaly compared to their Hmox1 littermates. Focal segmental glomerulosclerosis-type lesions and interstitial inflammatory infiltrates were prominent morphologic findings and were associated with increased blood urea nitrogen, serum creatinine and albuminuria. There was no increase in iron deposition in glomeruli, tubules or interstitium. Iron deposition in spleen and liver was reduced. Electron microscopic examination of glomeruli revealed edematous podocytes with scant areas of foot process effacement but otherwise well preserved processes and slit-diaphragms. Of the filtration barrier proteins examined, ß-catenin expression was markedly reduced both in glomeruli and extrarenal tissues. Since the rat is the preferred laboratory animal in experimental physiology and pathophysiology, the rat model of HO-1 deficiency may provide a novel tool for investigation of the role of this enzyme in renal function and disease.
[Mh] Termos MeSH primário: Heme Oxigenase-1/genética
Nefropatias/genética
Estresse Oxidativo/genética
[Mh] Termos MeSH secundário: Animais
Creatinina/sangue
Técnicas de Inativação de Genes
Ferro/metabolismo
Rim/metabolismo
Rim/patologia
Nefropatias/sangue
Nefropatias/patologia
Podócitos/metabolismo
Ratos
Baço/metabolismo
Baço/patologia
beta Catenina/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (beta Catenin); AYI8EX34EU (Creatinine); E1UOL152H7 (Iron); EC 1.14.14.18 (Heme Oxygenase-1)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180117
[Lr] Data última revisão:
180117
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161026
[St] Status:MEDLINE
[do] DOI:10.1007/s11248-016-9986-9


  10 / 6636 MEDLINE  
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[PMID]:29203625
[Au] Autor:Kaartokallio T; Utge S; Klemetti MM; Paananen J; Pulkki K; Romppanen J; Tikkanen I; Heinonen S; Kajantie E; Kere J; Kivinen K; Pouta A; Lakkisto P; Laivuori H
[Ad] Endereço:From Medical and Clinical Genetics, Helsinki University Hospital (T.K., S.U., M.M.K., H.L.), Obstetrics and Gynaecology, Helsinki University Hospital (M.M.K., S.H.), Abdominal Center, Nephrology, Helsinki University Hospital (I.T.), Clinical Chemistry and Hematology, Helsinki University Hospital (P.
[Ti] Título:Fetal Microsatellite in the Heme Oxygenase 1 Promoter Is Associated With Severe and Early-Onset Preeclampsia.
[So] Source:Hypertension;71(1):95-102, 2018 01.
[Is] ISSN:1524-4563
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Preeclampsia is a vascular pregnancy disorder that often involves impaired placental development. HO-1 (heme oxygenase 1, encoded by ) is a stress response enzyme crucial for endothelial and placental function. Long version of the guanine-thymine (GT ) microsatellite in the promoter decreases HO-1 expression, and the long maternal repeat is associated with late-onset preeclampsia. Our aim was to study whether the length of fetal repeat is associated with mother's preeclampsia, whether the length of fetal and maternal repeats affect HO-1 levels in placenta and maternal serum, and whether HO-1 levels are altered in preeclampsia. We genotyped the repeat in the cord blood of 609 preeclamptic and 745 nonpreeclamptic neonates. HO-1 levels were measured in 36 placental samples, and in the first (222 cases/243 controls) and third (176 cases/53 controls) pregnancy trimester serum samples using enzyme-linked immunosorbent assay. The long fetal GT repeat was associated with preeclampsia and its severe and early-onset subtypes. Interaction analysis suggested the maternal and fetal effects to be independent. Placental or serum HO-1 levels were not altered in preeclamptics, possibly reflecting heterogeneity of preeclampsia. Carriers of the long fetal and maternal repeats had lower placental and serum HO-1 levels, respectively, providing functional evidence for the association. We conclude that the long fetal GT repeat may increase mother's risk for especially severe and early-onset preeclampsia. The fetal and maternal risk alleles likely predispose to different disease subtypes.
[Mh] Termos MeSH primário: Feto/fisiologia
Heme Oxigenase-1/genética
Repetições de Microssatélites/genética
Placentação/genética
Pré-Eclâmpsia
[Mh] Termos MeSH secundário: Adulto
Feminino
Predisposição Genética para Doença
Heme Oxigenase-1/metabolismo
Seres Humanos
Pré-Eclâmpsia/diagnóstico
Pré-Eclâmpsia/genética
Pré-Eclâmpsia/fisiopatologia
Gravidez
Regiões Promotoras Genéticas/fisiologia
Índice de Gravidade de Doença
Fatores de Tempo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
EC 1.14.14.18 (HMOX1 protein, human); EC 1.14.14.18 (Heme Oxygenase-1)
[Em] Mês de entrada:1712
[Cu] Atualização por classe:180113
[Lr] Data última revisão:
180113
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171206
[St] Status:MEDLINE
[do] DOI:10.1161/HYPERTENSIONAHA.117.10425



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