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[PMID]:27773823
[Au] Autor:Iannucci LF; Sun J; Singh BK; Zhou J; Kaddai VA; Lanni A; Yen PM; Sinha RA
[Ad] Endereço:Dipartimento di Scienze e Tecnologie Ambientali, Biologiche e Farmaceutiche, Seconda Università degli Studi di Napoli, Caserta, Italy.
[Ti] Título:Short chain fatty acids induce UCP2-mediated autophagy in hepatic cells.
[So] Source:Biochem Biophys Res Commun;480(3):461-467, 2016 Nov 18.
[Is] ISSN:1090-2104
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Short-chain fatty acids (SCFAs) are gut microbial fermentation products derived from dietary fiber sources. Although depletion of gut microflora has been linked to the development of liver disease, the direct effects of SCFAs on intracellular hepatic processes are not well understood. In this study, we demonstrated that the SCFAs, propionate and butyrate, regulated autophagic flux in hepatic cells in a cell-autonomous manner. Induction of autophagy by SCFAs required PPARγ stimulation of Uncoupling Protein 2 (UCP2) expression that was associated with reduced intracellular ATP levels and activation of PRKAA1/AMPK (protein kinase, AMP-activated, alpha 1 catalytic subunit). In addition, elimination of gut flora by chronic antibiotic treatment diminished basal hepatic autophagy in mice suggesting that gut microbiota can regulate hepatic autophagy. These findings provide novel insights into the interplay between diet, gut microbiota, short chain fatty acids, and hepatic autophagic signaling.
[Mh] Termos MeSH primário: Autofagia/fisiologia
Microbioma Gastrointestinal/fisiologia
Hepatócitos/citologia
Hepatócitos/metabolismo
Proteína Desacopladora 2/metabolismo
[Mh] Termos MeSH secundário: Animais
Butiratos/metabolismo
Linhagem Celular
Células Cultivadas
Ácidos Graxos/metabolismo
Masculino
Camundongos
Camundongos Endogâmicos C57BL
Propionatos/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Butyrates); 0 (Fatty Acids); 0 (Propionates); 0 (Uncoupling Protein 2)
[Em] Mês de entrada:1705
[Cu] Atualização por classe:171127
[Lr] Data última revisão:
171127
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161106
[St] Status:MEDLINE


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[PMID]:28771482
[Au] Autor:Heise V; Zsoldos E; Suri S; Sexton C; Topiwala A; Filippini N; Mahmood A; Allan CL; Singh-Manoux A; Kivimäki M; Mackay CE; Ebmeier KP
[Ad] Endereço:OHBA, Oxford Centre for Human Brain Activity, University of Oxford, Oxford, United Kingdom.
[Ti] Título:Uncoupling protein 2 haplotype does not affect human brain structure and function in a sample of community-dwelling older adults.
[So] Source:PLoS One;12(8):e0181392, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Uncoupling protein 2 (UCP2) is a mitochondrial membrane protein that plays a role in uncoupling electron transport from adenosine triphosphate (ATP) formation. Polymorphisms of the UCP2 gene in humans affect protein expression and function and have been linked to survival into old age. Since UCP2 is expressed in several brain regions, we investigated in this study whether UCP2 polymorphisms might 1) affect occurrence of neurodegenerative or mental health disorders and 2) affect measures of brain structure and function. We used structural magnetic resonance imaging (MRI), diffusion-weighted MRI and resting-state functional MRI in the neuroimaging sub-study of the Whitehall II cohort. Data from 536 individuals aged 60 to 83 years were analyzed. No association of UCP2 polymorphisms with the occurrence of neurodegenerative disorders or grey and white matter structure or resting-state functional connectivity was observed. However, there was a significant effect on occurrence of mood disorders in men with the minor alleles of -866G>A (rs659366) and Ala55Val (rs660339)) being associated with increasing odds of lifetime occurrence of mood disorders in a dose dependent manner. This result was not accompanied by effects of UCP2 polymorphisms on brain structure and function, which might either indicate that the sample investigated here was too small and underpowered to find any significant effects, or that potential effects of UCP2 polymorphisms on the brain are too subtle to be picked up by any of the neuroimaging measures used.
[Mh] Termos MeSH primário: Encéfalo/citologia
Encéfalo/fisiologia
Haplótipos
Habitação
Distribuição Espacial da População
Proteína Desacopladora 2/genética
[Mh] Termos MeSH secundário: Idoso
Idoso de 80 Anos ou mais
Encéfalo/diagnóstico por imagem
Feminino
Substância Cinzenta/citologia
Substância Cinzenta/diagnóstico por imagem
Substância Cinzenta/fisiologia
Seres Humanos
Imagem por Ressonância Magnética
Masculino
Transtornos Mentais/genética
Meia-Idade
Doenças Neurodegenerativas/genética
Neuroimagem
Polimorfismo Genético
Substância Branca/citologia
Substância Branca/diagnóstico por imagem
Substância Branca/fisiologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Uncoupling Protein 2)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170906
[Lr] Data última revisão:
170906
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170804
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0181392


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[PMID]:28683125
[Au] Autor:Yan P; Chen K; Wang Q; Yang D; Li; Yang Y
[Ad] Endereço:Department of Cardiology, Chengdu Military General Hospital, Chengdu, Sichuan, P.R. China.
[Ti] Título:UCP-2 is involved in angiotensin-II-induced abdominal aortic aneurysm in apolipoprotein E-knockout mice.
[So] Source:PLoS One;12(7):e0179743, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:UCP-2 shows an important role in modulating of mitochondrial membrane potential and cell apoptosis. Whether or not UCP-2 could been a critical factor in preventing AAA formation is not known. We report that UCP-2 protein and mRNA expression were significantly higher in Ang-â…¡-induced AAA of mice. The incident rate of AAA in UCP-2-/-ApoE-/- mice after Ang-â…¡treatment was higher than the rate in the UCP-2+/+ApoE-/- mice. The abdominal aorta from UCP-2-/-ApoE-/- mice showed the medial hypertrophy, fragmentation of elastic lamellas and depletion of α-SMA. The NADPH oxidase activity and level of MDA was significantly higher in UCP-2-/-ApoE-/- mice than UCP-2+/+ApoE-/- or WT mice. Besides, the SOD activity is increased in UCP-2+/+ApoE-/- mice as compared with WT mice, whereas deficiency of UCP-2 decreased the increasing SOD activity in Ang-â…¡ treated ApoE-/- mice. UCP-2 knockout up-regulated the MMP2 and MMP9 expression in aortic aneurysm. Ang-â…¡ induced apoptosis of VSMCs was increased in UCP-2-/-ApoE-/- mice. And the expression of eNOS in vascular tissue from UCP-2-/-ApoE-/- mice is lower than WT and UCP-2+/+ApoE-/- mice. This study provides a mechanism by which UCP-2, via anti-oxidants and anti-apoptosis, participates in the preventing of AAA formation.
[Mh] Termos MeSH primário: Angiotensina II/farmacologia
Aorta Abdominal/efeitos dos fármacos
Aneurisma da Aorta Abdominal/genética
Apolipoproteínas E/genética
Proteína Desacopladora 2/genética
[Mh] Termos MeSH secundário: Actinas/genética
Actinas/metabolismo
Animais
Aorta Abdominal/metabolismo
Aorta Abdominal/patologia
Aneurisma da Aorta Abdominal/induzido quimicamente
Aneurisma da Aorta Abdominal/metabolismo
Aneurisma da Aorta Abdominal/patologia
Apolipoproteínas E/deficiência
Apoptose/efeitos dos fármacos
Células Endoteliais/efeitos dos fármacos
Células Endoteliais/metabolismo
Células Endoteliais/patologia
Regulação da Expressão Gênica
Malondialdeído/metabolismo
Metaloproteinase 2 da Matriz/genética
Metaloproteinase 2 da Matriz/metabolismo
Metaloproteinase 9 da Matriz/genética
Metaloproteinase 9 da Matriz/metabolismo
Potencial da Membrana Mitocondrial/efeitos dos fármacos
Camundongos
Camundongos Endogâmicos C57BL
Camundongos Knockout
NADPH Oxidases/genética
NADPH Oxidases/metabolismo
Óxido Nítrico Sintase Tipo III/genética
Óxido Nítrico Sintase Tipo III/metabolismo
RNA Mensageiro/genética
RNA Mensageiro/metabolismo
Transdução de Sinais
Superóxido Dismutase/genética
Superóxido Dismutase/metabolismo
Proteína Desacopladora 2/deficiência
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Actins); 0 (Apolipoproteins E); 0 (RNA, Messenger); 0 (Ucp2 protein, mouse); 0 (Uncoupling Protein 2); 0 (alpha-smooth muscle actin, mouse); 11128-99-7 (Angiotensin II); 4Y8F71G49Q (Malondialdehyde); EC 1.14.13.39 (Nitric Oxide Synthase Type III); EC 1.14.13.39 (Nos3 protein, mouse); EC 1.15.1.1 (Superoxide Dismutase); EC 1.6.3.- (NADPH Oxidases); EC 3.4.24.24 (Matrix Metalloproteinase 2); EC 3.4.24.24 (Mmp2 protein, mouse); EC 3.4.24.35 (Matrix Metalloproteinase 9); EC 3.4.24.35 (Mmp9 protein, mouse)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170707
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0179743


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[PMID]:28574619
[Au] Autor:Sreedhar A; Lefort J; Petruska P; Gu X; Shi R; Miriyala S; Panchatcharam M; Zhao Y
[Ad] Endereço:Department of Pharmacology, Toxicology and Neuroscience, LSU Health Sciences Center in Shreveport, Shreveport, Louisiana.
[Ti] Título:UCP2 upregulation promotes PLCγ-1 signaling during skin cell transformation.
[So] Source:Mol Carcinog;56(10):2290-2300, 2017 Oct.
[Is] ISSN:1098-2744
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Uncoupling protein 2 (UCP2), whose physiological role is to decrease mitochondrial membrane potential and reactive oxygen species (ROS) production, is often overexpressed in human cancers. UCP2 upregulation has recently been proposed as a novel survival mechanism for cancer cells. However, until now, how exactly UCP2 promotes tumorigenesis remains inconclusive. Based on a widely used skin cell transformation model, our data demonstrated that UCP2 differentially regulated ROS. UCP2 upregulation decreased superoxide whereas it increased hydrogen peroxide production with concomitant increase in the expression and activity of manganese superoxide dismutase (MnSOD), the primary mitochondrial antioxidant enzyme. Furthermore, hydrogen peroxide was responsible for induction of lipid peroxidation, and PLCγ-1 activation in UCP2 overexpressed cells. Additionally, PLCγ-1 activation enhanced skin cell transformation, and pharmacological, and siRNA mediated inhibition of PLCγ-1, markedly reduced colony formation, and 3D cell growth. Moreover, hydrogen peroxide scavenger, catalase, suppressed lipid peroxidation, and dampened PLCγ-1 activity. Taken together, our data suggest that (i) UCP2 is an important regulator of mitochondrial redox status and lipid signaling; (ii) hydrogen peroxide might mediate UCP2's tumor promoting activity; and (iii) pharmacological disruption of PLCγ-1 and/or hydrogen peroxide may have clinical utility for UCP2 overexpressed cancers.
[Mh] Termos MeSH primário: Transformação Celular Neoplásica/metabolismo
Fosfolipase C gama/metabolismo
Espécies Reativas de Oxigênio/metabolismo
Pele/patologia
Proteína Desacopladora 2/metabolismo
[Mh] Termos MeSH secundário: Animais
Técnicas de Cultura de Células
Linhagem Celular
Proliferação Celular
Seres Humanos
Peróxido de Hidrogênio/metabolismo
Peroxidação de Lipídeos
Camundongos
Modelos Biológicos
Transdução de Sinais
Pele/metabolismo
Superóxidos/metabolismo
Regulação para Cima
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Reactive Oxygen Species); 0 (UCP2 protein, human); 0 (Uncoupling Protein 2); 11062-77-4 (Superoxides); BBX060AN9V (Hydrogen Peroxide); EC 3.1.4.11 (PLCG1 protein, human); EC 3.1.4.3 (Phospholipase C gamma)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171004
[Lr] Data última revisão:
171004
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170603
[St] Status:MEDLINE
[do] DOI:10.1002/mc.22684


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[PMID]:28424210
[Au] Autor:Zhou Y; Cai T; Xu J; Jiang L; Wu J; Sun Q; Zen K; Yang J
[Ad] Endereço:Center of Kidney Disease, Second Affiliated Hospital, Nanjing Medical University, Nanjing, China; and.
[Ti] Título:UCP2 attenuates apoptosis of tubular epithelial cells in renal ischemia-reperfusion injury.
[So] Source:Am J Physiol Renal Physiol;313(4):F926-F937, 2017 Oct 01.
[Is] ISSN:1522-1466
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Uncoupling protein-2 (UCP2) plays critical roles in energy metabolism and cell survival. Previous investigations showed that UCP2 regulated the production of extracellular matrix and renal fibrosis. However, little is known about UCP2 in acute kidney injury (AKI). Here, we used knockout mice to investigate the role of UCP2 in an AKI model generated by renal ischemia-reperfusion (I/R) injury. The global knockout mice were born and grew normally without kidney histological abnormality or renal dysfunction. Compared with littermates, deletion of exacerbated I/R-induced AKI whereas increase of UCP2 by conjugated linoleic acid (CLA) attenuated I/R injury. Tubular cell apoptosis and autophagy were induced by I/R. After injury, more tubular cell apoptosis and less autophagy were identified in the kidneys of knockout mice compared with their littermates, and less apoptosis and more autophagy were observed in mice fed with CLA. In vitro rotenone, an inhibitor of electron transport chain complex I, was applied to induce energy depletion in cultured tubular epithelial cells. As expected, rotenone-recovery (R/R) treatment induced tubular cell apoptosis and autophagy. UCP2 plasmid transfection reduced cell apoptosis and facilitated autophagy after R/R treatment, whereas UCP2 small interfering RNA (siRNA) transfection sensitized cell apoptosis but reduced autophagy induced by R/R treatment. Interference of autophagy by treatment with autophagy inhibitor 3-methyladenine or autophagy initiation protein Beclin-1 siRNA transfection resulted in tubular cell apoptosis. Thus UCP2 attenuates I/R-induced AKI, probably by reducing cell apoptosis through protection of autophagy.
[Mh] Termos MeSH primário: Lesão Renal Aguda/metabolismo
Traumatismo por Reperfusão/metabolismo
Proteína Desacopladora 2/metabolismo
[Mh] Termos MeSH secundário: Animais
Apoptose
Autofagia
Linhagem Celular
Ácido Linoleico
Camundongos Endogâmicos C57BL
Camundongos Knockout
Rotenona
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Ucp2 protein, mouse); 0 (Uncoupling Protein 2); 03L9OT429T (Rotenone); 9KJL21T0QJ (Linoleic Acid)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171019
[Lr] Data última revisão:
171019
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170421
[St] Status:MEDLINE
[do] DOI:10.1152/ajprenal.00118.2017


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[PMID]:28258342
[Au] Autor:Oleksiewicz U; Liloglou T; Tasopoulou KM; Daskoulidou N; Gosney JR; Field JK; Xinarianos G
[Ad] Endereço:Roy Castle Lung Cancer Research Programme, University of Liverpool Cancer Research Centre, 200 London Rd, Liverpool, L3 9TA, UK. u.oleksiewicz@gmail.com.
[Ti] Título:COL1A1, PRPF40A, and UCP2 correlate with hypoxia markers in non-small cell lung cancer.
[So] Source:J Cancer Res Clin Oncol;143(7):1133-1141, 2017 Jul.
[Is] ISSN:1432-1335
[Cp] País de publicação:Germany
[La] Idioma:eng
[Ab] Resumo:PURPOSE: Collagen 1A1 (COL1A1), RNA-binding and pre-mRNA Processing Factor (PRPF40A), and Uncoupling Protein 2 (UCP2) were identified as downstream effectors of cytoglobin (CYGB), which was shown implicated in tumour biology. Although these three genes have been previously associated with cancer, little is known about their status in lung malignancies. METHODS: Hereby, we investigated the expression and promoter methylation of COL1A1, PRPF40A, and UCP2 in 156 non-small cell lung cancer (NSCLC) and adjacent normal tissues. RESULTS: We demonstrate that COL1A1 and PRPF40A mRNAs are significantly overexpressed in NSCLC (p < 1 × 10 ), while UCP2 exhibits a trend of upregulation (p = 0.066). Only COL1A1 promoter revealed hypermethylation in NSCLCs (36%), which was particularly evident in squamous cell carcinomas (p = 0.024) and in the tumours with moderate-to-good differentiation (p = 0.01). Transcript level of COL1A1, as well as PRPF40A and UCP2, exhibited striking association (p ≤ 0.001) with the expression of hypoxia markers. In addition, we demonstrate in lung cancer cell lines exposed to hypoxia or oxidative stress that COL1A1 transcription significantly responds to oxygen depletion, while other genes showed the modest upregulation in stress conditions. CONCLUSION: In conclusion, our data revealed that COL1A1, UCP2, and PRPF40A are novel players implicated in the complex network of hypoxia response in NSCLC.
[Mh] Termos MeSH primário: Carcinoma Pulmonar de Células não Pequenas/patologia
Proteínas de Transporte/biossíntese
Colágeno Tipo I/biossíntese
Neoplasias Pulmonares/patologia
Proteína Desacopladora 2/biossíntese
[Mh] Termos MeSH secundário: Adulto
Idoso
Idoso de 80 Anos ou mais
Biomarcadores Tumorais/análise
Carcinoma Pulmonar de Células não Pequenas/genética
Proteínas de Transporte/genética
Hipóxia Celular/fisiologia
Colágeno Tipo I/genética
Metilação de DNA
Feminino
Perfilação da Expressão Gênica
Seres Humanos
Neoplasias Pulmonares/genética
Masculino
Meia-Idade
Reação em Cadeia da Polimerase
Regiões Promotoras Genéticas/genética
Transcriptoma
Proteína Desacopladora 2/genética
Regulação para Cima
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Biomarkers, Tumor); 0 (Carrier Proteins); 0 (Collagen Type I); 0 (PRPF40A protein, human); 0 (UCP2 protein, human); 0 (Uncoupling Protein 2); 0 (collagen type I, alpha 1 chain)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170918
[Lr] Data última revisão:
170918
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170305
[St] Status:MEDLINE
[do] DOI:10.1007/s00432-017-2381-y


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[PMID]:28242329
[Au] Autor:Tekin S; Erden Y; Ozyalin F; Cigremis Y; Colak C; Sandal S
[Ad] Endereço:Inonu University, Faculty of Medicine, Department of Physiology, Malatya, Turkey. Electronic address: tekinsuat@gmail.com.
[Ti] Título:The effects of intracerebroventricular infusion of irisin on feeding behaviour in rats.
[So] Source:Neurosci Lett;645:25-32, 2017 04 03.
[Is] ISSN:1872-7972
[Cp] País de publicação:Ireland
[La] Idioma:eng
[Ab] Resumo:Irisin, a novel exercise-induced myokine, has attracted attention with its effects on energy metabolism. This study was conducted to determine the possible effects of irisin on nutritional behaviour. In this study, 40 male Wistar Albino rats were separated into 4 groups (n=10 for each group). Osmotic mini-pumps were connected to metal cannulas implanted to lateral ventricle; and artificial cerebrospinal fluid (vehicle), and 10 and 100nM of irisin was infused for 7days. The daily food and water consumptions and body weights of rats were followed up. After the infusion, the animals were killed, and the hypothalamus and blood samples were collected. NPY, POMC, and UCP2 mRNA levels in the hypothalamus were examined by RT-PCR. In serum, leptin and ghrelin levels as well as the levels of metabolic parameters were measured by using ELISA. It was determined that irisin administration increased the daily food consumption (p<0.05), without causing significant changes in water consumption and body weight. Irisin also caused increases in ghrelin level in circulation and NPY and UCP2 mRNA levels in the hypothalamus, whereas it decreased the leptin level in circulation and POMC mRNA levels in the hypothalamus (p<0.05). Otherwise, irisin caused decrease in LDL, triglycerides and cholesterol levels, while increasing HDL and glucose levels (p<0.05). Results indicates that long-term irisin treatment increases food intake without increasing body weight associated with increased ghrelin, NPY and UCP2 mRNAs, and decreased leptin and POMC mRNA in the hypothalamus.
[Mh] Termos MeSH primário: Comportamento Alimentar
Fibronectinas/metabolismo
[Mh] Termos MeSH secundário: Animais
Peso Corporal
Comportamento de Ingestão de Líquido
Fibronectinas/farmacologia
Grelina/metabolismo
Hipotálamo/citologia
Hipotálamo/efeitos dos fármacos
Hipotálamo/metabolismo
Infusões Intraventriculares
Leptina/metabolismo
Masculino
Neurônios/metabolismo
Neuropeptídeo Y/genética
Neuropeptídeo Y/metabolismo
Pró-Opiomelanocortina/genética
Pró-Opiomelanocortina/metabolismo
RNA Mensageiro/metabolismo
Ratos Wistar
Proteína Desacopladora 2/genética
Proteína Desacopladora 2/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (FNDC5 protein, rat); 0 (Fibronectins); 0 (Ghrelin); 0 (Leptin); 0 (Neuropeptide Y); 0 (RNA, Messenger); 0 (Ucp2 protein, rat); 0 (Uncoupling Protein 2); 66796-54-1 (Pro-Opiomelanocortin)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171101
[Lr] Data última revisão:
171101
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170301
[St] Status:MEDLINE


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[PMID]:28239813
[Au] Autor:Jiang ZM; Yang QH; Zhu CQ
[Ad] Endereço:Department of Emergency, Renji Hospital, School of Medicine, Shanghai Jiaotong University, Shanghai, China. qianghuayang@sina.com.
[Ti] Título:UCP2 in early diagnosis and prognosis of sepsis.
[So] Source:Eur Rev Med Pharmacol Sci;21(3):549-553, 2017 Feb.
[Is] ISSN:2284-0729
[Cp] País de publicação:Italy
[La] Idioma:eng
[Ab] Resumo:OBJECTIVE: Sepsis, a systemic inflammatory response syndrome caused by infection, is a serious threat to the lives of patients. Sepsis can cause tissue hypoperfusion and septic shock which leads to organ dysfunction and death via a variety of mechanisms. Mitochondrial protein (UCP2) involves in immune response, regulation of oxidative stress, and maintenance of mitochondrial membrane potential as well as energy production. However, the role of UCP2 in sepsis remains to be further explored. PATIENTS AND METHODS: A total of 156 patients with sepsis from our hospital were included in this study (69 patients with sepsis and 87 patients with severe sepsis). A total of 69 healthy volunteers were included as controls. Levels of UCP2 in blood cells before and after treatment were measured using RT-PCR and Western blot. The correlation between levels of UCP2 and sepsis was analyzed. RESULTS: The level of UCPPC2 in blood cells of sepsis patients was significantly higher than that of healthy controls at both mRNA level and protein level. The expression level of UCP2 in blood cells of sepsis patients was significantly reduced after treatment, compared to that before treatment. No significant difference was found in the level of UCP2 in blood cells of healthy controls before and after treatment ((p=0.45). Also, the level of UCP2 in blood cells of patients with severe sepsis was significantly higher than that of patients with sepsis at the protein level (p<0.05). Moreover, a positive correlation was found between the level of UCP2 protein and the severity of sepsis. CONCLUSIONS: UCP2 in blood cells might be a specific biomarker for sepsis and the level of UCP2 is positively correlated with the severity of sepsis.
[Mh] Termos MeSH primário: Sepse/diagnóstico
Choque Séptico
Proteína Desacopladora 2/sangue
[Mh] Termos MeSH secundário: Adolescente
Adulto
Idoso
Idoso de 80 Anos ou mais
Biomarcadores/sangue
Estudos de Casos e Controles
Diagnóstico Precoce
Seres Humanos
Meia-Idade
Prognóstico
Adulto Jovem
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Biomarkers); 0 (UCP2 protein, human); 0 (Uncoupling Protein 2)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:170726
[Lr] Data última revisão:
170726
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170228
[St] Status:MEDLINE


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[PMID]:28222054
[Au] Autor:Brondani LA; Rech TH; Boelter G; Bauer AC; Leitão CB; Eizirik DL; Crispim D
[Ad] Endereço:1 Endocrine Division, Laboratory of Human Pancreatic Islet Biology, Hospital de Clinicas de Porto Alegre, Porto Alegre, RS, Brazil.2 Post-Graduate Program in Medical Sciences: Endocrinology, Universidade Federal do Rio Grande do Sul, Porto Alegre, RS, Brazil.3 ULB Center for Diabetes Research, Medical Faculty, Université Libre de Bruxelles, Brussels, Belgium.
[Ti] Título:UCP2 Expression Is Increased in Pancreas From Brain-Dead Donors and Involved in Cytokine-Induced ß Cells Apoptosis.
[So] Source:Transplantation;101(3):e59-e67, 2017 Mar.
[Is] ISSN:1534-6080
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Systemic inflammation associated with brain death (BD) decreases islet yield and quality, negatively affecting outcomes of human islet transplantation. A recent study from our group showed an increased expression of uncoupling protein-2 (UCP2) in pancreas from rats with BD as compared with controls. UCP2 is located in the mitochondrial inner membrane and regulates production of reactive oxygen species and glucose-stimulated insulin secretion. It has been suggested that UCP2 also plays a role in ß cell apoptosis, but these findings remain controversial. METHODS: We have presently performed a case-control study to assess UCP2 expression in pancreas from BD donors (cases) and subjects who underwent pancreatectomy (controls). We next investigated the role of Ucp2 in cytokine-induced apoptosis of rat insulin-producing INS-1E cells. RESULTS: UCP2 gene expression was higher in pancreas from BD donors compared with controls (1.73 ± 0.93 vs 0.75 ± 0.66; fold change, P < 0.05). Ucp2 knockdown (80% at the protein and messenger RNA levels) reduced by 30% cytokine-induced apoptosis and nitric oxide production in INS-1E cells. This protection was associated with decreased expression of cleaved (activated) caspases 9 and 3, suggesting that Ucp2 knockdown interferes with cytokine triggering of the intrinsic apoptotic pathway. Moreover, both messenger RNA and protein concentrations of the antiapoptotic protein Bcl-2 were increased after Ucp2 knockdown in INS-1E cells. CONCLUSIONS: These data suggest that UCP2 has an apoptotic effect in ß cells via regulation of the intrinsic pathway of apoptosis.
[Mh] Termos MeSH primário: Apoptose/efeitos dos fármacos
Morte Encefálica/metabolismo
Células Secretoras de Insulina/efeitos dos fármacos
Interferon gama/farmacologia
Transplante de Pâncreas/métodos
Transdução de Sinais/efeitos dos fármacos
Doadores de Tecidos
Fator de Necrose Tumoral alfa/farmacologia
Proteína Desacopladora 2/metabolismo
[Mh] Termos MeSH secundário: Animais
Proteínas Reguladoras de Apoptose/metabolismo
Morte Encefálica/patologia
Estudos de Casos e Controles
Linhagem Celular
Seres Humanos
Células Secretoras de Insulina/metabolismo
Células Secretoras de Insulina/patologia
Óxido Nítrico/metabolismo
Pancreatectomia
Estudos Prospectivos
Interferência de RNA
RNA Mensageiro/genética
RNA Mensageiro/metabolismo
Ratos
Superóxido Dismutase/metabolismo
Fatores de Tempo
Transfecção
Proteína Desacopladora 2/genética
Regulação para Cima
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Apoptosis Regulatory Proteins); 0 (RNA, Messenger); 0 (Tumor Necrosis Factor-alpha); 0 (UCP2 protein, human); 0 (Ucp2 protein, rat); 0 (Uncoupling Protein 2); 31C4KY9ESH (Nitric Oxide); 82115-62-6 (Interferon-gamma); EC 1.15.1.1 (Superoxide Dismutase); EC 1.15.1.1 (superoxide dismutase 2)
[Em] Mês de entrada:1705
[Cu] Atualização por classe:170523
[Lr] Data última revisão:
170523
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170222
[St] Status:MEDLINE
[do] DOI:10.1097/TP.0000000000001292


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[PMID]:28214555
[Au] Autor:Duffy CM; Xu H; Nixon JP; Bernlohr DA; Butterick TA
[Ad] Endereço:Minneapolis Veterans Affairs Health Care System, Research 151, One Veterans Dr, Minneapolis, MN 55417, USA; Department of Food Science and Nutrition, University of Minnesota, 1334 Eckles Ave, St. Paul, MN 55108, USA.
[Ti] Título:Identification of a fatty acid binding protein4-UCP2 axis regulating microglial mediated neuroinflammation.
[So] Source:Mol Cell Neurosci;80:52-57, 2017 Apr.
[Is] ISSN:1095-9327
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Hypothalamic inflammation contributes to metabolic dysregulation and the onset of obesity. Dietary saturated fats activate microglia via a nuclear factor-kappa B (NFκB) mediated pathway to release pro-inflammatory cytokines resulting in dysfunction or death of surrounding neurons. Fatty acid binding proteins (FABPs) are lipid chaperones regulating metabolic and inflammatory pathways in response to fatty acids. Loss of FABP4 in peripheral macrophages via either molecular or pharmacologic mechanisms results in reduced obesity-induced inflammation via a UCP2-redox based mechanism. Despite the widespread appreciation for the role of FABP4 in mediating peripheral inflammation, the expression of FABP4 and a potential FABP4-UCP2 axis regulating microglial inflammatory capacity is largely uncharacterized. To that end, we hypothesized that microglial cells express FABP4 and that inhibition would upregulate UCP2 and attenuate palmitic acid (PA)-induced pro-inflammatory response. Gene expression confirmed expression of FABP4 in brain tissue lysate from C57Bl/6J mice and BV2 microglia. Treatment of microglial cells with an FABP inhibitor (HTS01037) increased expression of Ucp2 and arginase in the presence or absence of PA. Moreover, cells exposed to HTS01037 exhibited attenuated expression of inducible nitric oxide synthase (iNOS) compared to PA alone indicating reduced NFκB signaling. Hypothalamic tissue from mice lacking FABP4 exhibit increased UCP2 expression and reduced iNOS, tumor necrosis factor-alpha (TNF-α), and ionized calcium-binding adapter molecule 1 (Iba1; microglial activation marker) expression compared to wild type mice. Further, this effect is negated in microglia lacking UCP2, indicating the FABP4-UCP2 axis is pivotal in obesity induced neuroinflammation. To our knowledge, this is the first report demonstrating a FABP4-UCP2 axis with the potential to modulate the microglial inflammatory response.
[Mh] Termos MeSH primário: Proteínas de Ligação a Ácido Graxo/metabolismo
Regulação da Expressão Gênica/fisiologia
Microglia/metabolismo
Proteína Desacopladora 2/genética
[Mh] Termos MeSH secundário: Animais
Anti-Inflamatórios/farmacologia
Arginase/metabolismo
Encéfalo/citologia
Proteínas de Ligação ao Cálcio/metabolismo
Linhagem Celular Transformada
Proteínas de Ligação a Ácido Graxo/antagonistas & inibidores
Proteínas de Ligação a Ácido Graxo/genética
Regulação da Expressão Gênica/efeitos dos fármacos
Hipotálamo/citologia
Camundongos
Camundongos Endogâmicos C57BL
Camundongos Transgênicos
Proteínas dos Microfilamentos/metabolismo
Microglia/efeitos dos fármacos
Óxido Nítrico Sintase Tipo II/metabolismo
Ácido Palmítico/farmacologia
RNA Interferente Pequeno/genética
RNA Interferente Pequeno/metabolismo
Espécies Reativas de Oxigênio/metabolismo
Transdução de Sinais/efeitos dos fármacos
Transdução de Sinais/genética
Fator de Necrose Tumoral alfa/metabolismo
Proteína Desacopladora 2/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Aif1 protein, mouse); 0 (Anti-Inflammatory Agents); 0 (Calcium-Binding Proteins); 0 (Fabp4 protein, mouse); 0 (Fatty Acid-Binding Proteins); 0 (Microfilament Proteins); 0 (RNA, Small Interfering); 0 (Reactive Oxygen Species); 0 (Tumor Necrosis Factor-alpha); 0 (Uncoupling Protein 2); 2V16EO95H1 (Palmitic Acid); EC 1.14.13.39 (Nitric Oxide Synthase Type II); EC 3.5.3.1 (Arg1 protein, mouse); EC 3.5.3.1 (Arginase)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170901
[Lr] Data última revisão:
170901
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170220
[St] Status:MEDLINE



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