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[PMID]:29318368
[Au] Autor:Mirlohi MS; Yaghooti H; Shirali S; Aminasnafi A; Olapour S
[Ad] Endereço:Hyperlipidemia Research Center, School of Allied Medical Sciences, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran.
[Ti] Título:Increased levels of advanced glycation end products positively correlate with iron overload and oxidative stress markers in patients with ß-thalassemia major.
[So] Source:Ann Hematol;97(4):679-684, 2018 Apr.
[Is] ISSN:1432-0584
[Cp] País de publicação:Germany
[La] Idioma:eng
[Ab] Resumo:The impaired biosynthesis of the ß-globin chain in ß-thalassemia leads to the accumulation of unpaired alpha globin chains, failure in hemoglobin formation, and iron overload due to frequent blood transfusion. Iron excess causes oxidative stress and massive tissue injuries. Advanced glycation end products (AGEs) are harmful agents, and their production accelerates in oxidative conditions. This study was conducted on 45 patients with major ß-thalassemia who received frequent blood transfusions and chelation therapy and were compared to 40 healthy subjects. Metabolic parameters including glycemic and iron indices, hepatic and renal functions tests, oxidative stress markers, and AGEs (carboxymethyl-lysine and pentosidine) levels were measured. All parameters were significantly increased in ß-thalassemia compared to the control except for glutathione levels. Blood glucose, iron, serum ferritin, non-transferrin-bound iron (NTBI), MDA, soluble form of low-density lipoprotein receptor, glutathione peroxidase, total reactive oxygen species (ROS), and AGE levels were significantly higher in the ß-thalassemia patients. Iron and ferritin showed a significant positive correlation with pentosidine (P < 0.01) but not with carboxymethyl-lysine. The NTBI was markedly increased in the ß-thalassemia patients, and its levels correlated significantly with both carboxymethyl-lysine and pentosidine (P < 0.05). Our findings confirm the oxidative status generated by the iron overload in ß-thalassemia major patients and highlight the enhanced formation of AGEs, which may play an important role in the pathogenesis of ß-thalassemia major.
[Mh] Termos MeSH primário: Transfusão de Sangue
Produtos Finais de Glicação Avançada/sangue
Sobrecarga de Ferro/etiologia
Estresse Oxidativo
Reação Transfusional/fisiopatologia
Talassemia beta/sangue
[Mh] Termos MeSH secundário: Adolescente
Adulto
Biomarcadores/sangue
Terapia por Quelação/efeitos adversos
Terapia Combinada/efeitos adversos
Estudos Transversais
Desferroxamina/uso terapêutico
Feminino
Seres Humanos
Irã (Geográfico)
Sobrecarga de Ferro/prevenção & controle
Masculino
Piridonas/uso terapêutico
Receptores Depuradores Classe E/sangue
Adulto Jovem
Talassemia beta/terapia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Biomarkers); 0 (Glycation End Products, Advanced); 0 (OLR1 protein, human); 0 (Pyridones); 0 (Scavenger Receptors, Class E); 2BTY8KH53L (deferiprone); J06Y7MXW4D (Deferoxamine)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180309
[Lr] Data última revisão:
180309
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180111
[St] Status:MEDLINE
[do] DOI:10.1007/s00277-017-3223-3


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[PMID]:28941610
[Au] Autor:Paquette M; Dufour R; Baass A
[Ad] Endereço:Nutrition, Metabolism, and Atherosclerosis Clinic, Institut de recherches cliniques de Montréal, Montréal, Québec, Canada.
[Ti] Título:Scavenger Receptor LOX1 Genotype Predicts Coronary Artery Disease in Patients With Familial Hypercholesterolemia.
[So] Source:Can J Cardiol;33(10):1312-1318, 2017 Oct.
[Is] ISSN:1916-7075
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Familial hypercholesterolemia (FH) is a monogenic disease associated with elevated low-density lipoprotein (LDL) cholesterol and oxidized LDL (oxLDL) leading to premature cardiovascular disease. Lectin-like oxLDL receptor-1 (LOX1) is one of the major contributors of oxLDL uptake and degradation in macrophages, which leads to foam cell formation and the development of atherosclerosis. This study investigated the effect of the rs11053646 genotype of the oxidized low-density lipoprotein receptor 1 (OLR1) gene on coronary artery disease (CAD) risk in a cohort of FH patients. METHODS: A total of 665 genetically confirmed heterozygous adult patients with FH were included in the analysis. We evaluated the association between the rs11053646 genotype (GG vs GC) and CAD. RESULTS: The GC genotype (K167N carriers) represented 12.9% of the study cohort (n = 86), whereas 87.1% of the participants were noncarriers (GG genotype) (n = 579). A significantly higher proportion of GC carriers experienced a CAD event (40.7%) than did GG carriers (29.0%; P = 0.03). The presence of a C allele remained significantly associated with an increased CAD risk, even when the regression model was corrected for all traditional CAD risk factors (odds ratio, 3.05; 95% confidence interval, 1.63-5.70; P = 0.0005). The negative impact of carrying the C allele on CAD risk was similar in both sexes but was significantly more important in smokers as well as in younger patients with FH. CONCLUSIONS: Carrying the C allele of the rs11053646 variant of the OLR1 gene was associated with an increased risk of CAD in heterozygous adult patients with FH, and this risk could be even greater in smokers as well as in younger patients.
[Mh] Termos MeSH primário: Doença da Artéria Coronariana/etiologia
DNA/genética
Hiperlipoproteinemia Tipo II/genética
Mutação
Receptores Depuradores Classe E/genética
[Mh] Termos MeSH secundário: Adulto
Alelos
Southern Blotting
Doença da Artéria Coronariana/sangue
Doença da Artéria Coronariana/diagnóstico
Análise Mutacional de DNA
Feminino
Genótipo
Heterozigoto
Seres Humanos
Hiperlipoproteinemia Tipo II/sangue
Hiperlipoproteinemia Tipo II/complicações
Masculino
Reação em Cadeia da Polimerase
Fatores de Risco
Receptores Depuradores Classe E/sangue
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (OLR1 protein, human); 0 (Scavenger Receptors, Class E); 9007-49-2 (DNA)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170929
[Lr] Data última revisão:
170929
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170925
[St] Status:MEDLINE


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[PMID]:28891395
[Au] Autor:Liu L; Nagai I; Gao Y; Matsushima Y; Kawai Y; Sayama K
[Ad] Endereço:a Graduate School of Science and Technology , Shizuoka University , Shizuoka , Japan.
[Ti] Título:Effects of catechins and caffeine on the development of atherosclerosis in mice.
[So] Source:Biosci Biotechnol Biochem;81(10):1948-1955, 2017 Oct.
[Is] ISSN:1347-6947
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Atherosclerosis is one of the diseases related to metabolic syndrome which is caused by obesity. Previous reports have shown that green tea and its components have anti-obesity effect. We examined whether catechins and caffeine can prevent the development of atherosclerosis by oral administration, singly or in combination to the atherosclerosis model mice. Results demonstrated that the number of atherosclerotic regions in the aorta was significantly reduced by the combined treatment, and the atherosclerotic area was also improved. Serum HDL-C increased by caffeine single treatment, but no effect on the TG and TC by any treatments. Moreover, ECG illuviated to atheromatous lesions in aorta and the illuviation was enhanced by caffeine. The mRNA expression levels of LOX-1 and TNF-α showed a tendency to suppress by the combined treatment. These results indicated that the combined administration of catechins and caffeine has the inhibitory effect on the development of atherosclerosis in mice.
[Mh] Termos MeSH primário: Aterosclerose/prevenção & controle
Cafeína/farmacologia
Catequina/farmacologia
[Mh] Termos MeSH secundário: Animais
Aorta/efeitos dos fármacos
Aterosclerose/sangue
Aterosclerose/genética
Aterosclerose/metabolismo
Peso Corporal/efeitos dos fármacos
Interações Medicamentosas
Ingestão de Alimentos/efeitos dos fármacos
Feminino
Regulação da Expressão Gênica/efeitos dos fármacos
Peroxidação de Lipídeos/efeitos dos fármacos
Lipídeos/sangue
Camundongos
Camundongos Endogâmicos C57BL
Receptores Depuradores Classe E/genética
Fator de Necrose Tumoral alfa/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Lipids); 0 (Olr1 protein, mouse); 0 (Scavenger Receptors, Class E); 0 (Tumor Necrosis Factor-alpha); 3G6A5W338E (Caffeine); 8R1V1STN48 (Catechin)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171017
[Lr] Data última revisão:
171017
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170912
[St] Status:MEDLINE
[do] DOI:10.1080/09168451.2017.1364618


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[PMID]:28860004
[Au] Autor:Arjuman A; Chandra NC
[Ad] Endereço:Department of Biochemistry, All India Institute of Medical Sciences, Ansari Nagar, New Delhi, 110029, India. Electronic address: albinaarjuman@hotmail.com.
[Ti] Título:LOX-1: A potential target for therapy in atherosclerosis; an in vitro study.
[So] Source:Int J Biochem Cell Biol;91(Pt A):65-80, 2017 Oct.
[Is] ISSN:1878-5875
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Pro-inflammatory signal generated from the interaction of oxLDL with its cognate receptor LOX-1 has been attenuated successfully by a novel combination siRNA (siLOX-1 ) targeting unique regions of Homo sapien LOX-1 mRNA. Signalling via LOX-1R was studied in a potentially pro-atherogenic arena recreated in a metabolic, pulse-chase set up. An initial pulse of oxLDL (20µg/mL;5h) was chased (without oxLDL) on a temporal scale upto 72h. Our study shows that the pro-inflammatory signal generated via oxLDL-LOX-1R interaction was mediated in two rungs, an initial sustained increase in LOX-1R expression up to 12h, and a renewal after 48h. TNF-α acted as a primary mediator of LOX-1R signalling, presumably also stimulating CD40 and MMP-9. Both TNF-α and IL-6 were involved in the second rung of LOX-1R signalling; maximum secretion of both was detected at 48h. Our study suggests a temporal sustenance of LOX-1R signalling by pro-inflammatory cytokines even on withdrawal of oxLDL. Also, siLOX-1 successfully abated LOX-1R expression along with its signalling intermediates, NO and NF-kB. Overall, LOX-1 signalling and the crucial role of cytokines in sustaining it is reported. Attenuation of this receptor may be of therapeutic value in atherosclerosis.
[Mh] Termos MeSH primário: Aterosclerose/metabolismo
Terapia de Alvo Molecular
Receptores Depuradores Classe E/metabolismo
[Mh] Termos MeSH secundário: Aterosclerose/tratamento farmacológico
Linhagem Celular Tumoral
Citocinas/metabolismo
Regulação da Expressão Gênica/efeitos dos fármacos
Técnicas de Silenciamento de Genes
Seres Humanos
RNA Interferente Pequeno/genética
Receptores Depuradores Classe E/deficiência
Receptores Depuradores Classe E/genética
Transdução de Sinais/efeitos dos fármacos
Transdução de Sinais/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Cytokines); 0 (OLR1 protein, human); 0 (RNA, Small Interfering); 0 (Scavenger Receptors, Class E)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171113
[Lr] Data última revisão:
171113
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170902
[St] Status:MEDLINE


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[PMID]:28844714
[Au] Autor:Wang B; Zhao H; Zhao L; Zhang Y; Wan Q; Shen Y; Bu X; Wan M; Shen C
[Ad] Endereço:Department of Pathology and Pathophysiology, Medical School, Southeast University, Nanjing, Jiangsu, People's Republic of China.
[Ti] Título:Up-regulation of OLR1 expression by TBC1D3 through activation of TNFα/NF-κB pathway promotes the migration of human breast cancer cells.
[So] Source:Cancer Lett;408:60-70, 2017 Nov 01.
[Is] ISSN:1872-7980
[Cp] País de publicação:Ireland
[La] Idioma:eng
[Ab] Resumo:Metastatic spread of cancer cells is the most life-threatening aspect of breast cancer and involves multiple steps including cell migration. We recently found that the TBC1D3 oncogene promotes the migration of breast cancer cells, and its interaction with CaM enhances the effects of TBC1D3. However, little is known regarding the mechanism by which TBC1D3 induces the migration of cancer cells. Here, we demonstrated that TBC1D3 stimulated the expression of oxidized low density lipoprotein receptor 1 (OLR1), a stimulator of cell migration, in breast cancer cells at the transcriptional level. Depletion of OLR1 by siRNAs or down-regulation of OLR1 expression using pomalidomide, a TNFα inhibitor, significantly decreased TBC1D3-induced migration of these cells. Notably, TBC1D3 overexpression activated NF-κB, a major effector of TNFα signaling, while inhibition of TNFα signaling suppressed the effects of TBC1D3. Consistent with this, NF-κB inhibition using its specific inhibitor caffeic acid phenethyl ester decreased both TBC1D3-induced OLR1 expression and cell migration, suggesting a critical role for TNFα/NF-κB signaling in TBC1D3-induced migration of breast cancer cells. Mechanistically, TBC1D3 induced activation of this signaling pathway on multiple levels, including by increasing the release of TNFα, elevating the transcription of TNFR1, TRAF1, TRAF5 and TRAF6, and decreasing the degradation of TNFR1. In summary, these studies identify the TBC1D3 oncogene as a novel regulator of TNFα/NF-κB signaling that mediates this oncogene-induced migration of human breast cancer cells by up-regulating OLR1.
[Mh] Termos MeSH primário: Neoplasias da Mama/tratamento farmacológico
Movimento Celular
Proteínas Ativadoras de GTPase/metabolismo
NF-kappa B/metabolismo
Proteínas Proto-Oncogênicas/metabolismo
Receptores Depuradores Classe E/metabolismo
Fator de Necrose Tumoral alfa/metabolismo
[Mh] Termos MeSH secundário: Apoptose
Neoplasias da Mama/enzimologia
Neoplasias da Mama/patologia
Proliferação Celular
Feminino
Proteínas Ativadoras de GTPase/genética
Regulação Neoplásica da Expressão Gênica
Seres Humanos
NF-kappa B/genética
Proteínas Proto-Oncogênicas/genética
RNA Interferente Pequeno/genética
Receptores Depuradores Classe E/antagonistas & inibidores
Receptores Depuradores Classe E/genética
Células Tumorais Cultivadas
Fator de Necrose Tumoral alfa/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (GTPase-Activating Proteins); 0 (NF-kappa B); 0 (OLR1 protein, human); 0 (Proto-Oncogene Proteins); 0 (RNA, Small Interfering); 0 (Scavenger Receptors, Class E); 0 (TBC1D3 protein, human); 0 (Tumor Necrosis Factor-alpha)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171101
[Lr] Data última revisão:
171101
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170829
[St] Status:MEDLINE


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[PMID]:28672042
[Au] Autor:Spaans F; Kao CK; Morton JS; Quon AL; Sawamura T; Tannetta DS; Sargent IL; Davidge ST
[Ad] Endereço:Department of Obstetrics and Gynecology, University of Alberta, Edmonton, AB, Canada.
[Ti] Título:Syncytiotrophoblast extracellular vesicles impair rat uterine vascular function via the lectin-like oxidized LDL receptor-1.
[So] Source:PLoS One;12(7):e0180364, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Syncytiotrophoblast extracellular vesicles (STBEVs) are placenta derived particles that are released into the maternal circulation during pregnancy. Abnormal levels of STBEVs have been proposed to affect maternal vascular function. The lectin-like oxidized low-density lipoprotein receptor-1 (LOX-1) is a multi-ligand scavenger receptor. Increased LOX-1 expression and activation has been proposed to contribute to endothelial dysfunction. As LOX-1 has various ligands, we hypothesized that, being essentially packages of lipoproteins, STBEVs are able to activate the LOX-1 receptor thereby impairing vascular function via the production of superoxide and decreased nitric oxide bioavailability. Uterine arteries were obtained in late gestation from Sprague-Dawley rats and incubated for 24h with or without human STBEVs (derived from a normal pregnant placenta) in the absence or presence of a LOX-1 blocking antibody. Vascular function was assessed using wire myography. Endothelium-dependent maximal vasodilation to methylcholine was impaired by STBEVs (MCh Emax: 57.7±5.9% in STBEV-incubated arteries vs. 77.8±2.9% in controls, p<0.05). This was prevented by co-incubation of STBEV-incubated arteries with LOX-1 blocking antibodies (MCh Emax: 78.8±4.3%, p<0.05). Pre-incubation of the vessels with a nitric oxide synthase inhibitor (L-NAME) demonstrated that the STBEV-induced impairment in vasodilation was due to decreased nitric oxide contribution (ΔAUC 12.2±11.7 in STBEV-arteries vs. 86.5±20 in controls, p<0.05), which was abolished by LOX-1 blocking antibody (ΔAUC 98.9±17, p<0.05). In STBEV-incubated vessels, LOX-1 inhibition resulted in an increased endothelial nitric oxide synthase expression (p<0.05), to a level similar to control vessels. The oxidant scavenger, superoxide dismutase, did not improve this impairment, nor were vascular superoxide levels altered. Our data support an important role for STBEVs in impairment of vascular function via activation of LOX-1 and reduced nitric oxide mediated vasodilation. Moreover, we postulate that the LOX-1 pathway could be a potential therapeutic target in pathologies associated with vascular dysfunction during pregnancy.
[Mh] Termos MeSH primário: Vesículas Extracelulares/fisiologia
Receptores Depuradores Classe E/fisiologia
Trofoblastos/citologia
Artéria Uterina/fisiologia
Vasodilatação
[Mh] Termos MeSH secundário: Animais
Feminino
Seres Humanos
Gravidez
Ratos
Ratos Sprague-Dawley
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Scavenger Receptors, Class E)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171006
[Lr] Data última revisão:
171006
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170704
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0180364


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[PMID]:28657156
[Au] Autor:Iacovelli F; Tucci FG; Macari G; Falconi M
[Ad] Endereço:Department of Biology, University of Rome "Tor Vergata", Rome, Italy.
[Ti] Título:Multiple molecular dynamics simulations of human LOX-1 and Trp150Ala mutant reveal the structural determinants causing the full deactivation of the receptor.
[So] Source:Proteins;85(10):1902-1912, 2017 Oct.
[Is] ISSN:1097-0134
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Multiple classical molecular dynamics simulations have been applied to the human LOX-1 receptor to clarify the role of the Trp150Ala mutation in the loss of binding activity. Results indicate that the substitution of this crucial residue, located at the dimer interface, markedly disrupts the wild-type receptor dynamics. The mutation causes an irreversible rearrangement of the subunits interaction pattern that in the wild-type protein allows the maintaining of a specific symmetrical motion of the monomers. The subunits dislocation determines a loss of linearity of the arginines residues composing the basic spine and a consequent alteration of the long-range electrostatic attraction of the substrate. Moreover, the anomalous subunits arrangement observed in the mutated receptor also affects the integrity of the hydrophobic tunnel, actively involved in the short-range hydrophobic recognition of the substrate. The combined effect of these structural rearrangements generates the impairing of the receptor function.
[Mh] Termos MeSH primário: Substituição de Aminoácidos/genética
Proteínas Mutantes/química
Receptores Depuradores Classe E/química
[Mh] Termos MeSH secundário: Sítios de Ligação
Seres Humanos
Interações Hidrofóbicas e Hidrofílicas
Simulação de Dinâmica Molecular
Proteínas Mutantes/genética
Mutação/genética
Ligação Proteica
Receptores Depuradores Classe E/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Mutant Proteins); 0 (OLR1 protein, human); 0 (Scavenger Receptors, Class E)
[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:170629
[St] Status:MEDLINE
[do] DOI:10.1002/prot.25344


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[PMID]:28595908
[Au] Autor:Zhao Y; Li Y; Ning X; Chen K; Zhang S
[Ad] Endereço:State Key Laboratory of Cardiovascular Disease, Fuwai Hospital, National Center for Cardiovascular Diseases, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, China.
[Ti] Título:Association of angiotensin II receptor 1 and lectin-like oxidized low-density lipoprotein receptor-1 mediates the cardiac hypertrophy induced by oxidized low-density lipoprotein.
[So] Source:Biochem Biophys Res Commun;490(1):55-61, 2017 Aug 12.
[Is] ISSN:1090-2104
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:To date the molecular mechanism of cardiac hypertrophy has not been completely elucidated. Since oxidized low-density lipoprotein (ox-LDL) is considered a risk marker for early ventricular remodeling, we speculated that ox-LDL may be related to cardiac hypertrophy. We observed the significantly upregulation of plasma ox-LDL and hypertrophic responses, such as cardiomyocyte size and specific gene expressions in Apo E mice fed with high fat diet, accompanied by the upregulation of AT1-R and lectin-like oxidized low-density protein receptor 1 (LOX-1). Ox-LDL treatment with neonatal rat cardiomyocyte for 24 h significantly induced similar hypertrophic responses and also upregulation of AT1-R and LOX-1. The analysis of co-immunoprecipitation and the bimolecular fluorescence complementation assay proved that LOX-1 and AT1-R could directly bind together in the presence of ox-LDL, suggesting a critical role of the association between LOX-1 and AT1-R in ox-LDL-induced cardiac hypertrophy. Furthermore, we found that the AT1-R blocker Losartan and LOX-1 neutralizing antibody through inhibiting AT1-R or LOX-1 could both decline ox-LDL-induced hypertrophic responses whereas angiotensin converting enzyme inhibitor Enalapril only partially inhibited the responses stimulated by ox-LDL. These findings suggested that ox-LDL could induce cardiac hypertrophy through the direct association of AT1-R and LOX-1.
[Mh] Termos MeSH primário: Proteínas Adaptadoras de Transdução de Sinal/metabolismo
Cardiomegalia/metabolismo
Lipoproteínas LDL/metabolismo
Receptores Depuradores Classe E/metabolismo
[Mh] Termos MeSH secundário: Animais
Cardiomegalia/patologia
Células Cultivadas
Masculino
Camundongos
Camundongos Knockout
Miócitos Cardíacos/metabolismo
Miócitos Cardíacos/patologia
Ratos
Ratos Sprague-Dawley
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Adaptor Proteins, Signal Transducing); 0 (Agtrap protein, mouse); 0 (Lipoproteins, LDL); 0 (Olr1 protein, mouse); 0 (Scavenger Receptors, Class E); 0 (oxidized low density lipoprotein)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170922
[Lr] Data última revisão:
170922
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170610
[St] Status:MEDLINE


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[PMID]:28571642
[Au] Autor:Pothineni NVK; Karathanasis SK; Ding Z; Arulandu A; Varughese KI; Mehta JL
[Ad] Endereço:Division of Cardiovascular Medicine, Central Arkansas Veterans Healthcare System, Little Rock, Arkansas; Division of Cardiovascular Medicine, University of Arkansas for Medical Sciences, Little Rock, Arkansas.
[Ti] Título:LOX-1 in Atherosclerosis and Myocardial Ischemia: Biology, Genetics, and Modulation.
[So] Source:J Am Coll Cardiol;69(22):2759-2768, 2017 Jun 06.
[Is] ISSN:1558-3597
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Lectin-like oxidized low-density lipoprotein receptor-1 (LOX-1), one of the scavenger receptors for oxidized low-density lipoprotein cholesterol (ox-LDL), plays a crucial role in the uptake of ox-LDL by cells in the arterial wall. Mounting evidence suggests a role for LOX-1 in various steps of the atherosclerotic process, from initiation to plaque destabilization. Studies of the genetic structure of LOX-1 have also uncovered various genetic polymorphisms that could modulate the risk of atherosclerotic cardiovascular events. As evidence supporting the vital role of LOX-1 in atherogenesis keeps accumulating, there is growing interest in LOX-1 as a potential therapeutic target. This review discusses the discovery and genetics of LOX-1; describes existing evidence supporting the role of LOX-1 in atherogenesis and its major complication, myocardial ischemia; and summarizes LOX-1 modulation by some naturally occurring compounds and efforts toward development of small molecules and biologics that could be of therapeutic use.
[Mh] Termos MeSH primário: Aterosclerose/genética
Isquemia Miocárdica/genética
Polimorfismo Genético
Receptores Depuradores Classe E/genética
[Mh] Termos MeSH secundário: Aterosclerose/metabolismo
Seres Humanos
Isquemia Miocárdica/metabolismo
Receptores Depuradores Classe E/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (OLR1 protein, human); 0 (Scavenger Receptors, Class E)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170809
[Lr] Data última revisão:
170809
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170603
[St] Status:MEDLINE


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[PMID]:28546421
[Au] Autor:Wang S; Xie X; Lei T; Zhang K; Lai B; Zhang Z; Guan Y; Mao G; Xiao L; Wang N
[Ad] Endereço:Cardiovascular Research Center, School of Medicine, Xi'an Jiaotong University, Xi'an , People's Republic of China (S.W., X.X., T.L., K.Z., B.L., Z.Z., L.X., N.W.); The Advanced Institute for Medical Sciences, Dalian Medical University, Dalian, People's Republic of China (Y.G., N.W.); and Department
[Ti] Título:Statins Attenuate Activation of the NLRP3 Inflammasome by Oxidized LDL or TNF in Vascular Endothelial Cells through a PXR-Dependent Mechanism.
[So] Source:Mol Pharmacol;92(3):256-264, 2017 Sep.
[Is] ISSN:1521-0111
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Excessive activation of the NLRP3 inflammasome is implicated in cardiovascular diseases. Statins exert an anti-inflammatory effect independent of their cholesterol-lowering effect. This study investigated the potential role of statins in the activation of the NLRP3 inflammasome in endothelial cells (ECs). Western blotting and quantitative reverse-transcription polymerase chain reaction showed that oxidized low-density lipoprotein (ox-LDL) or tumor necrosis factor α (TNF ) activated the NLRP3 inflammasome in ECs. Simvastatin or mevastatin significantly suppressed the effects of ox-LDL or TNF Promoter reporter assays and small interfering RNA knockdown revealed that statins inhibit ox-LDL-mediated NLRP3 inflammasome activation via the pregnane X receptor (PXR). In addition, PXR agonists (rifampicin and SR12813) or overexpression of a constitutively active PXR markedly suppressed the NLRP3 inflammasome activation. Conversely, PXR knockdown abrogated the suppressive effect of rifampicin on NLRP3 inflammasome activation. Knockdown of lectin-like ox-LDL receptor or overexpression of I B -attenuated ox-LDL- or TNF -triggered activation of the NLRP3 inflammasome. Chromatin immunoprecipitation assays indicated that mevastatin inhibited nuclear factor-κB binding to the promoter regions of the human NLRP3 gene. Collectively, these results demonstrate that the statin activation of PXR inhibits the activation of NLRP3 inflammasome in response to atherogenic stimuli such as ox-LDL and TNF in ECs, providing a new mechanism for the cardiovascular benefit of statins.
[Mh] Termos MeSH primário: Inibidores de Hidroximetilglutaril-CoA Redutases/farmacologia
Lipoproteínas LDL/antagonistas & inibidores
Proteína 3 que Contém Domínio de Pirina da Família NLR/antagonistas & inibidores
Receptores de Esteroides/fisiologia
Fator de Necrose Tumoral alfa/antagonistas & inibidores
[Mh] Termos MeSH secundário: Células Cultivadas
Células Endoteliais/metabolismo
Seres Humanos
Lipoproteínas LDL/farmacologia
NF-kappa B/fisiologia
Proteína 3 que Contém Domínio de Pirina da Família NLR/genética
Proteína 3 que Contém Domínio de Pirina da Família NLR/fisiologia
Regiões Promotoras Genéticas
Receptores de Esteroides/agonistas
Receptores Depuradores Classe E/fisiologia
Transdução de Sinais/efeitos dos fármacos
Fator de Necrose Tumoral alfa/farmacologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Hydroxymethylglutaryl-CoA Reductase Inhibitors); 0 (Lipoproteins, LDL); 0 (NF-kappa B); 0 (NLR Family, Pyrin Domain-Containing 3 Protein); 0 (NLRP3 protein, human); 0 (OLR1 protein, human); 0 (Receptors, Steroid); 0 (Scavenger Receptors, Class E); 0 (Tumor Necrosis Factor-alpha); 0 (oxidized low density lipoprotein); 0 (pregnane X receptor)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170830
[Lr] Data última revisão:
170830
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170527
[St] Status:MEDLINE
[do] DOI:10.1124/mol.116.108100



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