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[PMID]:28468674
[Au] Autor:Cunningham DA; Lin JW; Brugat T; Jarra W; Tumwine I; Kushinga G; Ramesar J; Franke-Fayard B; Langhorne J
[Ad] Endereço:The Francis Crick Institute, London, NW1 1AT, UK. Deirdre.Cunningham@crick.ac.uk.
[Ti] Título:ICAM-1 is a key receptor mediating cytoadherence and pathology in the Plasmodium chabaudi malaria model.
[So] Source:Malar J;16(1):185, 2017 05 03.
[Is] ISSN:1475-2875
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Parasite cytoadherence within the microvasculature of tissues and organs of infected individuals is implicated in the pathogenesis of several malaria syndromes. Multiple host receptors may mediate sequestration. The identity of the host receptor(s), or the parasite ligand(s) responsible for sequestration of Plasmodium species other than Plasmodium falciparum is largely unknown. The rodent malaria parasites may be useful to model interactions of parasite species, which lack the var genes with their respective hosts, as other multigene families are shared between the species. The role of the endothelial receptors ICAM-1 and CD36 in cytoadherence and in the development of pathology was investigated in a Plasmodium chabaudi infection in C57BL/6 mice lacking these receptors. The schizont membrane-associated cytoadherence (SMAC) protein of Plasmodium berghei has been shown to exhibit reduced CD36-associated cytoadherence in P. berghei ANKA-infected mice. METHODS: Parasite tissue sequestration and the development of acute stage pathology in P. chabaudi infections of mice lacking CD36 or ICAM-1, their respective wild type controls, and in infections with mutant P. chabaudi parasites lacking the smac gene were compared. Peripheral blood parasitaemia, red blood cell numbers and weight change were monitored throughout the courses of infection. Imaging of bioluminescent parasites in isolated tissues (spleen, lungs, liver, kidney and gut) was used to measure tissue parasite load. RESULTS: This study shows that neither the lack of CD36 nor the deletion of the smac gene from P. chabaudi significantly impacted on acute-stage pathology or parasite sequestration. By contrast, in the absence of ICAM-1, infected animals experience less anaemia and weight loss, reduced parasite accumulation in both spleen and liver and higher peripheral blood parasitaemia during acute stage malaria. The reduction in parasite tissue sequestration in infections of ICAM-1 null mice is maintained after mosquito transmission. CONCLUSIONS: These results indicate that ICAM-1-mediated cytoadherence is important in the P. chabaudi model of malaria and suggest that for rodent malarias, as for P. falciparum, there may be multiple host and parasite molecules involved in sequestration.
[Mh] Termos MeSH primário: Antígenos CD36/genética
Molécula 1 de Adesão Intercelular/genética
Malária/parasitologia
Plasmodium chabaudi/fisiologia
Proteínas de Protozoários/genética
[Mh] Termos MeSH secundário: Animais
Antígenos CD36/metabolismo
Feminino
Molécula 1 de Adesão Intercelular/metabolismo
Camundongos
Camundongos Endogâmicos C57BL
Plasmodium chabaudi/genética
Proteínas de Protozoários/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (CD36 Antigens); 0 (Icam1 protein, mouse); 0 (Protozoan Proteins); 126547-89-5 (Intercellular Adhesion Molecule-1)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180223
[Lr] Data última revisão:
180223
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170505
[St] Status:MEDLINE
[do] DOI:10.1186/s12936-017-1834-8


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[PMID]:29258822
[Au] Autor:Huangfu N; Xu Z; Zheng W; Wang Y; Cheng J; Chen X
[Ad] Endereço:Department of Cardiology, Ningbo First Hospital, Ningbo, PR China.
[Ti] Título:LncRNA MALAT1 regulates oxLDL-induced CD36 expression via activating ß-catenin.
[So] Source:Biochem Biophys Res Commun;495(3):2111-2117, 2018 01 15.
[Is] ISSN:1090-2104
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The expression of scavenger receptors in macrophages regulating lipid uptake plays an important role in foam cell formation and the subsequent atherosclerotic plaque formation. Long non-coding RNA MALAT1 is abundantly expressed in THP-1-derived macrophages, and oxidized low-density lipoprotein promotes its transcription by qRT-PCR and RNA FISH detection. Through chemical inhibitor treatments and by performing a dual luciferase reporter analysis, we found that oxLDL induces MALAT1 transcription through the NF-κB pathway. The knockdown of MALAT1 using siRNA transfection affects lipid uptake in macrophages. To understand the details, we checked the scavenger receptors, which mainly control lipid uptake, and found that MALAT1 knockdown decreased CD36 expression. Additionally, we also incubated macrophages with actinomycin D, combined with a dual luciferase reporter analysis, and we found that MALAT1 influenced CD36 expression at the transcription level. We aim to investigate the detailed mechanism by which MALAT1 promotes CD36 transcription, and thus, we designed and synthesized biotin-TEG labeled oligonucleotides to precipitate the MALAT1 RNA-DNA-protein complex in vivo. Combined with SDS-PAGE electrophoresis and a subsequent mass spectra analysis, ß-catenin, a transcription factor that promotes CD36 transcription, was found in the complex. By performing R-IPs, we validated that ß-catenin was bound to MALAT1 under the oxLDL treatment. In addition, using VAX939, a chemical inhibitor of ß-catenin, MALAT1 was demonstrated to promote CD36 transcription partly via ß-catenin. We also performed chips to detect whether MALAT1 affects ß-catenin accumulation in the binding sites of the CD36 promoter and found that MALAT1 knockdown decreases ß-catenin binding to the CD36 promoter and vice versa. In conclusion, oxLDL induced MALAT1 transcription and MALAT1 recruits ß-catenin to binding sites on the CD36 promoter to induce CD36 expression, which enhances lipid uptake in macrophages.
[Mh] Termos MeSH primário: Antígenos CD36/metabolismo
Metabolismo dos Lipídeos/fisiologia
Lipoproteínas LDL/metabolismo
Macrófagos/metabolismo
RNA Longo não Codificante/metabolismo
beta Catenina/metabolismo
[Mh] Termos MeSH secundário: Regulação da Expressão Gênica/fisiologia
Seres Humanos
Células THP-1
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (CD36 Antigens); 0 (CTNNB1 protein, human); 0 (Lipoproteins, LDL); 0 (MALAT1 long non-coding RNA, human); 0 (RNA, Long Noncoding); 0 (beta Catenin); 0 (oxidized low density lipoprotein)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180213
[Lr] Data última revisão:
180213
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171221
[St] Status:MEDLINE


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[PMID]:28464262
[Au] Autor:Reales G; Rovaris DL; Jacovas VC; Hünemeier T; Sandoval JR; Salazar-Granara A; Demarchi DA; Tarazona-Santos E; Felkl AB; Serafini MA; Salzano FM; Bisso-Machado R; Comas D; Paixão-Côrtes VR; Bortolini MC
[Ad] Endereço:Departamento de Genética, Instituto de Biociências, Universidade Federal do Rio Grande do Sul, Porto Alegre, Brazil.
[Ti] Título:A tale of agriculturalists and hunter-gatherers: Exploring the thrifty genotype hypothesis in native South Americans.
[So] Source:Am J Phys Anthropol;163(3):591-601, 2017 07.
[Is] ISSN:1096-8644
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:OBJECTIVES: To determine genetic differences between agriculturalist and hunter-gatherer southern Native American populations for selected metabolism-related markers and to test whether Neel's thrifty genotype hypothesis (TGH) could explain the genetic patterns observed in these populations. MATERIALS AND METHODS: 375 Native South American individuals from 17 populations were genotyped using six markers (APOE rs429358 and rs7412; APOA2 rs5082; CD36 rs3211883; TCF7L2 rs11196205; and IGF2BP2 rs11705701). Additionally, APOE genotypes from 39 individuals were obtained from the literature. AMOVA, main effects, and gene-gene interaction tests were performed. RESULTS: We observed differences in allele distribution patterns between agriculturalists and hunter-gatherers for some markers. For instance, between-groups component of genetic variance (F ) for APOE rs429358 showed strong differences in allelic distributions between hunter-gatherers and agriculturalists (p = 0.00196). Gene-gene interaction analysis indicated that the APOE E4/CD36 TT and APOE E4/IGF2BP2 A carrier combinations occur at a higher frequency in hunter-gatherers, but this combination is not replicated in archaic (Neanderthal and Denisovan) and ancient (Anzick, Saqqaq, Ust-Ishim, Mal'ta) hunter-gatherer individuals. DISCUSSION: A complex scenario explains the observed frequencies of the tested markers in hunter-gatherers. Different factors, such as pleotropic alleles, rainforest selective pressures, and population dynamics, may be collectively shaping the observed genetic patterns. We conclude that although TGH seems a plausible hypothesis to explain part of the data, other factors may be important in our tested populations.
[Mh] Termos MeSH primário: Agricultura/história
Índios Sul-Americanos/genética
Índios Sul-Americanos/história
Polimorfismo de Nucleotídeo Único/genética
[Mh] Termos MeSH secundário: Antropologia Física
Apolipoproteínas E/genética
Antígenos CD36/genética
Genótipo
História Antiga
Seres Humanos
Proteínas de Ligação a RNA/genética
[Pt] Tipo de publicação:HISTORICAL ARTICLE; JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (ApoE protein, human); 0 (Apolipoproteins E); 0 (CD36 Antigens); 0 (IGF2BP2 protein, human); 0 (RNA-Binding Proteins)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:180214
[Lr] Data última revisão:
180214
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170503
[St] Status:MEDLINE
[do] DOI:10.1002/ajpa.23233


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[PMID]:29198193
[Au] Autor:Cai Z; Mai K; Ai Q
[Ad] Endereço:Key Laboratory of Aquaculture Nutrition and Feed (Ministry of Agriculture) & Key Laboratory of Mariculture (Ministry of Education),Ocean University of China,5 Yushan Road,Qingdao,Shandong 266003,People's Republic of China.
[Ti] Título:Regulation of hepatic lipid deposition by phospholipid in large yellow croaker.
[So] Source:Br J Nutr;118(12):999-1009, 2017 Dec.
[Is] ISSN:1475-2662
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Dietary phospholipid (PL) supplementation has been shown to reduce lipid accumulation in the tissues of farmed fish; however, the mechanisms underlying this effect are largely unknown. Thus, the present study was conducted to evaluate the potential impacts of PL on hepatic lipid metabolism both in vivo and in vitro. For in vivo study, four experimental diets - low lipid and low PL diet, as control diet (LL-LP diet, containing 12 % lipid and 1·5 % PL), low-lipid and high-PL diet (containing 12 % lipid and 8 % PL), high-lipid and low-PL diet (HL-LP diet, containing 20 % lipid and 1·5 % PL) and high-lipid and high-PL diet (HL-HP diet, containing 20 % lipid and 8 % PL) - were randomly allocated to four groups of large yellow croaker (Larimichthys crocea) (three cages per group) with similar initial body weight (approximately 8 g). For in vitro study, primary hepatocytes isolated from large yellow croaker were incubated either with graded levels of phosphatidylcholine (PC) (0-250 µm) or small interfering RNA (siRNA) for CTP: choline phosphate cytidylyltranferase α (CCTα) (siRNA-CCTα). Results showed that survival was independent of dietary treatments (P>0·05). Weight gain and feed efficiency in the HL-HP group were significantly higher than in the LL-LP and HL-LP groups (P<0·05). High level of dietary PL could markedly reduce abnormal hepatic lipid accumulation induced by the HL-LP diet (P<0·05). Similarly, compared with the corresponding controls, a significant decrease/increase in lipid content was observed in primary hepatocytes incubated with PC/siRNA-CCTα (P<0·05). High level of dietary PL reversed the HL-LP diet-induced increased levels of mRNA of fatty acid uptake and lipid synthesis related genes (P<0·05). In addition, High level of dietary PL markedly down-regulated the transcript levels of fatty acid oxidation-related genes and enhanced the transcript levels of VLDL assembly-related genes regardless of dietary lipid levels (P<0·05). Compared with corresponding controls, primary hepatocytes treated with PC showed significantly higher mRNA expression of lipid synthesis and VLDL assembly-related genes and lower mRNA expression of fatty acid oxidation-related genes, with hepatocytes treated with siRNA-CCTα exhibiting the opposite trend (P<0·05). In summary, these results demonstrated that high level of dietary PL might reverse the HL-LP diet-induced abnormal lipid accumulation in the liver through inhibiting fatty acid uptake and lipid synthesis, together with promoting the lipid export at the transcriptional level. Lipid export-promoting effect of PC was confirmed by in vitro studies. The present study showed for the first time that PL or PC could influence various metabolic pathways to regulate hepatic lipid deposition in fish at least at the transcriptional level.
[Mh] Termos MeSH primário: Dieta/veterinária
Metabolismo dos Lipídeos
Fígado/metabolismo
Perciformes/metabolismo
Fosfolipídeos/administração & dosagem
[Mh] Termos MeSH secundário: Ração Animal
Animais
Antígenos CD36/genética
Antígenos CD36/metabolismo
Células Cultivadas
Diacilglicerol O-Aciltransferase/genética
Diacilglicerol O-Aciltransferase/metabolismo
Ácido Graxo Sintases/genética
Ácido Graxo Sintases/metabolismo
Proteínas de Transporte de Ácido Graxo/genética
Proteínas de Transporte de Ácido Graxo/metabolismo
Proteínas de Ligação a Ácido Graxo/genética
Proteínas de Ligação a Ácido Graxo/metabolismo
Ácidos Graxos/metabolismo
Proteínas de Peixes/genética
Proteínas de Peixes/metabolismo
Hepatócitos/metabolismo
Lipase/genética
Lipase/metabolismo
Lipase Lipoproteica/genética
Lipase Lipoproteica/metabolismo
Fosfatidilcolinas/administração & dosagem
Proteína de Ligação a Elemento Regulador de Esterol 1/genética
Proteína de Ligação a Elemento Regulador de Esterol 1/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (CD36 Antigens); 0 (Fatty Acid Transport Proteins); 0 (Fatty Acid-Binding Proteins); 0 (Fatty Acids); 0 (Fish Proteins); 0 (Phosphatidylcholines); 0 (Phospholipids); 0 (Sterol Regulatory Element Binding Protein 1); EC 2.3.1.20 (Diacylglycerol O-Acyltransferase); EC 2.3.1.85 (Fatty Acid Synthases); EC 3.1.1.3 (Lipase); EC 3.1.1.34 (Lipoprotein Lipase)
[Em] Mês de entrada:1712
[Cu] Atualização por classe:171227
[Lr] Data última revisão:
171227
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171205
[St] Status:MEDLINE
[do] DOI:10.1017/S000711451700294X


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[PMID]:29016649
[Au] Autor:Ohn JH; Hwang JY; Moon MK; Ahn HY; Kim HH; Koo YD; Kim KI; Chang HJ; Lee HS; Jang HC; Park YJ
[Ad] Endereço:Department of Internal Medicine, Seoul National University Bundang Hospital, Seongnam, Republic of Korea.
[Ti] Título:Small heterodimer partner (SHP) deficiency protects myocardia from lipid accumulation in high fat diet-fed mice.
[So] Source:PLoS One;12(10):e0186021, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The small heterodimer partner (SHP) regulates fatty acid oxidation and lipogenesis in the liver by regulating peroxisome proliferator-activated receptor (PPAR) γ expression. SHP is also abundantly expressed in the myocardium. We investigated the effect of SHP expression on myocardia assessing not only heart structure and function but also lipid metabolism and related gene expression in a SHP deletion animal model. Transcriptional profiling with a microarray revealed that genes participating in cell growth, cytokine signalling, phospholipid metabolism, and extracellular matrix are up-regulated in the myocardia of SHP knockout (KO) mice compared to those of wild-type (WT) mice (nominal p value < 0.05). Consistent with these gene expression changes, the left ventricular masses of SHP KO mice were significantly higher than WT mice (76.8 ± 20.5 mg vs. 52.8 ± 6.8 mg, P = 0.0093). After 12 weeks of high fat diet (HFD), SHP KO mice gained less weight and exhibited less elevation in serum-free fatty acid and less ectopic lipid accumulation in the myocardium than WT mice. According to microarray analysis, genes regulated by PPARγ1 and PPARα were down-regulated in myocardia of SHP KO mice compared to their expression in WT mice after HFD, suggesting that the reduction in lipid accumulation in the myocardium resulted from a decrease in lipogenesis regulated by PPARγ. We confirmed the reduced expression of PPARγ1 and PPARα target genes such as CD36, medium-chain acyl-CoA dehydrogenase, long-chain acyl-CoA dehydrogenase, and very long-chain acyl-CoA dehydrogenase by SHP KO after HFD.
[Mh] Termos MeSH primário: Lipogênese/genética
Miocárdio/metabolismo
Obesidade/genética
Receptores Citoplasmáticos e Nucleares/genética
Transcriptoma
[Mh] Termos MeSH secundário: Acil-CoA Desidrogenase/genética
Acil-CoA Desidrogenase/metabolismo
Acil-CoA Desidrogenase de Cadeia Longa/deficiência
Acil-CoA Desidrogenase de Cadeia Longa/genética
Acil-CoA Desidrogenase de Cadeia Longa/metabolismo
Animais
Antígenos CD36/genética
Antígenos CD36/metabolismo
Citocinas/genética
Citocinas/metabolismo
Dieta Hiperlipídica
Ácidos Graxos/metabolismo
Perfilação da Expressão Gênica
Erros Inatos do Metabolismo Lipídico/genética
Erros Inatos do Metabolismo Lipídico/metabolismo
Fígado/metabolismo
Fígado/patologia
Masculino
Camundongos
Camundongos Knockout
Doenças Mitocondriais/genética
Doenças Mitocondriais/metabolismo
Doenças Musculares/genética
Doenças Musculares/metabolismo
Miocárdio/patologia
Obesidade/etiologia
Obesidade/metabolismo
Obesidade/patologia
Análise de Sequência com Séries de Oligonucleotídeos
PPAR alfa/genética
PPAR alfa/metabolismo
PPAR gama/genética
PPAR gama/metabolismo
Fatores de Proteção
Receptores Citoplasmáticos e Nucleares/deficiência
Transdução de Sinais
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (CD36 Antigens); 0 (Cytokines); 0 (Fatty Acids); 0 (PPAR alpha); 0 (PPAR gamma); 0 (Receptors, Cytoplasmic and Nuclear); 0 (nuclear receptor subfamily 0, group B, member 2); EC 1.3.8.7 (Acyl-CoA Dehydrogenase); EC 1.3.8.8 (Acyl-CoA Dehydrogenase, Long-Chain)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171011
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0186021


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[PMID]:28965954
[Au] Autor:Li BR; Xia LQ; Liu J; Liao LL; Zhang Y; Deng M; Zhong HJ; Feng TT; He PP; Ouyang XP
[Ad] Endereço:Department of Physiology, Shaoyang Medical College, Shaoyang, Hunan 422000, China.
[Ti] Título:miR-758-5p regulates cholesterol uptake via targeting the CD36 3'UTR.
[So] Source:Biochem Biophys Res Commun;494(1-2):384-389, 2017 Dec 09.
[Is] ISSN:1090-2104
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:miR-758-3p plays an important role via regulting ABCA1-mediated cholesterol efflux in atherosclerosis. However, the mechanism of miR-758-5p in cholesterol metabolism is still unclear. Here, we revealed that miR-758-5p decreased total cholesterol accumulation in THP-1 macrophage derived foam cells through markedly reducing cholesterol uptake, and no effect on the cholesterol efflux. Interestingly, computational analysis suggests that CD36 may be a target gene of miR-758-5p. Our study further demonstrated that miR-758-5p decreased CD36 expression at both protein and mRNA levels via targeting the CD36 3'UTR in THP-1 macrophage derived foam cells. The present present study concluded that miR-758-5p decreases lipid accumulation of foam cell via regulating CD36-mediated the cholesterol uptake. Therefore, targeting miR-758-5p may offer a promising strategy to treat atherosclerotic vascular disease.
[Mh] Termos MeSH primário: Regiões 3´ não Traduzidas
Antígenos CD36/genética
Colesterol/metabolismo
Células Espumosas/metabolismo
MicroRNAs/genética
Isoformas de RNA/genética
[Mh] Termos MeSH secundário: Sequência de Bases
Sítios de Ligação
Transporte Biológico
Antígenos CD36/metabolismo
Linhagem Celular
Células Espumosas/citologia
Regulação da Expressão Gênica
Seres Humanos
MicroRNAs/metabolismo
Isoformas de RNA/metabolismo
Transdução de Sinais
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (3' Untranslated Regions); 0 (CD36 Antigens); 0 (MIRN758 microRNA, human); 0 (MicroRNAs); 0 (RNA Isoforms); 97C5T2UQ7J (Cholesterol)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171003
[St] Status:MEDLINE


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[PMID]:28935758
[Au] Autor:Marcovecchio PM; Thomas GD; Mikulski Z; Ehinger E; Mueller KAL; Blatchley A; Wu R; Miller YI; Nguyen AT; Taylor AM; McNamara CA; Ley K; Hedrick CC
[Ad] Endereço:From the Department of Medicine, University of California San Diego School of Medicine, La Jolla (P.M.M., Y.I.M.); Division of Inflammation Biology, La Jolla Institute for Allergy and Immunology, CA (P.M.M., G.D.T., Z.M., E.E., K.A.L.M., A.B., R.W., K.L., C.C.H.); Department of Cardiology and Circul
[Ti] Título:Scavenger Receptor CD36 Directs Nonclassical Monocyte Patrolling Along the Endothelium During Early Atherogenesis.
[So] Source:Arterioscler Thromb Vasc Biol;37(11):2043-2052, 2017 Nov.
[Is] ISSN:1524-4636
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:OBJECTIVE: Nonclassical monocytes (NCM) function to maintain vascular homeostasis by crawling or patrolling along the vessel wall. This subset of monocytes responds to viruses, tumor cells, and other pathogens to aid in protection of the host. In this study, we wished to determine how early atherogenesis impacts NCM patrolling in the vasculature. APPROACH AND RESULTS: To study the role of NCM in early atherogenesis, we quantified the patrolling behaviors of NCM in ApoE (apolipoprotein E) and C57BL/6J mice fed a Western diet. Using intravital imaging, we found that NCM from Western diet-fed mice display a 4-fold increase in patrolling activity within large peripheral blood vessels. Both human and mouse NCM preferentially engulfed OxLDL (oxidized low-density lipoprotein) in the vasculature, and we observed that OxLDL selectively induced NCM patrolling in vivo. Induction of patrolling during early atherogenesis required scavenger receptor CD36, as CD36 mice revealed a significant reduction in patrolling activity along the femoral vasculature. Mechanistically, we found that CD36-regulated patrolling was mediated by a SFK (src family kinase) through DAP12 (DNAX activating protein of 12KDa) adaptor protein. CONCLUSIONS: Our studies show a novel pathway for induction of NCM patrolling along the vascular wall during early atherogenesis. Mice fed a Western diet showed increased NCM patrolling activity with a concurrent increase in SFK phosphorylation. This patrolling activity was lost in the absence of either CD36 or DAP12. These data suggest that NCM function in an atheroprotective manner through sensing and responding to oxidized lipoprotein moieties via scavenger receptor engagement during early atherogenesis.
[Mh] Termos MeSH primário: Aterosclerose/metabolismo
Antígenos CD36/metabolismo
Células Endoteliais/metabolismo
Endotélio Vascular/metabolismo
Artéria Femoral/metabolismo
Migração e Rolagem de Leucócitos
Monócitos/metabolismo
[Mh] Termos MeSH secundário: Citoesqueleto de Actina/metabolismo
Proteínas Adaptadoras de Transdução de Sinal/metabolismo
Animais
Apolipoproteínas E/deficiência
Apolipoproteínas E/genética
Aterosclerose/genética
Aterosclerose/patologia
Antígenos CD36/deficiência
Antígenos CD36/genética
Dieta Ocidental
Modelos Animais de Doenças
Células Endoteliais/patologia
Endotélio Vascular/patologia
Artéria Femoral/patologia
Predisposição Genética para Doença
Seres Humanos
Microscopia Intravital
Lipoproteínas LDL/metabolismo
Camundongos Endogâmicos C57BL
Camundongos Knockout
Monócitos/patologia
Fenótipo
Transdução de Sinais
Fatores de Tempo
Quinases da Família src/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; VIDEO-AUDIO MEDIA
[Nm] Nome de substância:
0 (Adaptor Proteins, Signal Transducing); 0 (Apolipoproteins E); 0 (CD36 Antigens); 0 (Lipoproteins, LDL); 0 (Tyrobp protein, mouse); 0 (oxidized low density lipoprotein); EC 2.7.10.2 (src-Family Kinases)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170923
[St] Status:MEDLINE
[do] DOI:10.1161/ATVBAHA.117.309123


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[PMID]:28866086
[Au] Autor:Chu Y; Lao W; Jin G; Dai D; Chen L; Kang H
[Ad] Endereço:Department of Laboratory Medicine, The First Affiliated Hospital of China Medical University, Shenyang 110001, Liaoning Province, China.
[Ti] Título:Evaluation of the relationship between CD36 and MARCO single-nucleotide polymorphisms and susceptibility to carotid atherosclerosis in a Chinese Han population.
[So] Source:Gene;633:66-70, 2017 Oct 30.
[Is] ISSN:1879-0038
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:OBJECTIVE: This study analyzed the genetic association between two scavenger receptors single nucleotide polymorphisms (CD36 rs1761667, MARCO rs12998782) and carotid atherosclerosis in a Chinese Han population. METHODS: Samples of genomic DNA collected from patients (n=215) and healthy control subjects (n=252) were analyzed by the polymerase chain reaction with high-resolution melting analysis. Odds ratios and 95% confidence intervals were used to evaluate the association between the two SNPs and carotid atherosclerosis. RESULTS: There was no difference between the SNPs regarding their association with the frequency of carotid atherosclerosis in the case and control groups or in the male case group and control group. Female patients of genotype GA for CD36 rs1761667 and CT for MARCO rs12998782 were at an increased risk for carotid atherosclerosis. The presence of rs1761667 GA and rs12998782 CT may increase the risk for carotid atherosclerosis among postmenopausal females. CONCLUSIONS: CD36 and MARCO are associated with the susceptibility of Chinese Han females to carotid atherosclerosis. Menopausal status may affect the association between gene polymorphisms and carotid atherosclerosis in the female Chinese Han population.
[Mh] Termos MeSH primário: Antígenos CD36/genética
Doenças das Artérias Carótidas/genética
Predisposição Genética para Doença/genética
Polimorfismo de Nucleotídeo Único
Receptores Imunológicos/genética
[Mh] Termos MeSH secundário: Grupo com Ancestrais do Continente Asiático/genética
Doenças das Artérias Carótidas/epidemiologia
China/epidemiologia
Feminino
Estudos de Associação Genética
Seres Humanos/genética
Masculino
Meia-Idade
Razão de Chances
Pós-Menopausa/genética
Fatores de Risco
Fatores Sexuais
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (CD36 Antigens); 0 (MARCO protein, human); 0 (Receptors, Immunologic)
[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:170904
[St] Status:MEDLINE


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[PMID]:28806616
[Au] Autor:Janovitz T; Wong S; Young NS; Oliveira T; Falck-Pedersen E
[Ad] Endereço:Tri-Institutional MD-PhD Program, USA; Department of Microbiology and Immunology, Weill Medical College of Cornell University, New York, NY 10065, USA.
[Ti] Título:Parvovirus B19 integration into human CD36+ erythroid progenitor cells.
[So] Source:Virology;511:40-48, 2017 Nov.
[Is] ISSN:1096-0341
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The pathogenic autonomous human parvovirus B19 (B19V) productively infects erythroid progenitor cells (EPCs). Functional similarities between B19V nonstructural protein (NS1), a DNA binding endonuclease, and the Rep proteins of Adeno-Associated Virus (AAV) led us to hypothesize that NS1 may facilitate targeted nicking of the human genome and B19 vDNA integration. We adapted an integration capture sequencing protocol (IC-Seq) to screen B19V infected human CD36+ EPCs for viral integrants, and discovered 40,000 unique B19V integration events distributed throughout the human genome. Computational analysis of integration patterns revealed strong correlations with gene intronic regions, H3K9me3 sites, and the identification of 41 base pair consensus sequence with an octanucleotide core motif. The octanucleotide core has homology to a single region of B19V, adjacent to the P6 promoter TATA box. We present the first direct evidence that B19V infection of erythroid progenitor cells disrupts the human genome and facilitates viral DNA integration.
[Mh] Termos MeSH primário: Proteínas de Ligação a DNA/metabolismo
DNA/metabolismo
Endonucleases/metabolismo
Células Precursoras Eritroides/virologia
Parvovirus B19 Humano/fisiologia
Proteínas não Estruturais Virais/metabolismo
Integração Viral
[Mh] Termos MeSH secundário: Antígenos CD36/análise
Células Cultivadas
Células Precursoras Eritroides/química
Seres Humanos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (CD36 Antigens); 0 (DNA-Binding Proteins); 0 (Viral Nonstructural Proteins); 9007-49-2 (DNA); EC 3.1.- (Endonucleases)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170815
[St] Status:MEDLINE


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[PMID]:28789920
[Au] Autor:Li J; Yu C; Wang R; Xu J; Chi Y; Qin J; Liu Q
[Ad] Endereço:Key Laboratory of Carbohydrate and Lipid Metabolism Research, College of Life Science and Technology, Dalian University, 10-Xuefu Avenue, Dalian Economical and Technological Development Zone, Liaoning 116622, China; School of Life Science and Biotechnology, Dalian University of Technology, Dalian 11
[Ti] Título:The ω-carboxyl group of 7-ketocholesteryl-9-carboxynonanoate mediates the binding of oxLDL to CD36 receptor and enhances caveolin-1 expression in macrophages.
[So] Source:Int J Biochem Cell Biol;90:121-135, 2017 Sep.
[Is] ISSN:1878-5875
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:CD36 signal transduction modulates the uptake of oxidized low-density lipoprotein (oxLDL) and foam cell formation. We previously observed that 7-ketocholesteryl-9-carboxynonanoate (oxLig-1), the lipid moiety of oxLDL, activates the CD36-Src-JNK/ERK1/2 signalling pathway. In this study, we assessed the role of the ω-carboxyl group in the binding of oxLig-1 to CD36 and investigated whether the binding of the ω-carboxyl group to CD36 triggers CD36-mediated signalling, thereby resulting in the upregulation of caveolin-1 expression. Our results showed that oxLig-1 bound to CD36 and that the ω-carboxyl group was critical for this binding. Furthermore, immunoprecipitation and Western blot analyses showed that interaction between the ω-carboxyl group of oxLig-1 and CD36 triggered intracellular Src-JNK/ERK1/2 signal transduction. Moreover, the binding of the ω-carboxyl group to CD36 induced caveolin-1 expression and translocation to the membrane in macrophages. Additionally, inhibitors of Src, JNK and ERK and siRNA targeting CD36 and NF-κB significantly suppressed the enhanced caveolin-1 expression induced by oxLig-1. In conclusion, these observations suggest that oxLig-1 is a critical epitope of oxLDL that mediates the binding of oxLDL to CD36 and activates downstream Src-JNK/ERK1/2-NF-κB signal transduction, resulting in upregulation of caveolin-1 expression in macrophages.
[Mh] Termos MeSH primário: Antígenos CD36/metabolismo
Caveolina 1/metabolismo
Ésteres do Colesterol/química
Ésteres do Colesterol/farmacologia
Regulação da Expressão Gênica/efeitos dos fármacos
Lipoproteínas LDL/metabolismo
Macrófagos/efeitos dos fármacos
[Mh] Termos MeSH secundário: Antígenos CD36/química
Linhagem Celular
MAP Quinases Reguladas por Sinal Extracelular/metabolismo
Seres Humanos
Proteínas Quinases JNK Ativadas por Mitógeno/metabolismo
Lipoproteínas LDL/química
Sistema de Sinalização das MAP Quinases/efeitos dos fármacos
Macrófagos/citologia
Macrófagos/metabolismo
Simulação de Acoplamento Molecular
NF-kappa B/metabolismo
Ligação Proteica/efeitos dos fármacos
Conformação Proteica
Transporte Proteico/efeitos dos fármacos
Proteínas Proto-Oncogênicas c-fyn/metabolismo
Relação Estrutura-Atividade
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (7-ketocholesteryl-9-carboxynonanoate); 0 (CD36 Antigens); 0 (Caveolin 1); 0 (Cholesterol Esters); 0 (Lipoproteins, LDL); 0 (NF-kappa B); 0 (oxidized low density lipoprotein); EC 2.7.10.2 (Proto-Oncogene Proteins c-fyn); EC 2.7.11.24 (Extracellular Signal-Regulated MAP Kinases); EC 2.7.11.24 (JNK Mitogen-Activated Protein Kinases)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170810
[St] Status:MEDLINE



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