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[PMID]:29419393
[Au] Autor:Ford TJ; Rocchiccioli P
[Ad] Endereço:British Heart Foundation Glasgow Cardiovascular Research Centre, Institute of Cardiovascular and Medical Sciences, University of Glasgow, Glasgow, UK.
[Ti] Título:A keen eye for risk.
[So] Source:BMJ;360:j5884, 2018 02 01.
[Is] ISSN:1756-1833
[Cp] País de publicação:England
[La] Idioma:eng
[Mh] Termos MeSH primário: Arco Senil/diagnóstico
Doenças da Córnea/diagnóstico
Doença da Artéria Coronariana/diagnóstico
Hiperlipoproteinemia Tipo II/diagnóstico
Receptores de LDL/genética
[Mh] Termos MeSH secundário: Anticorpos Monoclonais/administração & dosagem
Anticorpos Monoclonais/uso terapêutico
Anticolesterolemiantes/administração & dosagem
Anticolesterolemiantes/uso terapêutico
Arco Senil/etiologia
Colesterol/sangue
Doenças da Córnea/etiologia
Doença da Artéria Coronariana/complicações
Doença da Artéria Coronariana/etiologia
Feminino
Seres Humanos
Inibidores de Hidroximetilglutaril-CoA Redutases/uso terapêutico
Hiperlipoproteinemia Tipo II/sangue
Hiperlipoproteinemia Tipo II/tratamento farmacológico
Hiperlipoproteinemia Tipo II/genética
Injeções Subcutâneas
Meia-Idade
Mutação
Pró-Proteína Convertase 9/antagonistas & inibidores
Xantomatose/diagnóstico
Xantomatose/etiologia
[Pt] Tipo de publicação:CASE REPORTS; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antibodies, Monoclonal); 0 (Anticholesteremic Agents); 0 (Hydroxymethylglutaryl-CoA Reductase Inhibitors); 0 (Receptors, LDL); 97C5T2UQ7J (Cholesterol); EC 3.4.21.- (PCSK9 protein, human); EC 3.4.21.- (Proprotein Convertase 9); LKC0U3A8NJ (evolocumab)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180305
[Lr] Data última revisão:
180305
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:180209
[St] Status:MEDLINE
[do] DOI:10.1136/bmj.j5884


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[PMID]:28460556
[Au] Autor:Perani CV; Langgartner D; Uschold-Schmidt N; Füchsl AM; Neumann ID; Reber SO; Slattery DA
[Ad] Endereço:a Department of Behavioural and Molecular Neurobiology , University of Regensburg , Regensburg , Germany.
[Ti] Título:Adrenal gland plasticity in lactating rats and mice is sufficient to maintain basal hypersecretion of corticosterone.
[So] Source:Stress;20(3):303-311, 2017 May.
[Is] ISSN:1607-8888
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Increased basal glucocorticoid secretion and a reduced glucocorticoid response during acute stress, despite only minor changes in the secretion of the major secretagogue adrenocorticotropic hormone (ACTH), have been documented in the peripartum period in several species. We recently showed that the adrenal gland, the site of glucocorticoid synthesis, undergoes substantial postpartum-associated plasticity in the rat at mid-lactation. Here, we asked the question whether adrenal changes already take place around parturition in the rat and in another species, namely the mouse. After demonstrating that several components of the adrenal machinery mediating cholesterol supply for steroidogenesis, including protein levels of hormone-sensitive lipase, low-density lipoprotein receptor (LDLR) and scavenger receptor class-B type-1 (SRB1), are upregulated, while hydroxymethylglutaryl coenzyme A reductase (HMGCR) is downregulated in the lactating rat one day after delivery, as previously observed at mid-lactation, we demonstrated profound changes in the mouse. In detail, protein expression of LDLR, SRB1, HMGCR and adrenal lipid store density were increased in the mouse adrenal one day after parturition as tested via western blot analysis and oil-red lipid staining, respectively. Moreover, using in vitro culture techniques, we observed that isolated adrenal explants from lactating mice secreted higher levels of corticosterone under basal conditions, but showed impaired responsiveness to ACTH, mimicking the in vivo scenario. These results suggest that mechanisms of adaptation in the maternal adrenal after delivery, namely increased cholesterol availability and decreased ACTH sensitivity, are crucial for the basal increase in circulating glucocorticoids and maternal stress hyporesponsiveness that are typical of this period.
[Mh] Termos MeSH primário: Glândulas Suprarrenais/secreção
Corticosterona/secreção
Lactação/metabolismo
[Mh] Termos MeSH secundário: Hormônio Adrenocorticotrópico/metabolismo
Animais
Colesterol/metabolismo
Feminino
Hidroximetilglutaril-CoA Redutases/metabolismo
Camundongos
Fosfoproteínas/metabolismo
Período Pós-Parto/metabolismo
Ratos
Receptores da Corticotropina/metabolismo
Receptores de LDL/metabolismo
Receptores Depuradores Classe B/metabolismo
Esterol Esterase/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Phosphoproteins); 0 (Receptors, Corticotropin); 0 (Receptors, LDL); 0 (Scavenger Receptors, Class B); 0 (steroidogenic acute regulatory protein); 9002-60-2 (Adrenocorticotropic Hormone); 97C5T2UQ7J (Cholesterol); EC 1.1.1.- (Hydroxymethylglutaryl CoA Reductases); EC 3.1.1.13 (Sterol Esterase); W980KJ009P (Corticosterone)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180228
[Lr] Data última revisão:
180228
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170503
[St] Status:MEDLINE
[do] DOI:10.1080/10253890.2017.1325462


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[PMID]:29428127
[Au] Autor:Liao J; Liu X; Gao M; Wang M; Wang Y; Wang F; Huang W; Liu G
[Ad] Endereço:Department of Cardiology, Institute of Cardiovascular Diseases, First Affiliated Hospital of Dalian Medical University, Dalian 116011, China; Institute of Cardiovascular Sciences and Key Laboratory of Molecular Cardiovascular Sciences, Ministry of Education, Peking University Health Science Center,
[Ti] Título:Dyslipidemia, steatohepatitis and atherogenesis in lipodystrophic apoE deficient mice with Seipin deletion.
[So] Source:Gene;648:82-88, 2018 Mar 30.
[Is] ISSN:1879-0038
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:SEIPIN is an integral membrane protein located in the endoplasmic reticulum, regulating adipocytes differentiation and lipolysis. Deficiency of Seipin in mice causes severe general lipodystrophy, accompanied by insulin resistance, postprandial hypertriglyceridemia and steatohepatitis. In atherosclerosis-prone Ldlr null (Ldlr ) mice, lipodystrophy caused by Seipin deletion even led to severe hypercholesteremia and accelerated atherogenesis, when challenged with an atherogenic diet. However, whether the phenotypes observed in Seipin Ldlr mice were a common consequence due to lipodystrophy, rather than genetic background restricted or diet dependent, was unknown. Herein we explored the lipodystrophy-related dyslipidemia, steatohepatitis and atherogenesis in another atherosclerosis-prone murine model, apolipoprotein E null (apoE ) mice. Besides, we also compared phenotypes between sexes in apoE mice with Seipin deletion (Seipin apoE ). We found that compared with apoE controls, Seipin apoE mice also developed severe general lipodystrophy with hyperlipidemia, steatohepatitis and increased atherogenesis. Although the severity of adipose loss in female and male Seipin apoE mice were similar, hyperlipidemia, steatohepatitis and atherosclerosis were less severe in females than in males. Therefore, we demonstrated that lipodystrophy-related metabolic disorders, caused by Seipin deletion, were independent of genetic background and experimental diet, as seen in Ldlr and apoE mice. However, gender factor affected the disease progression, with females more resistant to developing lipodystrophy-related metabolic consequences.
[Mh] Termos MeSH primário: Apolipoproteínas E/genética
Aterosclerose/genética
Dislipidemias/genética
Fígado Gorduroso/genética
Proteínas Heterotriméricas de Ligação ao GTP/genética
Lipodistrofia/genética
[Mh] Termos MeSH secundário: Animais
Apolipoproteínas E/deficiência
Aterosclerose/metabolismo
Aterosclerose/patologia
Progressão da Doença
Dislipidemias/metabolismo
Dislipidemias/patologia
Fígado Gorduroso/metabolismo
Fígado Gorduroso/patologia
Feminino
Proteínas Heterotriméricas de Ligação ao GTP/deficiência
Lipodistrofia/metabolismo
Lipodistrofia/patologia
Masculino
Camundongos Endogâmicos C57BL
Camundongos Knockout
Receptores de LDL/deficiência
Receptores de LDL/genética
Índice de Gravidade de Doença
Fatores Sexuais
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Apolipoproteins E); 0 (Bscl2 protein, mouse); 0 (Receptors, LDL); EC 3.6.5.1 (Heterotrimeric GTP-Binding Proteins)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180226
[Lr] Data última revisão:
180226
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180212
[St] Status:MEDLINE


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[PMID]:29329335
[Au] Autor:Kyrklund M; Kummu O; Kankaanpää J; Akhi R; Nissinen A; Turunen SP; Pussinen P; Wang C; Hörkkö S
[Ad] Endereço:Medical Microbiology and Immunology, Research Unit of Biomedicine, Faculty of Medicine, University of Oulu, Oulu, Finland.
[Ti] Título:Immunization with gingipain A hemagglutinin domain of Porphyromonas gingivalis induces IgM antibodies binding to malondialdehyde-acetaldehyde modified low-density lipoprotein.
[So] Source:PLoS One;13(1):e0191216, 2018.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Treatment of periodontitis has beneficial effects on systemic inflammation markers that relate to progression of atherosclerosis. We aimed to investigate whether immunization with A hemagglutinin domain (Rgp44) of Porphyromonas gingivalis (Pg), a major etiologic agent of periodontitis, would lead to an antibody response cross-reacting with oxidized low-density lipoprotein (OxLDL) and how it would affect the progression of atherosclerosis in low-density lipoprotein receptor-deficient (LDLR-/-) mice. The data revealed a prominent IgM but not IgG response to malondialdehyde-acetaldehyde modified LDL (MAA-LDL) after Rgp44 and Pg immunizations, implying that Rgp44/Pg and MAA adducts may share cross-reactive epitopes that prompt IgM antibody production and consequently confer atheroprotection. A significant negative association was observed between atherosclerotic lesion and plasma IgA to Rgp44 in Rgp44 immunized mice, supporting further the anti-atherogenic effect of Rgp44 immunization. Plasma IgA levels to Rgp44 and to Pg in both Rgp44- and Pg-immunized mice were significantly higher than those in saline control, suggesting that IgA to Rgp44 could be a surrogate marker of immunization in Pg-immunized mice. Distinct antibody responses in plasma IgA levels to MAA-LDL, to Pg lipopolysaccharides (Pg-LPS), and to phosphocholine (PCho) were observed after Rgp44 and Pg immunizations, indicating that different immunogenic components between Rpg44 and Pg may behave differently in regard of their roles in the development of atherosclerosis. Immunization with Rgp44 also displayed atheroprotective features in modulation of plaque size through association with plasma levels of IL-1α whereas whole Pg bacteria achieved through regulation of anti-inflammatory cytokine levels of IL-5 and IL-10. The present study may contribute to refining therapeutic approaches aiming to modulate immune responses and inflammatory/anti-inflammatory processes in atherosclerosis.
[Mh] Termos MeSH primário: Adesinas Bacterianas/imunologia
Anticorpos Antibacterianos/biossíntese
Proteínas de Bactérias/imunologia
Cisteína Endopeptidases/imunologia
Imunoglobulina M/biossíntese
Lipoproteínas LDL/imunologia
Porphyromonas gingivalis/imunologia
[Mh] Termos MeSH secundário: Acetaldeído/análogos & derivados
Adesinas Bacterianas/química
Animais
Anticorpos Antibacterianos/metabolismo
Aterosclerose/etiologia
Aterosclerose/imunologia
Aterosclerose/prevenção & controle
Proteínas de Bactérias/química
Infecções por Bacteroidaceae/complicações
Infecções por Bacteroidaceae/imunologia
Infecções por Bacteroidaceae/microbiologia
Reações Cruzadas
Cisteína Endopeptidases/química
Modelos Animais de Doenças
Feminino
Seres Humanos
Imunização
Imunoglobulina M/metabolismo
Lectinas/química
Lectinas/imunologia
Lipoproteínas LDL/química
Malondialdeído/análogos & derivados
Malondialdeído/imunologia
Camundongos
Camundongos Knockout
Periodontite/complicações
Periodontite/imunologia
Periodontite/microbiologia
Domínios Proteicos
Receptores de LDL/deficiência
Receptores de LDL/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Adhesins, Bacterial); 0 (Antibodies, Bacterial); 0 (Bacterial Proteins); 0 (Immunoglobulin M); 0 (Lectins); 0 (Lipoproteins, LDL); 0 (Receptors, LDL); 0 (hemagglutinin A, Porphyromonas gingivalis); 0 (malondialdehyde-low density lipoprotein, mouse); 4Y8F71G49Q (Malondialdehyde); EC 3.4.22.- (Cysteine Endopeptidases); EC 3.4.22.37 (argingipain, Porphyromonas gingivalis); GO1N1ZPR3B (Acetaldehyde)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180226
[Lr] Data última revisão:
180226
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180113
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0191216


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[PMID]:29346401
[Au] Autor:van Puijvelde GHM; Foks AC; van Bochove RE; Bot I; Habets KLL; de Jager SC; Ter Borg MND; van Osch P; Boon L; Vos M; de Waard V; Kuiper J
[Ad] Endereço:Division of Biopharmaceutics, Leiden Academic Centre for Drug Research, Leiden University, Leiden, The Netherlands.
[Ti] Título:CD1d deficiency inhibits the development of abdominal aortic aneurysms in LDL receptor deficient mice.
[So] Source:PLoS One;13(1):e0190962, 2018.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:An abdominal aortic aneurysm (AAA) is a dilatation of the abdominal aorta leading to serious complications and mostly to death. AAA development is associated with an accumulation of inflammatory cells in the aorta including NKT cells. An important factor in promoting the recruitment of these inflammatory cells into tissues and thereby contributing to the development of AAA is angiotensin II (Ang II). We demonstrate that a deficiency in CD1d dependent NKT cells under hyperlipidemic conditions (LDLr-/-CD1d-/- mice) results in a strong decline in the severity of angiotensin II induced aneurysm formation when compared with LDLr-/- mice. In addition, we show that Ang II amplifies the activation of NKT cells both in vivo and in vitro. We also provide evidence that type I NKT cells contribute to AAA development by inducing the expression of matrix degrading enzymes in vSMCs and macrophages, and by cytokine dependently decreasing vSMC viability. Altogether, these data prove that CD1d-dependent NKT cells contribute to AAA development in the Ang II-mediated aneurysm model by enhancing aortic degradation, establishing that therapeutic applications which target NKT cells can be a successful way to prevent AAA development.
[Mh] Termos MeSH primário: Antígenos CD1d/genética
Aneurisma da Aorta Abdominal/prevenção & controle
Receptores de LDL/genética
[Mh] Termos MeSH secundário: Angiotensina II/administração & dosagem
Animais
Apoptose/imunologia
Citometria de Fluxo
Ativação Linfocitária
Masculino
Camundongos
Camundongos Endogâmicos C57BL
Camundongos Transgênicos
Músculo Liso Vascular/imunologia
Músculo Liso Vascular/patologia
Células NIH 3T3
Células T Matadoras Naturais/imunologia
Reação em Cadeia da Polimerase em Tempo Real
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Antigens, CD1d); 0 (Cd1d1 protein, mouse); 0 (Receptors, LDL); 11128-99-7 (Angiotensin II)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180221
[Lr] Data última revisão:
180221
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180119
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0190962


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[PMID]:28470529
[Au] Autor:Thormählen AS; Runz H
[Ad] Endereço:Institute of Human Genetics, University of Heidelberg, Heidelberg, 69120, Germany.
[Ti] Título:Systematic Cell-Based Phenotyping of Missense Alleles.
[So] Source:Methods Mol Biol;1601:215-228, 2017.
[Is] ISSN:1940-6029
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Sequencing of the protein-coding genome, the exome, has proven powerful to unravel links between genetic variation and disease for both Mendelian and complex conditions. Importantly, however, the increasing number of sequenced human exomes and mapping of disease-associated alleles is accompanied by a simultaneous, yet exponential increase in the overall number of rare and low frequency alleles identified. For most of these novel alleles, biological consequences remain unknown since reliable experimental approaches to better characterize their impact on protein function are only slowly emerging.Here we review a scalable, cell-based strategy that we have recently established to systematically profile the biological impact of rare and low frequency missense variants in vitro. By applying this approach to missense alleles identified through cohort-level exome sequencing in the low-density lipoprotein receptor (LDLR) we are able to distinguish rare alleles that predispose to familial hypercholesterolemia and myocardial infarction from alleles without obvious impact on LDLR levels or functions. We propose that systematic implementation of such and similar strategies will significantly advance our understanding of the protein-coding human genome and how rare and low frequency genetic variation impacts on health and disease.
[Mh] Termos MeSH primário: Alelos
Hiperlipoproteinemia Tipo II/genética
Mutação de Sentido Incorreto
Infarto do Miocárdio/genética
Receptores de LDL/genética
Receptores de LDL/metabolismo
[Mh] Termos MeSH secundário: DNA Complementar/química
Exoma/genética
Predisposição Genética para Doença
Proteínas de Fluorescência Verde/química
Células HeLa
Seres Humanos
Fenótipo
RNA Interferente Pequeno
Análise de Sequência de DNA
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (DNA, Complementary); 0 (LDLR protein, human); 0 (RNA, Small Interfering); 0 (Receptors, LDL); 147336-22-9 (Green Fluorescent Proteins)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180219
[Lr] Data última revisão:
180219
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170505
[St] Status:MEDLINE
[do] DOI:10.1007/978-1-4939-6960-9_17


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[PMID]:29298067
[Au] Autor:Thomas M; Kim S; Guo W; Collins FW; Wise ML; Meydani M
[Ad] Endereço:Vascular Biology Laboratory, Jean Mayer USDA Human Nutrition Research Center on Aging at Tufts University , 711 Washington Street, Boston, Massachusetts 02111, United States.
[Ti] Título:High Levels of Avenanthramides in Oat-Based Diet Further Suppress High Fat Diet-Induced Atherosclerosis in Ldlr Mice.
[So] Source:J Agric Food Chem;66(2):498-504, 2018 Jan 17.
[Is] ISSN:1520-5118
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Oats, in addition to cholesterol-lowering properties, contain unique antioxidants called avenanthramides (Avns), which inhibit both inflammatory cytokines and adhesion molecules in endothelial cells in culture. This study evaluated the effects of Avns of oats on atherosclerosis in Ldlr mice, one of the most commonly used atherosclerosis mouse models with their similar cholesterol distributions to humans. The Ldlr mice were fed a low fat, high fat, high fat containing regular oat brans with low levels of Avns (HFLA), or high fat containing regular oat brans with high levels of Avns (HFHA) diet. After 16 weeks of intervention, blood cholesterol and extent of aortic lesions were evaluated. We found that both oat-based diets reduced high fat diet-induced atheroma lesions in the aortic valve (p < 0.01). Furthermore, the effects of oat-based diets are more profound in HFHA mice than mice fed HFLA. Total plasma cholesterol levels were similarly reduced in both oat-supplemented mice. We concluded that oat bran diets reduce atheroma lesions and higher levels of Avns further reduce aortic lesions compared to regular oat bran. These preliminary in vivo data indicate that consumption of oats bran, with high Avns, has demonstrable beneficial effects on prevention of cardiovascular disease.
[Mh] Termos MeSH primário: Aterosclerose/dietoterapia
Avena/metabolismo
Extratos Vegetais/metabolismo
Receptores de LDL/deficiência
ortoaminobenzoatos/metabolismo
[Mh] Termos MeSH secundário: Animais
Aterosclerose/etiologia
Aterosclerose/metabolismo
Avena/química
Colesterol/metabolismo
Dieta Hiperlipídica/efeitos adversos
Fibras na Dieta/metabolismo
Suplementos Nutricionais/análise
Seres Humanos
Masculino
Camundongos
Extratos Vegetais/análise
Receptores de LDL/genética
ortoaminobenzoatos/análise
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Dietary Fiber); 0 (Plant Extracts); 0 (Receptors, LDL); 0 (avenanthramide-2C); 0 (ortho-Aminobenzoates); 97C5T2UQ7J (Cholesterol)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180205
[Lr] Data última revisão:
180205
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180104
[St] Status:MEDLINE
[do] DOI:10.1021/acs.jafc.7b04860


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[PMID]:28465464
[Au] Autor:Sun Y; Lin Z; Liu CH; Gong Y; Liegl R; Fredrick TW; Meng SS; Burnim SB; Wang Z; Akula JD; Pu WT; Chen J; Smith LEH
[Ad] Endereço:Department of Ophthalmology, Harvard Medical School, Boston Children's Hospital, Boston, MA 02115.
[Ti] Título:Inflammatory signals from photoreceptor modulate pathological retinal angiogenesis via c-Fos.
[So] Source:J Exp Med;214(6):1753-1767, 2017 Jun 05.
[Is] ISSN:1540-9538
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Pathological neovessels growing into the normally avascular photoreceptors cause vision loss in many eye diseases, such as age-related macular degeneration and macular telangiectasia. Ocular neovascularization is strongly associated with inflammation, but the source of inflammatory signals and the mechanisms by which these signals regulate the disruption of avascular privilege in photoreceptors are unknown. In this study, we found that c-Fos, a master inflammatory regulator, was increased in photoreceptors in a model of pathological blood vessels invading photoreceptors: the very low-density lipoprotein receptor-deficient ( ) mouse. Increased c-Fos induced inflammatory cytokines interleukin 6 (IL-6) and tumor necrosis factor (TNF), leading to activation of signal transducer and activator of transcription 3 (STAT3) and increased TNFα-induced protein 3 (TNFAIP3) in photoreceptors. IL-6 activated the STAT3/vascular endothelial growth factor A (VEGFA) pathway directly, and elevated TNFAIP3 suppressed SOCS3 (suppressor of cytokine signaling 3)-activated STAT3/VEGFA indirectly. Inhibition of c-Fos using photoreceptor-specific (adeno-associated virus)- (human rhodopsin kinase)- or a chemical inhibitor substantially reduced the pathological neovascularization and rescued visual function in mice. These findings suggested that the photoreceptor c-Fos controls blood vessel growth into the normally avascular photoreceptor layer through the inflammatory signal-induced STAT3/VEGFA pathway.
[Mh] Termos MeSH primário: Inflamação/metabolismo
Inflamação/patologia
Células Fotorreceptoras de Vertebrados/metabolismo
Proteínas Proto-Oncogênicas c-fos/metabolismo
Neovascularização Retiniana/metabolismo
Neovascularização Retiniana/patologia
Transdução de Sinais
[Mh] Termos MeSH secundário: Animais
Dependovirus/metabolismo
Interleucina-6/metabolismo
Camundongos
Neurônios/efeitos dos fármacos
Neurônios/metabolismo
Células Fotorreceptoras de Vertebrados/efeitos dos fármacos
Células Fotorreceptoras de Vertebrados/patologia
RNA Interferente Pequeno/metabolismo
Receptores de LDL/deficiência
Receptores de LDL/metabolismo
Retina/efeitos dos fármacos
Retina/patologia
Retina/fisiopatologia
Retinoides/farmacologia
Fator de Transcrição STAT3/metabolismo
Transdução de Sinais/efeitos dos fármacos
Fator A de Crescimento do Endotélio Vascular/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Interleukin-6); 0 (Proto-Oncogene Proteins c-fos); 0 (RNA, Small Interfering); 0 (Receptors, LDL); 0 (Retinoids); 0 (SR 11302); 0 (STAT3 Transcription Factor); 0 (VLDL receptor); 0 (Vascular Endothelial Growth Factor A)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:180117
[Lr] Data última revisão:
180117
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170504
[St] Status:MEDLINE
[do] DOI:10.1084/jem.20161645


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[PMID]:27776640
[Au] Autor:Moreno-Gordaliza E; van der Lee SJ; Demirkan A; van Duijn CM; Kuiper J; Lindenburg PW; Hankemeier T
[Ad] Endereço:Division of Analytical Biosciences, Leiden Academic Centre for Drug Research, Faculty of Science, Universiteit Leiden, Einsteinweg 55, 2300 RA Leiden, The Netherlands. Electronic address: emorenog@ucm.es.
[Ti] Título:A novel method for serum lipoprotein profiling using high performance capillary isotachophoresis.
[So] Source:Anal Chim Acta;944:57-69, 2016 Nov 09.
[Is] ISSN:1873-4324
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:A new capillary isotachophoresis (cITP) method for lipoprotein profiling with superior lipoprotein coverage compared to previous methods has been developed, resolving twice as many lipoprotein species (18 peaks/fractions) in serum or plasma in less than 9.5 min. For this, a novel mixture of 24 spacers, including amino acids, dipeptides and sulfonic acids, was developed and fine-tuned, using predictive software (PeakMaster) and testing of spiked serum samples. Lipoprotein peaks were identified by serum-spiking with reference lipoproteins. Compatibility with common lipophilic stains for selective lipoprotein detection with either UV/Vis or laser-induced fluorescence was demonstrated. A special new capillary with a neutral coating (combining water-compatible OV1701-OH deactivation and methylation) was used for the first time for electrodriven separations, allowing very stable separations in a pH 8.8-9.4 gradient system, being functional for more than 100 injections. Excellent reproducibility was achieved, with coefficients of variation lower than 2.6% for absolute migration times. Comparison was performed with human plasma samples analyzed by NMR, leading to similar results with cITP after multivariate statistics, regarding group-clustering and lipoprotein species correlation. The new cITP method was applied to the analysis of serum samples from a LDL receptor knock-out mice model fed either a normal diet or a western-type diet. Differences in the lipoprotein levels and in the sublipoprotein types were detected, showing a shift to more atherogenic particles due to the high cholesterol diet. In summary, this novel method will allow more detailed and informative profiling of lipoprotein particle subtypes for cardiovascular disease research.
[Mh] Termos MeSH primário: Análise Química do Sangue/métodos
Eletroforese Capilar/métodos
Isotacoforese/métodos
Lipoproteínas/sangue
Lipoproteínas/isolamento & purificação
[Mh] Termos MeSH secundário: Animais
Técnicas de Inativação de Genes
Seres Humanos
Camundongos
Receptores de LDL/deficiência
Receptores de LDL/genética
Software
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Lipoproteins); 0 (Receptors, LDL)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180116
[Lr] Data última revisão:
180116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161026
[St] Status:MEDLINE


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[PMID]:29190422
[Au] Autor:Zhao Y; Liu J; Hao W; Zhu H; Liang N; He Z; Ma KY; Chen ZY
[Ad] Endereço:Food & Nutritional Sciences Programme, School of Life Sciences, The Chinese University of Hong Kong , Shatin, New Territories, Hong Kong, China.
[Ti] Título:Structure-Specific Effects of Short-Chain Fatty Acids on Plasma Cholesterol Concentration in Male Syrian Hamsters.
[So] Source:J Agric Food Chem;65(50):10984-10992, 2017 Dec 20.
[Is] ISSN:1520-5118
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Previous studies have shown that short-chain fatty acids (SCFAs) are capable of decreasing plasma cholesterol. However, the relative plasma-cholesterol-lowering activity of individual SCFAs and the underlying mechanisms by which SCFAs decrease plasma cholesterol remain largely unknown. The present study was done to compare the plasma-cholesterol-lowering potencies of four common SCFAs with 2-5 carbons and to investigate their interactions with gene expressions of key regulatory factors involved in cholesterol metabolism. For 6 weeks, five groups of male Golden hamsters were fed either a control high-cholesterol diet (HCD) or one of the four experimental HCDs containing 0.5 mol of acetate (Ac), propionate (Pr), butyrate (Bu), or valerate (Va) per kilogram of the diet. The results showed that Ac, Pr, and Bu significantly reduced plasma total cholesterol (TC) by 24, 18, and 17% (P < 0.05), respectively. All four SCFAs could decrease non-HDL cholesterol (non-HDL-C) and the non-HDL-C/HDL-C ratio. The addition of Ac, Pr, or Bu into the diet significantly promoted fecal excretion of bile acids by 121, 113, or 120% (P < 0.05), respectively, and upregulated the gene expressions of sterol-regulatory-element-binding protein 2 (SREBP2), low-density-lipoprotein receptor (LDLR), and cholesterol 7α-hydroxylase (CYP7A1) in the liver. It was concluded that SCFAs with 2-4 carbons (Ac, Pr, and Bu) are more hypocholesterolemic than Va, which has 5 carbons, via enhancing fecal excretion of bile acids and promoting the hepatic uptake of cholesterol from the blood.
[Mh] Termos MeSH primário: Anticolesterolemiantes/administração & dosagem
Colesterol/sangue
Ácidos Graxos Voláteis/administração & dosagem
Hipercolesterolemia/tratamento farmacológico
[Mh] Termos MeSH secundário: Animais
Anticolesterolemiantes/química
Colesterol 7-alfa-Hidroxilase/genética
Colesterol 7-alfa-Hidroxilase/metabolismo
Cricetinae
Ácidos Graxos Voláteis/química
Seres Humanos
Hipercolesterolemia/sangue
Hipercolesterolemia/genética
Hipercolesterolemia/metabolismo
Masculino
Mesocricetus
Receptores de LDL/genética
Receptores de LDL/metabolismo
Proteína de Ligação a Elemento Regulador de Esterol 2/genética
Proteína de Ligação a Elemento Regulador de Esterol 2/metabolismo
Triglicerídeos/sangue
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Anticholesteremic Agents); 0 (Fatty Acids, Volatile); 0 (Receptors, LDL); 0 (Sterol Regulatory Element Binding Protein 2); 0 (Triglycerides); 97C5T2UQ7J (Cholesterol); EC 1.14.14.23 (Cholesterol 7-alpha-Hydroxylase)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180110
[Lr] Data última revisão:
180110
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171201
[St] Status:MEDLINE
[do] DOI:10.1021/acs.jafc.7b04666



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