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[PMID]:29403051
[Au] Autor:Koch RE; Kavazis AN; Hasselquist D; Hood WR; Zhang Y; Toomey MB; Hill GE
[Ad] Endereço:Department of Biological Sciences, Auburn University, 331 Funchess Hall, Auburn, AL, 36849, USA. rebecca.adrian@monash.edu.
[Ti] Título:No evidence that carotenoid pigments boost either immune or antioxidant defenses in a songbird.
[So] Source:Nat Commun;9(1):491, 2018 02 05.
[Is] ISSN:2041-1723
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Dietary carotenoids have been proposed to boost immune system and antioxidant functions in vertebrate animals, but studies aimed at testing these physiological functions of carotenoids have often failed to find support. Here we subject yellow canaries (Serinus canaria), which possess high levels of carotenoids in their tissue, and white recessive canaries, which possess a knockdown mutation that results in very low levels of tissue carotenoids, to oxidative and pathogen challenges. Across diverse measures of physiological performance, we detect no differences between carotenoid-rich yellow and carotenoid-deficient white canaries. These results add further challenge to the assumption that carotenoids are directly involved in supporting physiological function in vertebrate animals. While some dietary carotenoids provide indirect benefits as retinoid precursors, our observations suggest that carotenoids themselves may play little to no direct role in key physiological processes in birds.
[Mh] Termos MeSH primário: Antioxidantes/metabolismo
Canários/imunologia
Carotenoides/metabolismo
Regulação da Expressão Gênica/imunologia
Imunidade Inata/efeitos dos fármacos
[Mh] Termos MeSH secundário: Animais
Canários/genética
Lipopolissacarídeos/metabolismo
Mutação
Pigmentação/genética
Pigmentação/imunologia
Pigmentos Biológicos
Receptores Depuradores Classe B/genética
Receptores Depuradores Classe B/metabolismo
Toxoide Tetânico/imunologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T; RESEARCH SUPPORT, U.S. GOV'T, NON-P.H.S.
[Nm] Nome de substância:
0 (Antioxidants); 0 (Lipopolysaccharides); 0 (Pigments, Biological); 0 (Scavenger Receptors, Class B); 0 (Tetanus Toxoid); 36-88-4 (Carotenoids)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180305
[Lr] Data última revisão:
180305
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180207
[St] Status:MEDLINE
[do] DOI:10.1038/s41467-018-02974-x


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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]:28935756
[Au] Autor:Trenteseaux C; Gaston AT; Aguesse A; Poupeau G; de Coppet P; Andriantsitohaina R; Laschet J; Amarger V; Krempf M; Nobecourt-Dupuy E; Ouguerram K
[Ad] Endereço:From the UMR 1280 Physiopathologie des Adaptations Nutritionnelles, INRA, Université de Nantes, France (C.T., G.P., P.d.C., V.A., M.K., E.N.-D., K.O.); Centre de Recherche en Nutrition Humaine Ouest, Nantes, France (C.T., A.A., M.K., K.O.); UMR1063 Stress Oxydant et Pathologies Métaboliques, INSERM,
[Ti] Título:Perinatal Hypercholesterolemia Exacerbates Atherosclerosis Lesions in Offspring by Altering Metabolism of Trimethylamine-N-Oxide and Bile Acids.
[So] Source:Arterioscler Thromb Vasc Biol;37(11):2053-2063, 2017 Nov.
[Is] ISSN:1524-4636
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:OBJECTIVE: Experimental studies suggest that maternal hypercholesterolemia may be relevant for the early onset of cardiovascular disease in offspring. We investigated the effect of perinatal hypercholesterolemia on the atherosclerosis development in the offspring of apolipoprotein E-deficient mice and the underlying mechanism. APPROACH AND RESULTS: Atherosclerosis and related parameters were studied in adult male or female apolipoprotein E-deficient mice offspring from either normocholesterolemic or hypercholesterolemic mothers and normocholesterolemic fathers. Female born to hypercholesterolemic mothers had more aortic root lesions than female born to normocholesterolemic mothers. Lesions in whole aorta did not differ between groups. Higher trimethylamine-N-oxide levels and hepatic gene expression were higher in female born to hypercholesterolemic mothers offspring compared with female born to normocholesterolemic mothers and male. Trimethylamine-N-oxide levels were correlated with the size of atherosclerotic root lesions. Levels of hepatic cholesterol and gallbladder bile acid were greater in male born to hypercholesterolemic mothers compared with male born to normocholesterolemic mothers. At 18 weeks of age, female born to hypercholesterolemic mothers showed lower hepatic and but higher gene expression compared with female born to normocholesterolemic mothers. Male born to hypercholesterolemic mothers showed an increase in and gene expression compared with male born to normocholesterolemic mothers. At 25 weeks of age, female born to hypercholesterolemic mothers had lower gene expression compared with female born to normocholesterolemic mothers. DNA methylation of , and promoter regions was slightly modified and may explain the mRNA expression modulation. CONCLUSIONS: Our findings suggest that maternal hypercholesterolemia may exacerbate the development of atherosclerosis in female offspring by affecting metabolism of trimethylamine-N-oxide and bile acids. These data could be explained by epigenetic alterations.
[Mh] Termos MeSH primário: Doenças da Aorta/metabolismo
Aterosclerose/metabolismo
Ácidos e Sais Biliares/metabolismo
Hipercolesterolemia/metabolismo
Metilaminas/metabolismo
Efeitos Tardios da Exposição Pré-Natal
[Mh] Termos MeSH secundário: Fatores Etários
Animais
Animais Recém-Nascidos
Aorta/metabolismo
Aorta/patologia
Doenças da Aorta/etiologia
Doenças da Aorta/genética
Doenças da Aorta/patologia
Apolipoproteínas E/deficiência
Apolipoproteínas E/genética
Aterosclerose/etiologia
Aterosclerose/genética
Aterosclerose/patologia
Colesterol/metabolismo
Colesterol 7-alfa-Hidroxilase/genética
Colesterol 7-alfa-Hidroxilase/metabolismo
Metilação de DNA
Modelos Animais de Doenças
Feminino
Vesícula Biliar/metabolismo
Predisposição Genética para Doença
Hipercolesterolemia/complicações
Hipercolesterolemia/genética
Fígado/metabolismo
Masculino
Camundongos Knockout
Oxigenases/genética
Oxigenases/metabolismo
Fenótipo
Placa Aterosclerótica
Gravidez
Regiões Promotoras Genéticas
Receptores Citoplasmáticos e Nucleares/genética
Receptores Citoplasmáticos e Nucleares/metabolismo
Receptores de LDL/genética
Receptores de LDL/metabolismo
Receptores Depuradores Classe B/genética
Receptores Depuradores Classe B/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Apolipoproteins E); 0 (Bile Acids and Salts); 0 (Methylamines); 0 (Receptors, Cytoplasmic and Nuclear); 0 (Receptors, LDL); 0 (Scarb1 protein, mouse); 0 (Scavenger Receptors, Class B); 0 (farnesoid X-activated receptor); 97C5T2UQ7J (Cholesterol); EC 1.13.- (Oxygenases); EC 1.14.13.8 (dimethylaniline monooxygenase (N-oxide forming)); EC 1.14.14.23 (Cholesterol 7-alpha-Hydroxylase); EC 1.14.14.23 (Cyp7a1 protein, mouse); FLD0K1SJ1A (trimethyloxamine)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171107
[Lr] Data última revisão:
171107
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170923
[St] Status:MEDLINE
[do] DOI:10.1161/ATVBAHA.117.309923


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[PMID]:28910310
[Au] Autor:Leiva A; Contreras-Duarte S; Amigo L; Sepúlveda E; Boric M; Quiñones V; Busso D; Rigotti A
[Ad] Endereço:Cellular and Molecular Physiology Laboratory (CMPL), Division of Obstetrics and Gynaecology, School of Medicine, Pontificia Universidad Católica de Chile, Santiago, Chile.
[Ti] Título:Gugulipid causes hypercholesterolemia leading to endothelial dysfunction, increased atherosclerosis, and premature death by ischemic heart disease in male mice.
[So] Source:PLoS One;12(9):e0184280, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:For proper cholesterol metabolism, normal expression and function of scavenger receptor class B type I (SR-BI), a high-density lipoprotein (HDL) receptor, is required. Among the factors that regulate overall cholesterol homeostasis and HDL metabolism, the nuclear farnesoid X receptor plays an important role. Guggulsterone, a bioactive compound present in the natural product gugulipid, is an antagonist of this receptor. This natural product is widely used globally as a natural lipid-lowering agent, although its anti-atherogenic cardiovascular benefit in animal models or humans is unknown. The aim of this study was to determine the effects of gugulipid on cholesterol homeostasis and development of mild and severe atherosclerosis in male mice. For this purpose, we evaluated the impact of gugulipid treatment on liver histology, plasma lipoprotein cholesterol, endothelial function, and development of atherosclerosis and/or ischemic heart disease in wild-type mice; apolipoprotein E knockout mice, a model of atherosclerosis without ischemic complications; and SR-B1 knockout and atherogenic-diet-fed apolipoprotein E hypomorphic (SR-BI KO/ApoER61h/h) mice, a model of lethal ischemic heart disease due to severe atherosclerosis. Gugulipid administration was associated with histological abnormalities in liver, increased alanine aminotransferase levels, lower hepatic SR-BI content, hypercholesterolemia due to increased HDL cholesterol levels, endothelial dysfunction, enhanced atherosclerosis, and accelerated death in animals with severe ischemic heart disease. In conclusion, our data show important adverse effects of gugulipid intake on HDL metabolism and atherosclerosis in male mice, suggesting potential and unknown deleterious effects on cardiovascular health in humans. In addition, these findings reemphasize the need for rigorous preclinical and clinical studies to provide guidance on the consumption of natural products and regulation of their use in the general population.
[Mh] Termos MeSH primário: Aterosclerose/metabolismo
Endotélio Vascular/metabolismo
Hipercolesterolemia/metabolismo
Isquemia Miocárdica/metabolismo
Extratos Vegetais/toxicidade
Gomas Vegetais/toxicidade
[Mh] Termos MeSH secundário: Animais
Aterosclerose/induzido quimicamente
Aterosclerose/genética
Aterosclerose/patologia
Endotélio Vascular/patologia
Hipercolesterolemia/induzido quimicamente
Hipercolesterolemia/genética
Hipercolesterolemia/patologia
Proteínas Relacionadas a Receptor de LDL/deficiência
Masculino
Camundongos
Camundongos Knockout
Isquemia Miocárdica/induzido quimicamente
Isquemia Miocárdica/genética
Isquemia Miocárdica/patologia
Receptores Depuradores Classe B/deficiência
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (LDL-Receptor Related Proteins); 0 (Plant Extracts); 0 (Plant Gums); 0 (Scarb1 protein, mouse); 0 (Scavenger Receptors, Class B); 0 (guggulu extract)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171012
[Lr] Data última revisão:
171012
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170915
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0184280


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[PMID]:28902926
[Au] Autor:Guo N; Zhang N; Yan L; Cao X; Lv F; Wang J; Wang Y; Cong H
[Ad] Endereço:Department of Cardiology, Tianjin Chest Hospital, Tianjin Medical University, Tianjin, China.
[Ti] Título:Down-regulation of single-stranded DNA-binding protein 1 expression induced by HCMV infection promotes lipid accumulation in cells.
[So] Source:Braz J Med Biol Res;50(11):e6389, 2017 Sep 12.
[Is] ISSN:1414-431X
[Cp] País de publicação:Brazil
[La] Idioma:eng
[Ab] Resumo:The objective of this study was to observe the infection of human cytomegalovirus (HCMV) to human umbilical vein endothelial cells, and its effect on the expression of single-stranded DNA-binding protein (SSBP1) and on lipid metabolism in endothelial cells. We screened the differential expression of mRNAs after HCMV infection by suppression subtractive hybridization and the expression levels of SSBP1 mRNA and protein after HCMV infection by real-time PCR and western blot. After verification of successful infection by indirect immunofluorescent staining and RT-PCR, we found a differential expression of lipid metabolism-related genes including LDLR, SCARB, CETP, HMGCR, ApoB and LPL induced by HCMV infection. The expression levels of SSBP1 mRNA and protein after HCMV infection were significantly down-regulated. Furthermore, we found that upregulation of SSBP1 inhibited the expression of atherosclerosis-associated LDLR, SCARB, HMGCR, CETP as well as the accumulation of lipids in the cells. The results showed that the inhibition of SSBP1 by HCMV infection promotes lipid accumulation in the cells.
[Mh] Termos MeSH primário: Infecções por Citomegalovirus/metabolismo
Proteínas de Ligação a DNA/metabolismo
Células Endoteliais da Veia Umbilical Humana/metabolismo
Células Endoteliais da Veia Umbilical Humana/virologia
Metabolismo dos Lipídeos/fisiologia
Proteínas Mitocondriais/metabolismo
[Mh] Termos MeSH secundário: Aterosclerose/metabolismo
Aterosclerose/virologia
Colesterol/análise
Proteínas de Transferência de Ésteres de Colesterol/metabolismo
Proteínas de Ligação a DNA/genética
Regulação para Baixo
Seres Humanos
Hidroximetilglutaril-CoA Redutases/metabolismo
Metabolismo dos Lipídeos/genética
Proteínas Mitocondriais/genética
Receptores de LDL/metabolismo
Receptores Depuradores Classe B/metabolismo
Fatores de Tempo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (CETP protein, human); 0 (Cholesterol Ester Transfer Proteins); 0 (DNA-Binding Proteins); 0 (LDLR protein, human); 0 (Mitochondrial Proteins); 0 (Receptors, LDL); 0 (SCARB1 protein, human); 0 (SSBP1 protein, human); 0 (Scavenger Receptors, Class B); 97C5T2UQ7J (Cholesterol); EC 1.1.1.- (HMGCR protein, human); EC 1.1.1.- (Hydroxymethylglutaryl CoA Reductases)
[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:170914
[St] Status:MEDLINE


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[PMID]:28827115
[Au] Autor:Sadeghi S; Davari M; Asli E; Gharibzadeh S; Vaziri F; Jamnani FR; Fateh A; Siadat SD
[Ad] Endereço:Department of Biology, Karaj Branch, Islamic Azad University, Karaj, Iran.
[Ti] Título:Effect of IL15 rs10833 and SCARB1 rs10846744 on virologic responses in chronic hepatitis C patients treated with pegylated interferon-α and ribavirin.
[So] Source:Gene;630:28-34, 2017 Sep 30.
[Is] ISSN:1879-0038
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:The scavenger receptor type B class I (SCARBI) is known to be involved in the entry of hepatitis C virus (HCV) into the host, while interleukin-15 (IL15) is an important cytokine in both the innate and acquired immune responses against HCV infection. We investigated the association of IL15 rs10833 or SCARB1 rs10846744 polymorphisms with treatment responses in patients with chronic HCV (CHC). SCARB1 rs10846744 and IL15 rs10833 were identified in 365 treatment-naïve CHC patients through genotyping by TaqMan® Real-Time PCR and PCR-restriction fragment length polymorphism (RFLP), respectively. Of these 365 CHC treatment-naïve patients, rapid virological response (RVR), complete early virological response (cEVR), and sustained virological response (SVR) were observed in 53.2%, 76.4%, and 66.0% of the patients, respectively. Multivariate logistic regression analysis revealed that RVR was associated with sex (P=0.016), aspartate aminotransferase (AST) (P=0.026), IL15 rs10833 (AA) genotype (P<0.001), and SCARB1 rs10846744 (CC) genotype (P<0.001), while there was a relationship between alanine aminotransferase (ALT) (P=0.013) and IL15 rs10833 (AA) genotype (P<0.001) with cEVR. Age (<40years) (P=0.001), AST (P=0.029), ALP (P=0.028), HCV genotypes (P=0.005), HCV viral load (P=0.026), IL15 rs10833 (AA) genotype (P<0.001), and SCARB1 rs10846744 (CC) genotype (P=0.001) were strongly associated with SVR. In conclusion, the SCARB1 rs10846744 (CC) and IL15 rs10833 (AA) genotypes can be considered as powerful predictors of treatment responses in CHC patients treated with an interferon-based therapy.
[Mh] Termos MeSH primário: Antivirais/uso terapêutico
Hepatite C Crônica/genética
Interleucina-15/genética
Polimorfismo de Nucleotídeo Único
Receptores Depuradores Classe B/genética
Resposta Viral Sustentada
[Mh] Termos MeSH secundário: Adulto
Feminino
Hepatite C Crônica/tratamento farmacológico
Seres Humanos
Interferon-alfa/uso terapêutico
Masculino
Meia-Idade
Polietilenoglicóis/uso terapêutico
Proteínas Recombinantes/uso terapêutico
Ribavirina/uso terapêutico
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antiviral Agents); 0 (IL15 protein, human); 0 (Interferon-alpha); 0 (Interleukin-15); 0 (Recombinant Proteins); 0 (SCARB1 protein, human); 0 (Scavenger Receptors, Class B); 30IQX730WE (Polyethylene Glycols); 49717AWG6K (Ribavirin); Q46947FE7K (peginterferon alfa-2a)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170920
[Lr] Data última revisão:
170920
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170823
[St] Status:MEDLINE


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[PMID]:28765047
[Au] Autor:Chen L; Zhang J; Deng X; Liu Y; Yang X; Wu Q; Yu C
[Ad] Endereço:Institute of Life Science, Chongqing Medical University, Chongqing, 400016, PR China.
[Ti] Título:Lysophosphatidic acid directly induces macrophage-derived foam cell formation by blocking the expression of SRBI.
[So] Source:Biochem Biophys Res Commun;491(3):587-594, 2017 Sep 23.
[Is] ISSN:1090-2104
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The leading cause of morbidity and mortality is the result of cardiovascular disease, mainly atherosclerosis. The formation of macrophage foam cells by ingesting ox-LDL and focal retention in the subendothelial space are the hallmarks of the early atherosclerotic lesion. Lysophosphatidic acid (LPA), which is a low-molecular weight lysophospholipid enriched in oxidized LDL, exerts a range of effects on the cardiovascular system. Previous reports show that LPA increases the uptake of ox-LDL to promote the formation of foam cells. However, as the most active component of ox-LDL, there is no report showing whether LPA directly affects foam cell formation. The aim of this study was to investigate the effects of LPA on foam cell formation, as well as to elucidate the underlying mechanism. Oil red O staining and a Cholesterol/cholesteryl ester quantitation assay were used to evaluate foam cell formation in Raw264.7 macrophage cells. We utilized a Western blot and RT-PCR to investigate the relationship between LPA receptors and lipid transport related proteins. We found that LPA promoted foam cell formation, using 200 µM for 24 h. Meanwhile, the expression of the Scavenger receptor BI (SRBI), which promotes the efflux of free cholesterol, was decreased. Furthermore, the LPA receptor antagonist Ki16425 significantly abolished the LPA effects, indicating that LPA was involved in the foam cell formation and SRBI expression induced by LPA. Additionally, the LPA-induced foam cell formation was blocked with an AKT inhibitor. Our results suggest that LPA-enhanced foam cell formation is mediated by LPA -AKT activation and subsequent SRBI expression.
[Mh] Termos MeSH primário: Células Espumosas/citologia
Células Espumosas/fisiologia
Lisofosfolipídeos/metabolismo
Receptores de Ácidos Lisofosfatídicos/metabolismo
Receptores Depuradores Classe B/metabolismo
[Mh] Termos MeSH secundário: Animais
Diferenciação Celular
Regulação para Baixo/efeitos dos fármacos
Regulação para Baixo/fisiologia
Camundongos
Células RAW 264.7
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Lysophospholipids); 0 (Receptors, Lysophosphatidic Acid); 0 (Scarb1 protein, mouse); 0 (Scavenger Receptors, Class B); PG6M3969SG (lysophosphatidic acid)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170911
[Lr] Data última revisão:
170911
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170803
[St] Status:MEDLINE


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[PMID]:28669731
[Au] Autor:Lu X; He L; Zhou Q; Wang M; Shen WJ; Azhar S; Pan F; Guo Z; Hu Z
[Ad] Endereço:Jiangsu Key Laboratory for Molecular and Medical Biotechnology, College of Life Sciences, Nanjing Normal University, 1 WenYuan Road, Nanjing, 210023, China.
[Ti] Título:NHERF1 and NHERF2 regulation of SR-B1 stability via ubiquitination and proteasome degradation.
[So] Source:Biochem Biophys Res Commun;490(4):1168-1175, 2017 Sep 02.
[Is] ISSN:1090-2104
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Scavenger receptor class B type 1 (SR-B1), an HDL receptor plays a crucial role in cholesterol metabolism in the liver, steroidogenic tissues, and vascular cells including macrophages. SR-B1 is subject to regulation at the transcription, posttranscription and posttranslational levels. We previously provided evidence that PDZ domain containing NHERF1 and NHERF2 regulate SR-B1 protein levels post-transcriptionally, although the underlying mechanism(s) by which NHERF1 and NHERF2 regulate SR-B1 protein levels is not well understood. In this study, we demonstrate that SR-B1 is degraded intracellularly via ubiquitin-proteasome pathway and that SR-B1 can be ubiquitinated at K500 and K508 residues. Overexpression of NHERF1 or NHERF2 enhanced SR-B1 ubiquitination and degradation. NHERF1 and NHERF2 promote SR-B1 ubiquitination at sites K508 and K500, respectively. These results suggest that NHERF1 and NHERF2 down-regulated SR-B1 at least in part via the ubiquitin/proteasome pathway.
[Mh] Termos MeSH primário: Fosfoproteínas/metabolismo
Complexo de Endopeptidases do Proteassoma/metabolismo
Receptores Depuradores Classe B/metabolismo
Trocadores de Sódio-Hidrogênio/metabolismo
[Mh] Termos MeSH secundário: Animais
Células CHO
Células Cultivadas
Cricetulus
Estabilidade Proteica
Ratos
Ubiquitinação
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Phosphoproteins); 0 (Scarb1 protein, rat); 0 (Scavenger Receptors, Class B); 0 (Slc9a3r2 protein, rat); 0 (Sodium-Hydrogen Exchangers); 0 (sodium-hydrogen exchanger regulatory factor); EC 3.4.25.1 (Proteasome Endopeptidase Complex)
[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:170704
[St] Status:MEDLINE


  9 / 1684 MEDLINE  
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[PMID]:28552715
[Au] Autor:Zeng TT; Tang DJ; Ye YX; Su J; Jiang H
[Ad] Endereço:Department of Laboratory Medicine, West China Hospital, Sichuan University, Chengdu 610041, PR China.
[Ti] Título:Influence of SCARB1 gene SNPs on serum lipid levels and susceptibility to coronary heart disease and cerebral infarction in a Chinese population.
[So] Source:Gene;626:319-325, 2017 Aug 30.
[Is] ISSN:1879-0038
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:The SCARB1 gene encodes human scavenger receptor class B type I (SR-BI), the primary receptor for high-density lipoprotein (HDL)- cholesteryl ester uptake, and polymorphisms in this gene may influence SR-BI protein expression and serum lipid levels, modulating susceptibility to coronary heart disease (CHD) and cerebral infarction (CI). Therefore, we investigated the association between singlenucleotide polymorphisms (SNPs) in the SCARB1 gene and serum lipid levels as well as risk of CHD and CI in the Chinese Han population. Genotypes in 295 CHD patients, 302 CI patients and 312 healthy controls matched for age and gender were determined by high-resolution melting (HRM). Among the 5 SNPs investigated in this study, rs10846744 and rs2278986 were significantly associated with CHD risk. The frequency of the C allele for rs10846744 and that of the T allele for rs2278986 appeared to be significantly increased in the CHD group (OR: 1.416, 95%CI: 1.128-1.778, P=0.0058 and OR: 1.681, 95%CI: 1.327-2.130, P<0.0001, respectively). CHD patients with genotypes CC and CG for rs10846744 had a higher HDL-c level than those with genotype GG, and CHD patients with genotypes CC and CT for the rs2278986 SNP had a higher HDL-c level compared to those with the TT allele. The other 3 SNPs, rs5888, rs10744182 and rs838893, showed no significant association with serum lipid levels and CHD or CI risk in the Chinese population. The CCCTT and CCTTC haplotypes of rs5888, rs10846744, rs10744182, rs2278986 and rs838893 appear to significantly increase CHD risk, whereas the CGTTC, CCTCT and TGCTC haplotypes appear to significantly reduce risk. Overall, the CCTTC and TGTTC haplotypes acted as a significant risk for CI, with the CGCTC and CCCCT haplotypes conferring significantly reduced risk. These results suggest that SCARB1 gene polymorphisms may contribute to genetic susceptibility to CHD; in particular, the C allele of rs10846744 and the C allele of rs2278986 may serve as risk and protective factors for CHD, respectively.
[Mh] Termos MeSH primário: Infarto Cerebral/genética
Doença das Coronárias/genética
Polimorfismo de Nucleotídeo Único
Receptores Depuradores Classe B/genética
[Mh] Termos MeSH secundário: Adulto
Idoso
Idoso de 80 Anos ou mais
Estudos de Casos e Controles
China
HDL-Colesterol/sangue
HDL-Colesterol/genética
Feminino
Seres Humanos
Lipoproteínas HDL/sangue
Lipoproteínas HDL/genética
Masculino
Meia-Idade
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Cholesterol, HDL); 0 (Lipoproteins, HDL); 0 (SCARB1 protein, human); 0 (Scavenger Receptors, Class B)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170801
[Lr] Data última revisão:
170801
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170530
[St] Status:MEDLINE


  10 / 1684 MEDLINE  
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[PMID]:28549616
[Au] Autor:Zhu RG; Sun YD; Hou YT; Fan JG; Chen G; Li TP
[Ad] Endereço:Department of Food Science, College of Light Industry, Liaoning University, Liaoning Engineering Research Center for Food Bioprocessing, Shenyang Key Laboratory of Food Bioprocessing and Quality Control, Shenyang 110036, China. Electronic address: zhurugang@lnu.edu.cn.
[Ti] Título:Pectin penta-oligogalacturonide reduces cholesterol accumulation by promoting bile acid biosynthesis and excretion in high-cholesterol-fed mice.
[So] Source:Chem Biol Interact;272:153-159, 2017 Jun 25.
[Is] ISSN:1872-7786
[Cp] País de publicação:Ireland
[La] Idioma:eng
[Ab] Resumo:Haw pectin penta-oligogalacturonide (HPPS) has important role in improving cholesterol metabolism and promoting the conversion of cholesterol to bile acids (BA) in mice fed high-cholesterol diet (HCD). However, the mechanism is not clear. This study aims to investigate the effects of HPPS on cholesterol accumulation and the regulation of hepatic BA synthesis and transport in HCD-fed mice. Results showed that HPPS significantly decreased plasma and hepatic TC levels but increased plasma high-density lipoprotein cholesterol (HDL-C) and apolipoprotein A-I (apoA-I) levels, compared to HCD. BA analysis showed that HPPS markedly decreased hepatic and small intestine BA levels but increased the gallbladder BA levels, and finally decreased the total BA pool size, compared to HCD. Studies of molecular mechanism revealed that HPPS promoted hepatic ATP-binding cassette transporter A1 (ABCA1), ATP-binding cassette transporter G1 (ABCG1), and scavenger receptor BI (SR-BI) expression but did not affect ATB binding cassette transporter G5/G8 (ABCG5/8) expression. HPPS inactivated hepatic farnesoid X receptor (FXR) and target genes expression, which resulted in significant increase of cholesterol 7α-hydroxylase 1 (CYP7A1) and sterol 12α-hydroxylase (CYP8B1) expression, with up-regulations of 204.2% and 33.5% for mRNA levels, respectively, compared with HCD. In addition, HPPS markedly enhanced bile salt export pump (BSEP) expression but didn't affect the sodium/taurocholate co-transporting polypeptide (NTCP) expression. In conclusion, the study revealed that HPPS reduced cholesterol accumulation by promoting BA synthesis in the liver and excretion in the feces, and might promote macrophage-to-liver reverse cholesterol transport (RCT) but did not liver-to-fecal RCT.
[Mh] Termos MeSH primário: Ácidos e Sais Biliares/metabolismo
Colesterol/sangue
Expressão Gênica/efeitos dos fármacos
Oligossacarídeos/farmacologia
Pectinas/farmacologia
[Mh] Termos MeSH secundário: Transportador 1 de Cassete de Ligação de ATP/genética
Transportador 1 de Cassete de Ligação de ATP/metabolismo
Membro 1 da Subfamília G de Transportadores de Cassetes de Ligação de ATP/genética
Membro 1 da Subfamília G de Transportadores de Cassetes de Ligação de ATP/metabolismo
Animais
Apolipoproteína A-I/sangue
Colesterol 7-alfa-Hidroxilase/genética
Colesterol 7-alfa-Hidroxilase/metabolismo
HDL-Colesterol/sangue
Dieta Hiperlipídica
Intestino Delgado/efeitos dos fármacos
Intestino Delgado/metabolismo
Fígado/efeitos dos fármacos
Fígado/metabolismo
Masculino
Camundongos
Pectinas/química
Receptores Depuradores Classe B/genética
Receptores Depuradores Classe B/metabolismo
Esteroide 12-alfa-Hidroxilase/genética
Esteroide 12-alfa-Hidroxilase/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (ABCA1 protein, mouse); 0 (ABCG1 protein, mouse); 0 (ATP Binding Cassette Transporter 1); 0 (ATP Binding Cassette Transporter, Sub-Family G, Member 1); 0 (Apolipoprotein A-I); 0 (Bile Acids and Salts); 0 (Cholesterol, HDL); 0 (Oligosaccharides); 0 (Pectins); 0 (Scarb1 protein, mouse); 0 (Scavenger Receptors, Class B); 97C5T2UQ7J (Cholesterol); EC 1.14.14.23 (Cholesterol 7-alpha-Hydroxylase); EC 1.14.14.23 (Cyp7a1 protein, mouse); EC 1.14.18.8 (Steroid 12-alpha-Hydroxylase)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:170620
[Lr] Data última revisão:
170620
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170528
[St] Status:MEDLINE



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