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[PMID]:29288662
[Au] Autor:Zhang X; Zhang P; Gao J; Huang Q
[Ad] Endereço:Department of General Surgery, Affiliated Provincial Hospital of Anhui Medical University, Hefei, 230001, China.
[Ti] Título:Autophagy dysregulation caused by ApoM deficiency plays an important role in liver lipid metabolic disorder.
[So] Source:Biochem Biophys Res Commun;495(4):2643-2648, 2018 01 22.
[Is] ISSN:1090-2104
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Autophagy is thought to be a key mechanism in maintaining the balance of liver lipid metabolism. However, the relationship between apolipoprotein M (ApoM) and autophagy has not been reported, and the role of ApoM in triglyceride metabolism is still unclear. In this study, we investigated the correlation between ApoM and autophagy and liver triglyceride metabolism in ApoM-knockout animal and cellular models. First, we observed that spontaneous hepatic steatosis developed in the liver of adult ApoM mice, which was presented as the accumulation of large quantities of lipid droplets in hepatocytes under electron microscopy; Oil Red O staining showed significant accumulation of triglycerides. At the molecular level, the expression of lipid synthesis-associated proteins (primarily triglyceride synthesis) as well as acetyl-CoA carboxylase alpha (ACACA), fatty acid synthase (FASN) and sterol regulatory element-binding protein 1 (SREBP1) was upregulated. Moreover, lipid metabolic disorder and accumulation were accompanied by dysfunction in autophagy, which displayed predominantly as inhibition of the degradation pathway; for example, P62 protein accumulated and key proteins involved in the initiation of autophagy including ATG7, ATG5-12, Beclin1 and the LC3BII/LC3BI ratio were upregulated as a feedback response. When the autophagy dysfunction was ameliorated by the activation of autophagy pathways induced by starvation, the lipid metabolic disorder was corrected to a certain extent. This suggests that the autophagy dysfunction caused by the deficiency of ApoM is an important factor in hepatic steatosis (triglyceride accumulation). ApoM plays a key role in normal autophagy activity in the liver and thereby further regulates the metabolism of liver lipids, particularly triglycerides.
[Mh] Termos MeSH primário: Apolipoproteínas M/metabolismo
Autofagia
Fígado Gorduroso/metabolismo
Transtornos do Metabolismo dos Lipídeos/metabolismo
Fígado/metabolismo
Fígado/patologia
Triglicerídeos/metabolismo
[Mh] Termos MeSH secundário: Animais
Apolipoproteínas M/genética
Fígado Gorduroso/complicações
Fígado Gorduroso/patologia
Feminino
Transtornos do Metabolismo dos Lipídeos/complicações
Transtornos do Metabolismo dos Lipídeos/patologia
Masculino
Camundongos
Camundongos Knockout
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (ApoM protein, mouse); 0 (Apolipoproteins M); 0 (Triglycerides)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180222
[Lr] Data última revisão:
180222
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171231
[St] Status:MEDLINE


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[PMID]:28647361
[Au] Autor:Tian F; Wu CL; Yu BL; Liu L; Hu JR
[Ad] Endereço:Department of Cardiovascular Medicine, The Second Xiangya Hospital, Central South University, Changsha, Hunan 410011, China.
[Ti] Título:Apolipoprotein O expression in mouse liver enhances hepatic lipid accumulation by impairing mitochondrial function.
[So] Source:Biochem Biophys Res Commun;491(1):8-14, 2017 Sep 09.
[Is] ISSN:1090-2104
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Apolipoprotein O (ApoO) was recently observed in the cellular mitochondrial inner membrane, which plays a role in mitochondrial function and is associated with myocardiopathy. Empirical information on the physiological functions of apoO is therefore limited. In this study, we aimed to elucidate the effect of apoO on hepatic fatty acid metabolism. An adenoviral vector expressing hApoO was constructed and introduced into chow diet and high-fat diet induced mice and the L02 human hepatoma cell line. High levels of hApoO mRNA and protein were detected in the liver, and the expression of lipid metabolism genes was significantly altered compared with negative controls. The liver function indices (serum ALT and AST) were clearly elevated, and the ultrastructure of cellular mitochondria was distinctly altered in the liver after apoO overexpression. Further, mitochondrial membrane potential decreased with hApoO treatment in L02 cells. These results establish a link between apoO and lipid accumulation and could suggest a new pathway for regulating non-alcoholic fatty liver disease progression.
[Mh] Termos MeSH primário: Apolipoproteínas/metabolismo
Hepatócitos/metabolismo
Metabolismo dos Lipídeos/fisiologia
Lipocalinas/metabolismo
Fígado/metabolismo
Mitocôndrias Hepáticas/metabolismo
[Mh] Termos MeSH secundário: Animais
Apolipoproteínas/genética
Apolipoproteínas M
Células Cultivadas
Feminino
Hepatócitos/patologia
Seres Humanos
Lipocalinas/genética
Fígado/patologia
Masculino
Camundongos
Camundongos Endogâmicos C57BL
Camundongos Transgênicos
Mitocôndrias Hepáticas/patologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (APOM protein, human); 0 (Apolipoproteins); 0 (Apolipoproteins M); 0 (Lipocalins)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170626
[St] Status:MEDLINE


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[PMID]:28385702
[Au] Autor:Frej C; Mendez AJ; Ruiz M; Castillo M; Hughes TA; Dahlbäck B; Goldberg RB
[Ad] Endereço:From the Division of Clinical Chemistry, Department of Translational Medicine, Lund University, Malmö, Sweden (C.F., M.R., B.D.); Health Science Center, Department of Medicine, University of Tennessee, Memphis (T.A.H.); and Division of Endocrinology, Metabolism and Diabetes and Diabetes Research Ins
[Ti] Título:A Shift in ApoM/S1P Between HDL-Particles in Women With Type 1 Diabetes Mellitus Is Associated With Impaired Anti-Inflammatory Effects of the ApoM/S1P Complex.
[So] Source:Arterioscler Thromb Vasc Biol;37(6):1194-1205, 2017 Jun.
[Is] ISSN:1524-4636
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:OBJECTIVE: Type 1 diabetes mellitus (T1D) patients have an increased risk of cardiovascular disease despite high levels of high-density lipoproteins (HDL). Apolipoprotein M (apoM) and its ligand sphingosine 1-phospate (S1P) exert many of the anti-inflammatory effects of HDL. We investigated whether apoM and S1P are altered in T1D and whether apoM and S1P are important for HDL functionality in T1D. APPROACH AND RESULTS: ApoM and S1P were quantified in plasma from 42 healthy controls and 89 T1D patients. HDL was isolated from plasma and separated into dense, medium-dense, and light HDL by ultracentrifugation. Primary human aortic endothelial cells were challenged with tumor necrosis factor-α in the presence or absence of isolated HDL. Proinflammatory adhesion molecules E-selectin and vascular cellular adhesion molecule-1 were quantified by flow cytometry. Activation of the S1P - receptor was evaluated by analyzing downstream signaling targets and receptor internalization. There were no differences in plasma levels of apoM and S1P between controls and T1D patients, but the apoM/S1P complexes were shifted from dense to light HDL particles in T1D. ApoM/S1P in light HDL particles from women were less efficient in inhibiting expression of vascular cellular adhesion molecule-1 than apoM/S1P in denser particles. The light HDL particles were unable to activate Akt, whereas all HDL subfractions were equally efficient in activating Erk and receptor internalization. CONCLUSIONS: ApoM/S1P in light HDL particles were inefficient in inhibiting tumor necrosis factor-α-induced vascular cellular adhesion molecule-1 expression in contrast to apoM/S1P in denser HDL particles. T1D patients have a higher proportion of light particles and hence more dysfunctional HDL, which could contribute to the increased cardiovascular disease risk associated with T1D.
[Mh] Termos MeSH primário: Apolipoproteínas/sangue
Diabetes Mellitus Tipo 1/sangue
Inflamação/sangue
Lipocalinas/sangue
Lipoproteínas HDL/sangue
Lisofosfolipídeos/sangue
Esfingosina/análogos & derivados
[Mh] Termos MeSH secundário: Adulto
Apolipoproteínas M
Biomarcadores/sangue
Estudos de Casos e Controles
Células Cultivadas
Cromatografia Líquida
Diabetes Mellitus Tipo 1/complicações
Diabetes Mellitus Tipo 1/diagnóstico
Selectina E/metabolismo
Endocitose
Células Endoteliais/efeitos dos fármacos
Células Endoteliais/metabolismo
Ativação Enzimática
Ensaio de Imunoadsorção Enzimática
MAP Quinases Reguladas por Sinal Extracelular/metabolismo
Feminino
Seres Humanos
Inflamação/diagnóstico
Inflamação/etiologia
Inflamação/prevenção & controle
Masculino
Meia-Idade
Receptores de Lisoesfingolipídeo/metabolismo
Fatores de Risco
Esfingosina/sangue
Espectrometria de Massas em Tandem
Fator de Necrose Tumoral alfa/farmacologia
Molécula 1 de Adesão de Célula Vascular/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (APOM protein, human); 0 (Apolipoproteins); 0 (Apolipoproteins M); 0 (Biomarkers); 0 (E-Selectin); 0 (Lipocalins); 0 (Lipoproteins, HDL); 0 (Lysophospholipids); 0 (Receptors, Lysosphingolipid); 0 (S1PR1 protein, human); 0 (SELE protein, human); 0 (Tumor Necrosis Factor-alpha); 0 (Vascular Cell Adhesion Molecule-1); 26993-30-6 (sphingosine 1-phosphate); EC 2.7.11.24 (Extracellular Signal-Regulated MAP Kinases); NGZ37HRE42 (Sphingosine)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170408
[St] Status:MEDLINE
[do] DOI:10.1161/ATVBAHA.117.309275


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[PMID]:28179022
[Au] Autor:Ruiz M; Okada H; Dahlbäck B
[Ad] Endereço:Department of Translational Medicine, Skåne University Hospital, Lund University, Malmö, Sweden. mario.ruiz_garcia@med.lu.se.
[Ti] Título:HDL-associated ApoM is anti-apoptotic by delivering sphingosine 1-phosphate to S1P1 & S1P3 receptors on vascular endothelium.
[So] Source:Lipids Health Dis;16(1):36, 2017 Feb 08.
[Is] ISSN:1476-511X
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: High-density Lipoprotein (HDL) attenuates endothelial cell apoptosis induced by different cell-death stimuli such as oxidation or growth factor deprivation. HDL is the main plasma carrier of the bioactive lipid sphingosine 1-phosphate (S1P), which it is a signaling molecule that promotes cell survival in response to several apoptotic stimuli. In HDL, S1P is bound to Apolipoprotein M (ApoM), a Lipocalin that is only present in around 5% of the HDL particles. The goal of this study is to characterize ApoM-bound S1P role in endothelial apoptosis protection and the signaling pathways involved. METHODS: Human umbilical vein endothelial cells (HUVEC) cultures were switched to serum/grow factor deprivation medium to induce apoptosis and the effect caused by the addition of ApoM and S1P analyzed. RESULTS: The addition of HDL or recombinant ApoM-bound S1P promoted cell viability and blocked apoptosis, whereas HDL had no protective effect. Remarkably, S1P exerted a more potent anti-apoptotic effect when carried by ApoM as compared to albumin, or when added as free molecule. Mechanistically, cooperation between S1P1 and S1P3 was required for the HDL/ApoM/S1P-mediated anti-apoptotic ability. Furthermore, AKT and ERK phosphorylation was also necessary to achieve the anti-apoptotic effect of the HDL/ApoM/S1P complex. CONCLUSIONS: Altogether, our results indicate that ApoM and S1P are key elements of the anti-apoptotic activity of HDL and promote optimal endothelial function.
[Mh] Termos MeSH primário: Apolipoproteínas/metabolismo
Células Endoteliais da Veia Umbilical Humana/metabolismo
Lipocalinas/metabolismo
Lipoproteínas HDL/metabolismo
Lisofosfolipídeos/metabolismo
Receptores de Lisoesfingolipídeo/metabolismo
Esfingosina/análogos & derivados
[Mh] Termos MeSH secundário: Apolipoproteínas/genética
Apolipoproteínas/farmacologia
Apolipoproteínas M
Apoptose/efeitos dos fármacos
Sobrevivência Celular/efeitos dos fármacos
Meios de Cultura/química
Expressão Gênica
Células Endoteliais da Veia Umbilical Humana/citologia
Células Endoteliais da Veia Umbilical Humana/efeitos dos fármacos
Seres Humanos
Lipocalinas/genética
Lipocalinas/farmacologia
Lipoproteínas HDL/genética
Lipoproteínas HDL/farmacologia
Lisofosfolipídeos/farmacologia
Proteína Quinase 1 Ativada por Mitógeno/genética
Proteína Quinase 1 Ativada por Mitógeno/metabolismo
Proteína Quinase 3 Ativada por Mitógeno/genética
Proteína Quinase 3 Ativada por Mitógeno/metabolismo
Fosforilação
Proteínas Proto-Oncogênicas c-akt/genética
Proteínas Proto-Oncogênicas c-akt/metabolismo
Receptores de Lisoesfingolipídeo/genética
Albumina Sérica/farmacologia
Esfingosina/metabolismo
Esfingosina/farmacologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (APOM protein, human); 0 (Apolipoproteins); 0 (Apolipoproteins M); 0 (Culture Media); 0 (Lipocalins); 0 (Lipoproteins, HDL); 0 (Lysophospholipids); 0 (Receptors, Lysosphingolipid); 0 (Serum Albumin); 26993-30-6 (sphingosine 1-phosphate); EC 2.7.11.1 (Proto-Oncogene Proteins c-akt); EC 2.7.11.24 (MAPK1 protein, human); EC 2.7.11.24 (Mitogen-Activated Protein Kinase 1); EC 2.7.11.24 (Mitogen-Activated Protein Kinase 3); NGZ37HRE42 (Sphingosine)
[Em] Mês de entrada:1705
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170210
[St] Status:MEDLINE
[do] DOI:10.1186/s12944-017-0429-2


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[PMID]:28126827
[Au] Autor:Kurano M; Hara M; Ikeda H; Tsukamoto K; Yatomi Y
[Ad] Endereço:From the Department of Clinical Laboratory Medicine, Graduate School of Medicine, The University of Tokyo, Japan (M.K., H.I., Y.Y.); Department of Medicine IV, Mizonokuchi Hospital, Teikyo University School of Medicine, Kawasaki, Japan (M.H.); and Department of Metabolism, Diabetes and Nephrology, A
[Ti] Título:Involvement of CETP (Cholesteryl Ester Transfer Protein) in the Shift of Sphingosine-1-Phosphate Among Lipoproteins and in the Modulation of its Functions.
[So] Source:Arterioscler Thromb Vasc Biol;37(3):506-514, 2017 Mar.
[Is] ISSN:1524-4636
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:OBJECTIVE: Sphingosine-1-phosphate (S1P) is a vasoprotective lipid mediator. About two thirds of plasma S1P rides on high-density lipoprotein (HDL), and several pleiotropic properties of HDL have been ascribed to S1P. In human subjects, CETP (cholesteryl ester transfer protein) greatly influences HDL quantities. In this study, we attempted to elucidate the roles of CETP in the metabolism of S1P. APPROACH AND RESULTS: We overexpressed CETP in mice that lacked CETP and found that CETP overexpression decreased the HDL level but failed to modulate the levels of S1P and apolipoprotein M (apoM), a carrier of S1P, in the total plasma. We observed, however, that the distribution of S1P and apoM shifted from HDL to apoB-containing lipoproteins. When we administered C S1P bound to apoM-containing lipoprotein, C S1P and apoM were rapidly transferred to apoB-containing lipoproteins in CETP-overexpressing mice. When HDL containing C S1P was mixed with low-density lipoprotein ex vivo, C S1P shifted to the low-density lipoprotein fraction independent of the presence of CETP. Concordant with these results, apoM was distributed mainly to the same fraction as apo AI in a CETP-deficient subject, although apoM was also detected in apo AI-poor fractions in a corresponding hypercholesterolemia subject. About the bioactivities of S1P carried on each lipoprotein, S1P riding on apoB-containing lipoproteins induced the phosphorylation of Akt (AKT8 virus oncogene cellular homolog) and eNOS (endothelial nitric oxide synthase) in human umbilical vein endothelial cells, and CETP overexpression increased insulin secretion and sensitivity, which was inhibited by an S1P receptor 1 or 3 antagonist. CONCLUSIONS: CETP modulates the distribution of S1P among lipoproteins, which affects the bioactivities of S1P.
[Mh] Termos MeSH primário: Proteínas de Transferência de Ésteres de Colesterol/deficiência
Erros Inatos do Metabolismo Lipídico/sangue
Lipoproteínas/sangue
Lisofosfolipídeos/sangue
Esfingosina/análogos & derivados
[Mh] Termos MeSH secundário: Animais
Apolipoproteína B-100/sangue
Apolipoproteínas/sangue
Apolipoproteínas B/sangue
Apolipoproteínas M
Bile/metabolismo
Proteínas de Transferência de Ésteres de Colesterol/sangue
Proteínas de Transferência de Ésteres de Colesterol/genética
Proteínas de Transferência de Ésteres de Colesterol/metabolismo
Genótipo
Células Hep G2
Células Endoteliais da Veia Umbilical Humana/metabolismo
Seres Humanos
Erros Inatos do Metabolismo Lipídico/genética
Lipocalinas/sangue
Lipoproteínas HDL/sangue
Fígado/metabolismo
Masculino
Camundongos Endogâmicos C57BL
Camundongos Knockout
Camundongos Transgênicos
Fenótipo
Esfingosina/sangue
Fatores de Tempo
Transfecção
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (APOB protein, human); 0 (APOM protein, human); 0 (ApoM protein, mouse); 0 (Apob protein, mouse); 0 (Apolipoprotein B-100); 0 (Apolipoproteins); 0 (Apolipoproteins B); 0 (Apolipoproteins M); 0 (CETP protein, human); 0 (Cholesterol Ester Transfer Proteins); 0 (Lipocalins); 0 (Lipoproteins); 0 (Lipoproteins, HDL); 0 (Lysophospholipids); 26993-30-6 (sphingosine 1-phosphate); NGZ37HRE42 (Sphingosine)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170128
[St] Status:MEDLINE
[do] DOI:10.1161/ATVBAHA.116.308692


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[PMID]:28073663
[Au] Autor:Zhang P; Gao J; Pu C; Feng G; Wang L; Huang L; Zhang Y
[Ad] Endereço:Anhui Province Key Laboratory of Biological Macro-molecules Research, Wannan Medical College, China; Department of Clinical Laboratory, The Second Affiliated Hospital of Wannan Medical College, China.
[Ti] Título:ApoM/HDL-C and apoM/apoA-I ratios are indicators of diabetic nephropathy in healthy controls and type 2 diabetes mellitus.
[So] Source:Clin Chim Acta;466:31-37, 2017 Mar.
[Is] ISSN:1873-3492
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Apolipoprotein M (apoM) concentrations were decreased in type 2 diabetes mellitus (T2DM). ApoM was selectively expressed in renal tubular epithelial cells. We investigated the changes in plasma apoM concentrations in diabetic nephropathy (DN) patients and the potential of apoM as a biomarker of DN. METHODS: A total of 96 DN patients and 100 age- and sex-matched diabetic non-nephropathy (non-DN) patients and 110 healthy controls were included. All T2DM patients were divided into 3 groups according to urinary albumin excretion: normoalbuminuria (n=100), microalbuminuria (n=50) and macroalbuminuria (n=46). Plasma apoM concentrations were measured by enzyme-linked immunosorbent assay. RESULTS: DN Patients had higher plasma apoM concentrations than those in non-DN patients (22.23±11.69 vs. 18.96±7.85ng/µl, P<0.05). In addition, microalbuminuria group showed higher plasma apoM concentrations than those in normoalbuminuria group (22.67±11.40 vs. 18.96±7.85ng/µl, P<0.05). The areas under curve (AUC) of apoM using a receiver-operating characteristic (ROC) curve analysis showed that plasma apoM concentrations were not indicators for identification of DN from healthy people (AUC=0.478, P=0.585) and from T2DM (AUC=0.563, P=0.125). DN patients had higher ratios of apoM/HDL-C and apoM/apoA1 than those in healthy controls and in non-DN patients. ApoM/HDL-C and apoM/apoA1 ratios could be used as indicators for identification of DN from healthy people (AUC=0.597, P=0.016; AUC=0.665, P=0.000, respectively) and from T2DM (AUC=0.580, P=0.050; AUC=0.601, P=0.015, respectively). CONCLUSIONS: ApoM/HDL-C and apoM/apoA1 ratios could be used as indicators for identification of DN from healthy people and from T2DM patients.
[Mh] Termos MeSH primário: Apolipoproteína A-I/sangue
Apolipoproteínas/sangue
HDL-Colesterol/sangue
Diabetes Mellitus Tipo 2/sangue
Nefropatias Diabéticas/sangue
Lipocalinas/sangue
[Mh] Termos MeSH secundário: Fatores Etários
Albuminúria/urina
Apolipoproteínas M
Biomarcadores/sangue
Estudos de Casos e Controles
Estudos de Coortes
Nefropatias Diabéticas/diagnóstico
Feminino
Seres Humanos
Masculino
Meia-Idade
Fatores Sexuais
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (APOA1 protein, human); 0 (APOM protein, human); 0 (Apolipoprotein A-I); 0 (Apolipoproteins); 0 (Apolipoproteins M); 0 (Biomarkers); 0 (Cholesterol, HDL); 0 (Lipocalins)
[Em] Mês de entrada:1703
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170112
[St] Status:MEDLINE


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[PMID]:28039587
[Au] Autor:Ren K; Mo ZC; Liu X; Tang ZL; Jiang Y; Peng XS; Zhang QH; Shi JF; Yi GH
[Ad] Endereço:Institute of Cardiovascular Disease, Key Lab for Arteriosclerology of Hunan Province, University of South China, 28 W Changsheng Road, Hengyang, 421001, Hunan, China.
[Ti] Título:TGF-ß Down-regulates Apolipoprotein M Expression through the TAK-1-JNK-c-Jun Pathway in HepG2 Cells.
[So] Source:Lipids;52(2):109-117, 2017 Feb.
[Is] ISSN:1558-9307
[Cp] País de publicação:Germany
[La] Idioma:eng
[Ab] Resumo:Apolipoprotein M (apoM) is a relatively novel apolipoprotein that plays pivotal roles in many dyslipidemia-associated diseases; however, its regulatory mechanisms are poorly understood. Many cytokines have been identified that down-regulate apoM expression in HepG2 cells, among which transforming growth factor-ß (TGF-ß) exerts the most potent effects. In addition, c-Jun, a member of the activated protein 1 (AP-1) family whose activity is modulated by c-Jun N-terminal kinase (JNK), decreases apoM expression at the transcriptional level by binding to the regulatory element in the proximal apoM promoter. In this study, we investigated the molecular mechanisms through which TGF-ß decreases the apoM level in HepG2 cells. The results revealed that TGF-ß inhibited apoM expression at both the mRNA and protein levels in a dose- and time-dependent manner and that it suppressed apoM secretion. These effects were attenuated by treatment of cells with either SP600125 (JNK inhibitor) or c-Jun siRNA. 5Z-7-oxozeaenol [(a TGF-ß-activated kinase 1 (TAK-1) inhibitor)] also attenuated the TGF-ß-mediated inhibition of apoM expression and suppressed the activation of JNK and c-Jun. These results have demonstrated that TGF-ß suppresses apoM expression through the TAK-1-JNK-c-Jun pathway in HepG2 cells.
[Mh] Termos MeSH primário: Apolipoproteínas/genética
Apolipoproteínas/metabolismo
Lipocalinas/genética
Lipocalinas/metabolismo
MAP Quinase Quinase Quinases/metabolismo
Sistema de Sinalização das MAP Quinases/efeitos dos fármacos
Proteínas Proto-Oncogênicas c-jun/metabolismo
Fator de Crescimento Transformador beta/farmacologia
[Mh] Termos MeSH secundário: Antracenos/farmacologia
Apolipoproteínas M
Relação Dose-Resposta a Droga
Regulação Neoplásica da Expressão Gênica/efeitos dos fármacos
Células Hep G2
Seres Humanos
Lactonas/farmacologia
Regiões Promotoras Genéticas
Resorcinóis/farmacologia
Fatores de Tempo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (7-oxozeanol); 0 (APOM protein, human); 0 (Anthracenes); 0 (Apolipoproteins); 0 (Apolipoproteins M); 0 (Lactones); 0 (Lipocalins); 0 (Proto-Oncogene Proteins c-jun); 0 (Resorcinols); 0 (Transforming Growth Factor beta); 1TW30Y2766 (pyrazolanthrone); EC 2.7.11.25 (MAP Kinase Kinase Kinases); EC 2.7.11.25 (MAP kinase kinase kinase 7)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170101
[St] Status:MEDLINE
[do] DOI:10.1007/s11745-016-4227-9


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[PMID]:27879252
[Au] Autor:Ruiz M; Frej C; Holmér A; Guo LJ; Tran S; Dahlbäck B
[Ad] Endereço:From the Department of Translational Medicine, Skåne University Hospital, Lund University, Malmö, Sweden. mario.ruiz_garcia@med.lu.se.
[Ti] Título:High-Density Lipoprotein-Associated Apolipoprotein M Limits Endothelial Inflammation by Delivering Sphingosine-1-Phosphate to the Sphingosine-1-Phosphate Receptor 1.
[So] Source:Arterioscler Thromb Vasc Biol;37(1):118-129, 2017 Jan.
[Is] ISSN:1524-4636
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:OBJECTIVE: Plasma high-density lipoproteins (HDL) are potent antiatherogenic and anti-inflammatory particles. However, HDL particles are highly heterogenic in composition, and different HDL-mediated functions can be ascribed to different subclasses of HDL. Only a small HDL population contains apolipoprotein M (ApoM), which is the main plasma carrier of the bioactive lipid mediator sphingosine-1-phosphate (S1P). Vascular inflammation is modulated by S1P, but both pro- and anti-inflammatory roles have been ascribed to S1P. The goal of this study is to elucidate the role of ApoM and S1P in endothelial anti-inflammatory events related to HDL. APPROACH AND RESULTS: Aortic or brain human primary endothelial cells were challenged with tumor necrosis factor-α (TNF-α) as inflammatory stimuli. The presence of recombinant ApoM-bound S1P or ApoM-containing HDL reduced the abundance of adhesion molecules in the cell surface, whereas ApoM and ApoM-lacking HDL did not. Specifically, ApoM-bound S1P decreased vascular adhesion molecule-1 (VCAM-1) and E-selectin surface abundance but not intercellular adhesion molecule-1. Albumin, which is an alternative S1P carrier, was less efficient in inhibiting VCAM-1 than ApoM-bound S1P. The activation of the S1P receptor 1 was sufficient and required to promote anti-inflammation. Moreover, ApoM-bound S1P induced the rearrangement of the expression of S1P-related genes to counteract TNF-α. Functionally, HDL/ApoM/S1P limited monocyte adhesion to the endothelium and maintained endothelial barrier integrity under inflammatory conditions. CONCLUSIONS: ApoM-bound S1P is a key component of HDL and is responsible for several HDL-associated protective functions in the endothelium, including regulation of adhesion molecule abundance, leukocyte-endothelial adhesion, and endothelial barrier.
[Mh] Termos MeSH primário: Anti-Inflamatórios/farmacologia
Apolipoproteínas/farmacologia
Células Endoteliais da Veia Umbilical Humana/efeitos dos fármacos
Inflamação/prevenção & controle
Lipocalinas/farmacologia
Lisofosfolipídeos/farmacologia
Receptores de Lisoesfingolipídeo/agonistas
Esfingosina/análogos & derivados
[Mh] Termos MeSH secundário: Anti-Inflamatórios/metabolismo
Apolipoproteínas/metabolismo
Apolipoproteínas M
Permeabilidade Capilar/efeitos dos fármacos
Adesão Celular/efeitos dos fármacos
Linhagem Celular
Técnicas de Cocultura
Relação Dose-Resposta a Droga
Selectina E/metabolismo
Células Endoteliais da Veia Umbilical Humana/metabolismo
Células Endoteliais da Veia Umbilical Humana/patologia
Seres Humanos
Inflamação/metabolismo
Inflamação/patologia
Lipocalinas/metabolismo
Lipoproteínas HDL/metabolismo
Lisofosfolipídeos/metabolismo
Monócitos/efeitos dos fármacos
Monócitos/metabolismo
Ligação Proteica
Receptores de Lisoesfingolipídeo/metabolismo
Proteínas Recombinantes/farmacologia
Albumina Sérica/metabolismo
Albumina Sérica/farmacologia
Transdução de Sinais/efeitos dos fármacos
Esfingosina/metabolismo
Esfingosina/farmacologia
Fatores de Tempo
Fator de Necrose Tumoral alfa/farmacologia
Molécula 1 de Adesão de Célula Vascular/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (APOM protein, human); 0 (Anti-Inflammatory Agents); 0 (Apolipoproteins); 0 (Apolipoproteins M); 0 (E-Selectin); 0 (Lipocalins); 0 (Lipoproteins, HDL); 0 (Lysophospholipids); 0 (Receptors, Lysosphingolipid); 0 (Recombinant Proteins); 0 (S1PR1 protein, human); 0 (SELE protein, human); 0 (Serum Albumin); 0 (Tumor Necrosis Factor-alpha); 0 (Vascular Cell Adhesion Molecule-1); 26993-30-6 (sphingosine 1-phosphate); NGZ37HRE42 (Sphingosine)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161124
[St] Status:MEDLINE
[do] DOI:10.1161/ATVBAHA.116.308435


  9 / 152 MEDLINE  
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[PMID]:27841911
[Au] Autor:Zhang Y; Huang LZ; Yang QL; Liu Y; Zhou X
[Ad] Endereço:Department of Biochemistry and Molecular Biology, Wan Nan Medical College, Anhui 241000, China. Email: zhangyao@ahedu.gov.cn.
[Ti] Título:Correlation analysis between ApoM gene-promoter polymorphisms and coronary heart disease.
[So] Source:Cardiovasc J Afr;27(4):228-237, 2016 Jul/Aug.
[Is] ISSN:1680-0745
[Cp] País de publicação:South Africa
[La] Idioma:eng
[Ab] Resumo:OBJECTIVES: Apolipoprotein M (ApoM), a 25-kDa plasma protein belonging to the lipocalin protein family, is predominantly associated with high-density lipoprotein cholesterol (HDL-C). Studies have suggested ApoM to be important for the formation of pre-ß-HDL and to increase cholesterol efflux from macrophage foam cells. The aim of this study was to explore the association of single-nucleotide polymorphisms (SNPs) in the ApoM promoter with coronary atherosclerotic disease (CAD), and the contribution of latent factors. METHODS: ApoM was measured in samples from two separate case-control studies, of whom 88 patients developed CAD and 88 were controls. Whole-blood samples from subjects were genotyped by PCR-restriction fragment length polymorphism (PCR-RFLP). Luciferase activities were measured for HepG2 cells with two SNPs, rs805296 (T-778C) and rs940494 (T-855C), and after interfering with or overexpressing the predicted transcription factors. The ability of the SNPs to combine with nucleoproteins was analysed by electrophoretic mobility shift assay (EMSA). RESULTS: Mean plasma ApoM concentrations in the CAD and non-CAD groups were 9.58 ± 4.30 and 12.22 ± 6.59 µg/ ml, respectively. Correlation studies of ApoM concentrations with several analytes showed a marked positive correlation with HDL-C, fasting plasma glucose and triglyceride levels. The CC genotype showed lower luciferase activities compared to the TC and TT genotypes. The ApoM-855 mutant-type could bind to the AP-2α. Interference and overexpression of AP-2 increased and decreased luciferase activities of the wild and mutant types to different degrees. CONCLUSION: ApoM may be a biomarker of CAD. ApoM-855 T→C substitution provides binding sites for AP-2α and reduces ApoM transcription activity.
[Mh] Termos MeSH primário: Apolipoproteínas/genética
Doença da Artéria Coronariana/genética
Lipocalinas/genética
Polimorfismo de Nucleotídeo Único
Regiões Promotoras Genéticas
[Mh] Termos MeSH secundário: Idoso
Apolipoproteínas/sangue
Apolipoproteínas M
Sítios de Ligação
Estudos de Casos e Controles
Doença da Artéria Coronariana/sangue
Doença da Artéria Coronariana/diagnóstico
Ensaio de Desvio de Mobilidade Eletroforética
Feminino
Genes Reporter
Estudos de Associação Genética
Marcadores Genéticos
Predisposição Genética para Doença
Células Hep G2
Seres Humanos
Lipocalinas/sangue
Luciferases/biossíntese
Luciferases/genética
Masculino
Meia-Idade
Mutação
Nucleoproteínas/metabolismo
Fenótipo
Reação em Cadeia da Polimerase
Ligação Proteica
Fatores de Risco
Fator de Transcrição AP-2/metabolismo
Transcrição Genética
Transfecção
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (APOM protein, human); 0 (Apolipoproteins); 0 (Apolipoproteins M); 0 (Genetic Markers); 0 (Lipocalins); 0 (Nucleoproteins); 0 (Transcription Factor AP-2); EC 1.13.12.- (Luciferases)
[Em] Mês de entrada:1702
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161115
[St] Status:MEDLINE
[do] DOI:10.5830/CVJA-2016-001


  10 / 152 MEDLINE  
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[PMID]:27633510
[Au] Autor:Zhang P; Gao J; Pu C; Feng G; Wang L; Huang L; Tao Q; Zhang Y
[Ad] Endereço:Anhui Province Key Laboratory of Biological Macro-molecules Research (Wannan Medical College), Wuhu, China.
[Ti] Título:Effects of hyperlipidaemia on plasma apolipoprotein M levels in patients with type 2 diabetes mellitus: an independent case-control study.
[So] Source:Lipids Health Dis;15(1):158, 2016 Sep 15.
[Is] ISSN:1476-511X
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Apolipoprotein M (apoM) is mainly enriched in high-density lipoprotein (HDL) cholesterol and is slightly present in low-density lipoprotein (LDL) cholesterol and very low-density lipoprotein cholesterol. apoM is involved in HDL formation and HDL-mediated reverse cholesterol transport. apoM is also associated with hyperlipidaemia and type 2 diabetes mellitus (T2DM). Significantly high plasma apoM levels are detected in hyperlipidaemia mice with a defective LDL receptor. By contrast, low plasma apoM levels are observed in patients with T2DM, which is often accompanied with hyperlipidaemia. However, the underlying mechanism of this condition is poorly understood. This research aims to examine the changes in apoM levels in patients with hyperlipidaemia and to determine the effects of hyperlipidaemia on plasma apoM levels in patients with T2DM. METHODS: This study included patients with hyperlipidaemia (n = 79), patients with T2DM but without hyperlipidaemia (n = 125), patients with T2DM and hyperlipidaemia (n = 98), and healthy controls (n = 105). Their plasma apoM concentrations were measured with enzyme-linked immunosorbent assay. RESULTS: The average plasma apoM concentrations were 18 % higher in the hyperlipidaemia group (26.63 ± 10.35 ng/µL) than in the healthy controls (22.61 ± 10.81 ng/µL, P <0.01). The plasma apoM concentrations were lower in the T2DM without hyperlipidaemia group (18.54 ± 10.33 ng/µL, P <0.01) and the T2DM with hyperlipidaemia group (19.83 ± 7.41 ng/µL, P <0.05) than in the healthy controls. Similar to apoA-I (1.29 ± 0.33 g/L vs. 1.28 ± 0.31 g/L, P >0.05), the plasma apoM concentrations in the T2DM with hyperlipidaemia group did not significantly differ from those in the T2DM without hyperlipidaemia group (P >0.05). Multivariate linear regression analysis showed that hyperlipidaemia (ß = 5.18, P = 0.007) is an independent promoting factor of plasma apoM levels and diabetes (ß = -3.09, P = 0.005) is an inhibiting factor of plasma apoM levels. CONCLUSION: Plasma apoM concentrations are higher in patients with hyperlipidaemia than in healthy controls. Low plasma apoM levels in patients with T2DM are likely caused by diabetes but are not induced by hyperlipidaemia.
[Mh] Termos MeSH primário: Apolipoproteínas/sangue
LDL-Colesterol/sangue
Diabetes Mellitus Tipo 2/sangue
Hiperlipidemias/sangue
Lipocalinas/sangue
[Mh] Termos MeSH secundário: Adulto
Idoso
Animais
Apolipoproteínas M
Diabetes Mellitus Tipo 2/patologia
Feminino
Seres Humanos
Hiperlipidemias/patologia
Modelos Lineares
Masculino
Camundongos
Meia-Idade
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (APOM protein, human); 0 (Apolipoproteins); 0 (Apolipoproteins M); 0 (Cholesterol, LDL); 0 (Lipocalins)
[Em] Mês de entrada:1704
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160917
[St] Status:MEDLINE
[do] DOI:10.1186/s12944-016-0325-1



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