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[PMID]:29279524
[Au] Autor:Li X; Liang Y; Qiao Z; Yang J; Han P; Zhao B; Li F; Lv H; Guo J; Gao F; Li L
[Ad] Endereço:Department of Cardiology, Hongqi Hospital, Mudanjiang Medical College.
[Ti] Título:Transcriptional Analysis of Endothelial Cell Alternation Induced by Atrial Natriuretic Polypeptide in Human Umbilical Vein Endothelial Cells.
[So] Source:Int Heart J;59(1):197-202, 2018 Jan 27.
[Is] ISSN:1349-3299
[Cp] País de publicação:Japan
[La] Idioma:eng
[Ab] Resumo:The aim of this study was to explore how atrial natriuretic polypeptide (ANP) affects the properties and function of endothelial cells. Gene expression data GSE56976 generated at 0, 1, and 6 hours after ANP incubation in human umbilical vein endothelial cells (HUVEC) was used. Microarray data were preprocessed for differentially expressed genes (DEGs) in each time-dependent group. Next, gene ontology (GO), pathway analysis, and transcriptional regulation were performed. Co-expression clustering analysis of DEGs and functional enrichment analysis of co-expression modules were processed. RT-PCR analysis was performed to validate gene expression. DEGs were obtained and their counts were increased from 0 hours to 6 hours. No overlapping DEGs were obtained among the 3 groups. The DEGs of ANP_6hours, including TGFB2 (transforming growth factor, beta 2), LTF (lactotransferrin/lactoferrin), and ETV7 (Ets variant 7) were mainly related with cell apoptosis and immune responses. The DEGs in the network of ANP_0hour were mainly associated with epithelial ion transport processes. In addition, 3 co-expressed modules were detected. CSF2 (colony stimulating factor 2) and PF4 (platelet factor 4) of the blue module were related with cytolysis, while FXYD1 (FXYD domain containing ion transport regulator 1) and TGFB2 of the yellow module were mainly enriched in ion transport and the ovulation cycle. The expression of TGFB2 obtained by microarray analysis was consistent with that of RT-PCR. Ion transport could be affected promptly after ANP treatment, and subsequently, the cytolysis of vein endothelial cells may be promoted and endothelial permeability would be enhanced, followed by activated immune responses.
[Mh] Termos MeSH primário: Apoptose
Fator Natriurético Atrial/farmacologia
Regulação da Expressão Gênica
Células Endoteliais da Veia Umbilical Humana/metabolismo
Lactoferrina/genética
Proteínas Proto-Oncogênicas c-ets/genética
Fator de Crescimento Transformador beta2/genética
[Mh] Termos MeSH secundário: Células Cultivadas
Perfilação da Expressão Gênica
Células Endoteliais da Veia Umbilical Humana/efeitos dos fármacos
Células Endoteliais da Veia Umbilical Humana/patologia
Seres Humanos
Lactoferrina/biossíntese
Proteínas Proto-Oncogênicas c-ets/biossíntese
RNA/genética
Reação em Cadeia da Polimerase em Tempo Real
Fator de Crescimento Transformador beta2/biossíntese
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (ETV7 protein, human); 0 (LTF protein, human); 0 (Proto-Oncogene Proteins c-ets); 0 (TGFB2 protein, human); 0 (Transforming Growth Factor beta2); 63231-63-0 (RNA); 85637-73-6 (Atrial Natriuretic Factor); EC 3.4.21.- (Lactoferrin)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180206
[Lr] Data última revisão:
180206
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171228
[St] Status:MEDLINE
[do] DOI:10.1536/ihj.16-522


  2 / 1343 MEDLINE  
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[PMID]:29320969
[Au] Autor:Hachim MY; Hachim IY; Dai M; Ali S; Lebrun JJ
[Ad] Endereço:1 Cancer Research Program, Department of Medicine, McGill University Health Centre, Montreal, QC, Canada.
[Ti] Título:Differential expression of TGFß isoforms in breast cancer highlights different roles during breast cancer progression.
[So] Source:Tumour Biol;40(1):1010428317748254, 2018 Jan.
[Is] ISSN:1423-0380
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:While TGFß plays a critical role in tumor formation and progression, the role and contribution of its three different isoforms remain unclear. In this study, we aimed at elucidating the prognostic value of the TGFß isoforms and assessed their expression levels in breast cancer patients at different stages of the disease. We found higher levels of TGFß1 and TGFß3 in cancer patients compared to normal tissues, with no significant changes in TGFß2 expression. Similarly, TGFß1 and TGFß3, but not TGFß2, showed higher expression levels in advanced lymph node-positive and metastatic tumors, suggesting different roles for the different isoforms in tumor progression and the metastatic process, while in the least aggressive molecular subtype (luminal A), expression of the three TGFß isoforms significantly correlated with expression of both TGFß receptors, such correlation only occurred between TGFß1 and TGFß3 and the TGFß type II receptor (TßRII) in the highly aggressive basal-like subtype. Interestingly, a distinct and somehow opposite pattern was observed in HER-2 tumors, only showing significant association pattern between TGFß2 and the TGFß type I receptor (TßRI). Finally, the three TGFß isoforms showed distinct association patterns with patient outcome depending on the different molecular subtype, highlighting context-dependent, differential prognostic values.
[Mh] Termos MeSH primário: Neoplasias da Mama/genética
Perfilação da Expressão Gênica/métodos
Fator de Crescimento Transformador beta1/genética
Fator de Crescimento Transformador beta2/genética
Fator de Crescimento Transformador beta3/genética
[Mh] Termos MeSH secundário: Neoplasias da Mama/metabolismo
Neoplasias da Mama/patologia
Linhagem Celular Tumoral
Progressão da Doença
Feminino
Seres Humanos
Imuno-Histoquímica
Meia-Idade
RNA Mensageiro/genética
RNA Mensageiro/metabolismo
Receptores de Fatores de Crescimento Transformadores beta/genética
Receptores de Fatores de Crescimento Transformadores beta/metabolismo
Esferoides Celulares/metabolismo
Fator de Crescimento Transformador beta1/metabolismo
Fator de Crescimento Transformador beta2/metabolismo
Fator de Crescimento Transformador beta3/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (RNA, Messenger); 0 (Receptors, Transforming Growth Factor beta); 0 (Transforming Growth Factor beta1); 0 (Transforming Growth Factor beta2); 0 (Transforming Growth Factor beta3)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180129
[Lr] Data última revisão:
180129
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180112
[St] Status:MEDLINE
[do] DOI:10.1177/1010428317748254


  3 / 1343 MEDLINE  
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[PMID]:28448670
[Au] Autor:Futakuchi A; Inoue T; Fujimoto T; Kuroda U; Inoue-Mochita M; Takahashi E; Ohira S; Tanihara H
[Ad] Endereço:Department of Ophthalmology, Faculty of Life Sciences, Kumamoto University, Kumamoto, Japan.
[Ti] Título:Molecular Mechanisms Underlying the Filtration Bleb-Maintaining Effects of Suberoylanilide Hydroxamic Acid (SAHA).
[So] Source:Invest Ophthalmol Vis Sci;58(4):2421-2429, 2017 04 01.
[Is] ISSN:1552-5783
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Purpose: Suberoylanilide hydroxamic acid (SAHA) has been shown to support the maintenance of experimental filtration blebs in animal models. This study was performed to investigate the molecular mechanisms underlying the bleb-maintaining effects of SAHA in modulating wound healing activities of conjunctival fibroblasts. Methods: Human conjunctival fibroblasts (HConFs) were pretreated with SAHA before treatment with TGF-ß2. Microarray-based screening was used to investigate the gene expression profiles. Gene ontology (GO) analysis was conducted to categorize the gene functions. The expression of TGF-ß-induced signaling molecules, α-smooth muscle actin, and extracellular matrix (ECM) proteins were evaluated by Western blot analyses. Multiplex immunoassay was performed to evaluate supernatant cytokine concentrations. Tube formation assay was used to evaluate angiogenesis using human umbilical vein endothelial cells. Results: GO analysis showed that SAHA, in the presence of TGF-ß2, induced changes in expression of genes involved in the TGF-ß receptor signaling pathway, cell proliferation, extracellular matrix organization, inflammatory responses, and angiogenesis. Subsequent in vitro experiments showed that SAHA partly inhibited the phosphorylation of Smad2, Smad3, and Akt. SAHA pretreatment potently suppressed TGF-ß2-driven cell proliferation, myofibroblast differentiation, contraction, ECM production, and angiogenic cytokine expression. The supernatant of HConFs treated with SAHA inhibited tube formation. Conclusions: SAHA has been shown to suppress angiogenesis and activation of conjunctival fibroblasts partly via inhibition of Smad and non-Smad TGF-ß signaling. This in vitro study provides new evidence for the molecular basis of the potential bleb-maintaining effects of SAHA, a novel candidate drug in modulating scar formation after glaucoma filtration surgery.
[Mh] Termos MeSH primário: Inibidores da Angiogênese/farmacologia
Túnica Conjuntiva/efeitos dos fármacos
Fibroblastos/efeitos dos fármacos
Inibidores de Histona Desacetilases/farmacocinética
Ácidos Hidroxâmicos/farmacologia
[Mh] Termos MeSH secundário: Vesícula/metabolismo
Movimento Celular/efeitos dos fármacos
Proliferação Celular/efeitos dos fármacos
Células Cultivadas
Colágeno Tipo I/metabolismo
Túnica Conjuntiva/citologia
Citocinas/metabolismo
Proteínas da Matriz Extracelular/metabolismo
Fibroblastos/metabolismo
Cirurgia Filtrante
Perfilação da Expressão Gênica
Seres Humanos
Receptores de Fatores de Crescimento Transformadores beta/metabolismo
Transdução de Sinais/efeitos dos fármacos
Proteínas Smad/metabolismo
Análise Serial de Tecidos
Fator de Crescimento Transformador beta2/farmacologia
Cicatrização/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Angiogenesis Inhibitors); 0 (Collagen Type I); 0 (Cytokines); 0 (Extracellular Matrix Proteins); 0 (Histone Deacetylase Inhibitors); 0 (Hydroxamic Acids); 0 (Receptors, Transforming Growth Factor beta); 0 (Smad Proteins); 0 (Transforming Growth Factor beta2); 58IFB293JI (vorinostat)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:180118
[Lr] Data última revisão:
180118
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170428
[St] Status:MEDLINE
[do] DOI:10.1167/iovs.16-21403


  4 / 1343 MEDLINE  
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[PMID]:29190815
[Au] Autor:Thiagarajan D; O' Shea K; Sreejit G; Ananthakrishnan R; Quadri N; Li Q; Schmidt AM; Gabbay K; Ramasamy R
[Ad] Endereço:Diabetes Research Program, Department of Medicine, New York University Langone Medical Center, New York, New York, United States of America.
[Ti] Título:Aldose reductase modulates acute activation of mesenchymal markers via the ß-catenin pathway during cardiac ischemia-reperfusion.
[So] Source:PLoS One;12(11):e0188981, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Aldose reductase (AR: human, AKR1B1; mouse, AKR1B3), the first enzyme in the polyol pathway, plays a key role in mediating myocardial ischemia/reperfusion (I/R) injury. In earlier studies, using transgenic mice broadly expressing human AKR1B1 to human-relevant levels, mice devoid of Akr1b3, and pharmacological inhibitors of AR, we demonstrated that AR is an important component of myocardial I/R injury and that inhibition of this enzyme protects the heart from I/R injury. In this study, our objective was to investigate if AR modulates the ß-catenin pathway and consequent activation of mesenchymal markers during I/R in the heart. To test this premise, we used two different experimental models: in vivo, Akr1b3 null mice and wild type C57BL/6 mice (WT) were exposed to acute occlusion of the left anterior descending coronary artery (LAD) followed by recovery for 48 hours or 28 days, and ex-vivo, WT and Akr1b3 null murine hearts were perfused using the Langendorff technique (LT) and subjected to 30 min of global (zero-flow) ischemia followed by 60 min of reperfusion. Our in vivo results reveal reduced infarct size and improved functional recovery at 48 hours in mice devoid of Akr1b3 compared to WT mice. We demonstrate that the cardioprotection observed in Akr1b3 null mice was linked to acute activation of the ß-catenin pathway and consequent activation of mesenchymal markers and genes linked to fibrotic remodeling. The increased activity of the ß-catenin pathway at 48 hours of recovery post-LAD was not observed at 28 days post-infarction, thus indicating that the observed increase in ß-catenin activity was transient in the mice hearts devoid of Akr1b3. In ex vivo studies, inhibition of ß-catenin blocked the cardioprotection observed in Akr1b3 null mice hearts. Taken together, these data indicate that AR suppresses acute activation of ß-catenin and, thereby, blocks consequent induction of mesenchymal markers during early reperfusion after myocardial ischemia. Inhibition of AR might provide a therapeutic opportunity to optimize cardiac remodeling after I/R injury.
[Mh] Termos MeSH primário: Aldeído Redutase/metabolismo
Biomarcadores/metabolismo
Mesoderma/metabolismo
Traumatismo por Reperfusão Miocárdica/metabolismo
beta Catenina/metabolismo
[Mh] Termos MeSH secundário: Aldeído Redutase/genética
Animais
Regulação da Expressão Gênica
Camundongos
Camundongos Endogâmicos C57BL
Camundongos Knockout
Fator de Crescimento Transformador beta2/metabolismo
Regulação para Cima
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Biomarkers); 0 (Tgfb2 protein, mouse); 0 (Transforming Growth Factor beta2); 0 (beta Catenin); EC 1.1.1.21 (Aldehyde Reductase)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180101
[Lr] Data última revisão:
180101
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171201
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0188981


  5 / 1343 MEDLINE  
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[PMID]:28977001
[Au] Autor:Howe GA; Kazda K; Addison CL
[Ad] Endereço:Cancer Therapeutics Program, Ottawa Hospital Research Institute, Ottawa, ON, Canada.
[Ti] Título:MicroRNA-30b controls endothelial cell capillary morphogenesis through regulation of transforming growth factor beta 2.
[So] Source:PLoS One;12(10):e0185619, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The importance of microRNA (miRNA) to vascular biology is becoming increasingly evident; however, the function of a significant number of miRNA remains to be determined. In particular, the effect of growth factor regulation of miRNAs on endothelial cell morphogenesis is incomplete. Thus, we aimed to identify miRNAs regulated by pro-angiogenic vascular endothelial growth factor (VEGF) and determine the effects of VEGF-regulated miRNAs and their targets on processes important for angiogenesis. Human umbilical vein endothelial cells (HUVECs) were thus stimulated with VEGF and miRNA levels assessed using microarrays. We found that VEGF altered expression of many miRNA, and for this study focused on one of the most significantly down-regulated miRNA in HUVECs following VEGF treatment, miR-30b. Using specific miRNA mimics, we found that overexpression of miR-30b inhibited capillary morphogenesis in vitro, while depletion of endogenous miR-30b resulted in increased capillary morphogenesis indicating the potential significance of down-regulation of miR-30b as a pro-angiogenic response to VEGF stimulation. MiR-30b overexpression in HUVEC regulated transforming growth factor beta 2 (TGFß2) production, which led to increased phosphorylation of Smad2, indicating activation of an autocrine TGFß signaling pathway. Up-regulation of TGFß2 by miR-30b overexpression was found to be dependent on ATF2 activation, a transcription factor known to regulate TGFß2 expression, as miR-30b overexpressing cells exhibited increased levels of phosphorylated ATF2 and depletion of ATF2 inhibited miR-30b-induced TGFß2 expression. However, miR-30b effects on ATF2 were indirect and found to be via targeting of the known ATF2 repressor protein JDP2 whose mRNA levels were indirectly correlated with miR-30b levels. Increased secretion of TGFß2 from HUVEC was shown to mediate the inhibitory effects of miR-30b on capillary morphogenesis as treatment with a neutralizing antibody to TGFß2 restored capillary morphogenesis to normal levels in miR-30b overexpressing cells. These results support that the regulation of miR-30b by VEGF in HUVEC is important for capillary morphogenesis, as increased miR-30b expression inhibits capillary morphogenesis through enhanced expression of TGFß2.
[Mh] Termos MeSH primário: Capilares/crescimento & desenvolvimento
Endotélio Vascular/citologia
MicroRNAs/fisiologia
Fator de Crescimento Transformador beta2/metabolismo
[Mh] Termos MeSH secundário: Células Endoteliais da Veia Umbilical Humana
Seres Humanos
Morfogênese
Fosforilação
Fator de Crescimento Transformador beta2/biossíntese
Fator A de Crescimento do Endotélio Vascular/fisiologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (MIRN30 microRNA, human); 0 (MicroRNAs); 0 (Transforming Growth Factor beta2); 0 (Vascular Endothelial Growth Factor A)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171102
[Lr] Data última revisão:
171102
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171005
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0185619


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[PMID]:28913545
[Au] Autor:Yoshida S; Nakama T; Ishikawa K; Nakao S; Sonoda KH; Ishibashi T
[Ad] Endereço:Department of Ophthalmology, Kyushu University Graduate School of Medical Sciences, Fukuoka, 812-8582, Japan. usyosi@gmail.com.
[Ti] Título:Periostin in vitreoretinal diseases.
[So] Source:Cell Mol Life Sci;74(23):4329-4337, 2017 Dec.
[Is] ISSN:1420-9071
[Cp] País de publicação:Switzerland
[La] Idioma:eng
[Ab] Resumo:Proliferative vitreoretinal diseases such as diabetic retinopathy, proliferative vitreoretinopathy (PVR), and age-related macular degeneration are a leading cause of decreased vision and blindness in developed countries. In these diseases, retinal fibro(vascular) membrane (FVM) formation above and beneath the retina plays an important role. Gene expression profiling of human FVMs revealed significant upregulation of periostin. Subsequent analyses demonstrated increased periostin expression in the vitreous of patients with both proliferative diabetic retinopathy and PVR. Immunohistochemical analysis showed co-localization of periostin with α-SMA and M2 macrophage markers in FVMs. In vitro, periostin blockade inhibited migration and adhesion induced by PVR vitreous and transforming growth factor-ß2 (TGF-ß2). In vivo, a novel single-stranded RNAi agent targeting periostin showed the inhibitory effect on experimental retinal and choroidal FVM formation without affecting the viability of retinal cells. These results indicated that periostin is a pivotal molecule for FVM formation and a promising therapeutic target for these proliferative vitreoretinal diseases.
[Mh] Termos MeSH primário: Moléculas de Adesão Celular/genética
Neovascularização de Coroide/genética
Retinopatia Diabética/genética
Degeneração Macular/genética
Vitreorretinopatia Proliferativa/genética
[Mh] Termos MeSH secundário: Actinas/genética
Actinas/imunologia
Animais
Moléculas de Adesão Celular/antagonistas & inibidores
Moléculas de Adesão Celular/imunologia
Neovascularização de Coroide/imunologia
Neovascularização de Coroide/patologia
Neovascularização de Coroide/terapia
Retinopatia Diabética/imunologia
Retinopatia Diabética/patologia
Retinopatia Diabética/terapia
Regulação da Expressão Gênica
Inativação Gênica
Seres Humanos
Degeneração Macular/imunologia
Degeneração Macular/patologia
Degeneração Macular/terapia
Camundongos
RNA Interferente Pequeno/genética
RNA Interferente Pequeno/metabolismo
Retina/imunologia
Retina/patologia
Transdução de Sinais
Fator de Crescimento Transformador beta2/genética
Fator de Crescimento Transformador beta2/imunologia
Vitreorretinopatia Proliferativa/imunologia
Vitreorretinopatia Proliferativa/patologia
Vitreorretinopatia Proliferativa/terapia
Corpo Vítreo/imunologia
Corpo Vítreo/patologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (ACTA2 protein, human); 0 (Actins); 0 (Cell Adhesion Molecules); 0 (POSTN protein, human); 0 (RNA, Small Interfering); 0 (Transforming Growth Factor beta2)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171101
[Lr] Data última revisão:
171101
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170916
[St] Status:MEDLINE
[do] DOI:10.1007/s00018-017-2651-5


  7 / 1343 MEDLINE  
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[PMID]:28789942
[Au] Autor:Kim ML; Sung KR; Shin JA; Young Yoon J; Jang J
[Ad] Endereço:Biomedical Research Center, College of Medicine, University of Ulsan, Asan Medical Center, Seoul, South Korea.
[Ti] Título:Statins reduce TGF-beta2-modulation of the extracellular matrix in cultured astrocytes of the human optic nerve head.
[So] Source:Exp Eye Res;164:55-63, 2017 Nov.
[Is] ISSN:1096-0007
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Statins are cholesterol lowering drugs and have shown beneficial effects on glaucoma. With regard to the mechanism of statin action on glaucoma, we investigated the effects of statins on transforming growth factor-beta 2 (TGF-ß2)-induced expression of extracellular matrix (ECM) proteins in human astrocytes of the optic nerve head (ONH) lamina cribrosa (LC). By using primary human ONH astrocytes, we found that both simvastatin and lovastatin inhibited TGF-ß2-mediated expression of ECM proteins such as connective tissue growth factor, collagen I, fibronectin, and plasminogen activator inhibitor-1. Suppression of ECM related proteins is due to inhibition of Smad2/3 activation as statins inhibit TGF-ß2-induced Smad2 phosphorylation and Smad2/3 nuclear accumulation. In ONH astrocytes, TGF-ß2 does not induce MAPK activation. In this study we found an anti-fibrotic effect of statins in human astrocytes of the ONH and identified TGF-ß2 as a mediator of statin action, which may support a beneficial role for statins in blocking glaucomatous axonal damage induced by ECM remodeling.
[Mh] Termos MeSH primário: Astrócitos/efeitos dos fármacos
Matriz Extracelular/metabolismo
Inibidores de Hidroximetilglutaril-CoA Redutases/farmacologia
Disco Óptico/metabolismo
Fator de Crescimento Transformador beta2/fisiologia
[Mh] Termos MeSH secundário: Análise de Variância
Astrócitos/metabolismo
Células Cultivadas
Matriz Extracelular/efeitos dos fármacos
Proteínas do Olho/metabolismo
Seres Humanos
Lovastatina
Disco Óptico/citologia
Sinvastatina
Fator de Crescimento Transformador beta2/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Eye Proteins); 0 (Hydroxymethylglutaryl-CoA Reductase Inhibitors); 0 (Transforming Growth Factor beta2); 9LHU78OQFD (Lovastatin); AGG2FN16EV (Simvastatin)
[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:170810
[St] Status:MEDLINE


  8 / 1343 MEDLINE  
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[PMID]:28782576
[Au] Autor:Li J; Chen C; Bi X; Zhou C; Huang T; Ni C; Yang P; Chen S; Ye M; Duan S
[Ad] Endereço:Medical Genetics Center, School of Medicine, Ningbo University, Ningbo, Zhejiang 315211, China; The Affiliated Hospital, Ningbo University, Ningbo, Zhejiang 315000, China.
[Ti] Título:DNA methylation of CMTM3, SSTR2, and MDFI genes in colorectal cancer.
[So] Source:Gene;630:1-7, 2017 Sep 30.
[Is] ISSN:1879-0038
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Colorectal cancer (CRC) is increasingly common worldwide, including in China. Therefore, there is an increasing need to detect CRC at an early stage and to discover and evaluate diagnostic and prognostic biomarkers. DNA methylation of genes in CRC is a potential epigenetic biomarker for the early detection of CRC. This study was performed to analyze the methylation frequency of six candidate genes, CMTM3, SSTR2, MDFI, NDRG4, TGFB2, and BCL2L11, in fresh-frozen CRC tissues and adjacent normal colorectal tissues, from 42 patients with CRC. DNA isolation, bisulphite modification, and pyrosequencing were performed. The sensitivity, specificity, and the area under the receiver operator characteristic (ROC) curve (AUC) were evaluated to determine whether these genes showed any associations with tumor grade, stage, or diagnostic features. Among the tested genes, three genes, CMTM3, SSTR2, and MDFI were significantly methylated in CRC tissues when compared with adjacent normal colorectal tissues. The ROC analysis showed that a multigene model, including CMTM3, SSTR2, and MDFI, had a sensitivity of 81% and a specificity of 91% with an AUC value of 0.92. The findings of this study have shown that DNA methylation of the genes, CMTM3, SSTR2, and MDFI should be studied further with a view to determining their potential role as biomarkers for CRC.
[Mh] Termos MeSH primário: Biomarcadores Tumorais/genética
Neoplasias Colorretais/genética
Contactinas/genética
Metilação de DNA
Fatores de Regulação Miogênica/genética
Receptores de Somatostatina/genética
[Mh] Termos MeSH secundário: Proteína 11 Semelhante a Bcl-2/genética
Neoplasias Colorretais/patologia
Feminino
Seres Humanos
Masculino
Meia-Idade
Proteínas Musculares/genética
Proteínas do Tecido Nervoso/genética
Fator de Crescimento Transformador beta2/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (BCL2L11 protein, human); 0 (Bcl-2-Like Protein 11); 0 (Biomarkers, Tumor); 0 (CNTN3 protein, human); 0 (Contactins); 0 (Muscle Proteins); 0 (Myogenic Regulatory Factors); 0 (NDRG4 protein, human); 0 (Nerve Tissue Proteins); 0 (Receptors, Somatostatin); 0 (TGFB2 protein, human); 0 (Transforming Growth Factor beta2); 0 (somatostatin receptor subtype 2, human); 183511-66-2 (MDFI protein, human)
[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:170808
[St] Status:MEDLINE


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[PMID]:28729364
[Au] Autor:Angelov SN; Hu JH; Wei H; Airhart N; Shi M; Dichek DA
[Ad] Endereço:From the Department of Medicine, University of Washington School of Medicine, Seattle.
[Ti] Título:TGF-ß (Transforming Growth Factor-ß) Signaling Protects the Thoracic and Abdominal Aorta From Angiotensin II-Induced Pathology by Distinct Mechanisms.
[So] Source:Arterioscler Thromb Vasc Biol;37(11):2102-2113, 2017 Nov.
[Is] ISSN:1524-4636
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:OBJECTIVE: The role of TGF-ß (transforming growth factor-ß) signaling in abdominal aortic aneurysm (AAA) formation is controversial. Others reported that systemic blockade of TGF-ß by neutralizing antibodies accelerated AAA development in angiotensin II-infused mice. This result is consistent with other studies suggesting that TGF-ß signaling prevents AAA. Development of a therapy for AAA that exploits the protective actions of TGF-ß would be facilitated by identification of the mechanisms through which TGF-ß prevents AAA. We hypothesized that TGF-ß signaling prevents AAA by its actions on aortic medial smooth muscle cells. APPROACH AND RESULTS: We compared the prevalence, severity, and histopathology of angiotensin II-induced AAA among control mice (no TGF-ß blockade), mice with antibody-mediated systemic neutralization of TGF-ß, and mice with genetically based smooth muscle-specific loss of TGF-ß signaling. Surprisingly, we found that systemic-but not smooth muscle-specific-TGF-ß blockade significantly increased the prevalence of AAA and tended to increase AAA severity, adventitial thickening, and aortic wall macrophage accumulation. In contrast, abdominal aortas of mice with smooth muscle-specific loss of TGF-ß signaling differed from controls only in having a thinner media. We examined thoracic aortas of the same mice. Here we found that smooth muscle-specific loss of -but not systemic TGF-ß neutralization-significantly accelerated development of aortic pathology, including increased prevalence of intramural hematomas, medial thinning, and adventitial thickening. CONCLUSION: Our results suggest that TGF-ß signaling prevents both abdominal and thoracic aneurysmal disease but does so by distinct mechanisms. Smooth muscle extrinsic signaling protects the abdominal aorta and smooth muscle intrinsic signaling protects the thoracic aorta.
[Mh] Termos MeSH primário: Angiotensina II
Aneurisma da Aorta Abdominal/prevenção & controle
Aneurisma da Aorta Torácica/prevenção & controle
Músculo Liso Vascular/metabolismo
Transdução de Sinais
Fator de Crescimento Transformador beta/metabolismo
Remodelação Vascular
[Mh] Termos MeSH secundário: Túnica Adventícia/metabolismo
Túnica Adventícia/patologia
Animais
Anticorpos/farmacologia
Aorta Abdominal/efeitos dos fármacos
Aorta Abdominal/metabolismo
Aorta Abdominal/patologia
Aorta Torácica/efeitos dos fármacos
Aorta Torácica/metabolismo
Aorta Torácica/patologia
Aneurisma da Aorta Abdominal/induzido quimicamente
Aneurisma da Aorta Abdominal/metabolismo
Aneurisma da Aorta Abdominal/patologia
Aneurisma da Aorta Torácica/induzido quimicamente
Aneurisma da Aorta Torácica/metabolismo
Aneurisma da Aorta Torácica/patologia
Dilatação Patológica
Modelos Animais de Doenças
Feminino
Predisposição Genética para Doença
Masculino
Camundongos Endogâmicos C57BL
Camundongos Knockout
Músculo Liso Vascular/efeitos dos fármacos
Músculo Liso Vascular/patologia
Fenótipo
Proteínas Serina-Treonina Quinases/deficiência
Proteínas Serina-Treonina Quinases/genética
Receptores de Fatores de Crescimento Transformadores beta/deficiência
Receptores de Fatores de Crescimento Transformadores beta/genética
Índice de Gravidade de Doença
Transdução de Sinais/efeitos dos fármacos
Fator de Crescimento Transformador beta/antagonistas & inibidores
Fator de Crescimento Transformador beta1/antagonistas & inibidores
Fator de Crescimento Transformador beta1/metabolismo
Fator de Crescimento Transformador beta2/antagonistas & inibidores
Fator de Crescimento Transformador beta2/metabolismo
Fator de Crescimento Transformador beta3/antagonistas & inibidores
Fator de Crescimento Transformador beta3/metabolismo
Túnica Média/metabolismo
Túnica Média/patologia
Remodelação Vascular/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antibodies); 0 (Receptors, Transforming Growth Factor beta); 0 (Tgfb1 protein, mouse); 0 (Tgfb2 protein, mouse); 0 (Tgfb3 protein, mouse); 0 (Transforming Growth Factor beta); 0 (Transforming Growth Factor beta1); 0 (Transforming Growth Factor beta2); 0 (Transforming Growth Factor beta3); 11128-99-7 (Angiotensin II); EC 2.7.11.1 (Protein-Serine-Threonine Kinases); EC 2.7.11.30 (transforming growth factor-beta type II receptor)
[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:170722
[St] Status:MEDLINE
[do] DOI:10.1161/ATVBAHA.117.309401


  10 / 1343 MEDLINE  
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[PMID]:28719670
[Au] Autor:Matoba R; Morizane Y; Shiode Y; Hirano M; Doi S; Toshima S; Araki R; Hosogi M; Yonezawa T; Shiraga F
[Ad] Endereço:Department of Ophthalmology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama, Japan.
[Ti] Título:Suppressive effect of AMP-activated protein kinase on the epithelial-mesenchymal transition in retinal pigment epithelial cells.
[So] Source:PLoS One;12(7):e0181481, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The epithelial-mesenchymal transition (EMT) in retinal pigment epithelial (RPE) cells plays a central role in the development of proliferative vitreoretinopathy (PVR). The purpose of this study was to investigate the effect of AMP-activated protein kinase (AMPK), a key regulator of energy homeostasis, on the EMT in RPE cells. In this study, EMT-associated formation of cellular aggregates was induced by co-stimulation of cultured ARPE-19 cells with tumor necrosis factor (TNF)-α (10 ng/ml) and transforming growth factor (TGF)-ß2 (5 ng/ml). 5-Aminoimidazole-4-carboxamide-1-ß-D-ribofuranoside (AICAR), a potent activator of AMPK, significantly suppressed TNF-α and TGF-ß2-induced cellular aggregate formation (p < 0.01). Dipyridamole almost completely reversed the suppressive effect of AICAR, whereas 5'-amino-5'-deoxyadenosine restored aggregate formation by approximately 50%. AICAR suppressed the downregulation of E-cadherin and the upregulation of fibronectin and α-smooth muscle actin by TNF-α and TGF-ß2. The levels of matrix metalloproteinase (MMP)-2, MMP-9, interleukin-6, and vascular endothelial growth factor were significantly decreased by AICAR. Activation of the mitogen-activated protein kinase and mammalian target of rapamycin pathways, but not the Smad pathway, was inhibited by AICAR. These findings indicate that AICAR suppresses the EMT in RPE cells at least partially via activation of AMPK. AMPK is a potential target molecule for the prevention and treatment of PVR, so AICAR may be a promising candidate for PVR therapy.
[Mh] Termos MeSH primário: Proteínas Quinases Ativadas por AMP/metabolismo
Transição Epitelial-Mesenquimal/efeitos dos fármacos
Epitélio Pigmentado da Retina/citologia
[Mh] Termos MeSH secundário: Aminoimidazol Carboxamida/análogos & derivados
Aminoimidazol Carboxamida/farmacologia
Agregação Celular/efeitos dos fármacos
Linhagem Celular
Sinergismo Farmacológico
Ativação Enzimática/efeitos dos fármacos
Regulação Enzimológica da Expressão Gênica/efeitos dos fármacos
Seres Humanos
Interleucina-6/metabolismo
Metaloproteinase 2 da Matriz/metabolismo
Metaloproteinase 9 da Matriz/metabolismo
Ribonucleotídeos/farmacologia
Fator de Crescimento Transformador beta2/farmacologia
Fator de Necrose Tumoral alfa/farmacologia
Fator A de Crescimento do Endotélio Vascular/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Interleukin-6); 0 (Ribonucleotides); 0 (Transforming Growth Factor beta2); 0 (Tumor Necrosis Factor-alpha); 0 (Vascular Endothelial Growth Factor A); 360-97-4 (Aminoimidazole Carboxamide); EC 2.7.11.31 (AMP-Activated Protein Kinases); EC 3.4.24.24 (Matrix Metalloproteinase 2); EC 3.4.24.35 (Matrix Metalloproteinase 9); F0X88YW0YK (AICA ribonucleotide)
[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:170719
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0181481



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