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[PMID]:29232393
[Au] Autor:Larocca TF; Macêdo CT; Noya-Rabelo M; Lemos Correia LC; Moreira MI; Caldas AC; Torreão JA; Souza BSF; Vasconcelos JF; Carvalho da Silva AS; Ribeiro Dos Santos R; Soares MBP
[Ad] Endereço:Center for Biotechnology and Cell Therapy, São Rafael Hospital, Salvador, Bahia, Brazil.
[Ti] Título:Lack of association between serum syndecan-4, myocardial fibrosis and ventricular dysfunction in subjects with chronic Chagas disease.
[So] Source:PLoS One;12(12):e0189408, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Syndecan-4 is a transmembrane glycoprotein associated with inflammation and fibrosis. Increased syndecan-4 levels were previously detected after acute myocardial infarction and in subjects with heart failure. However, the levels of syndecan-4 in subjects with Chagas disease have not so far been investigated. The aim of this study was to investigate the potential role of serum sydencan-4 as a novel biomarker for myocardial fibrosis and cardiac dysfunction in subjects with Chagas disease. METHODS: This study comprised subjects with Chagas disease (n = 56), being 14 (25%) with the indeterminate form, 16 (29%) with the cardiac form without ventricular dysfunction, and 26 (46%) with the cardiac form with ventricular dysfunction. RESULTS: Syndecan-4 serum concentrations did not correlate with presence or absence of myocardial fibrosis (P = 0.386) nor disease severity in subjects with Chagas disease (P = 0.918). Additionally, no correlation was found either between the degree of myocardial fibrosis and serum syndecan-4 [r = 0.08; P = 0.567] or between left ventricular ejection fraction and syndecan-4 [r = 0.02; P = 0.864]. In contrast, NT-proBNP levels correlated with ejection fraction and myocardial fibrosis. CONCLUSIONS: Our results demonstrate the lack of correlations between serum syndecan-4, myocardial fibrosis and cardiac dysfunction in subjects with Chagas disease. Further studies are required to show if syndecan-4 concentrations can be marker for prognosis assessment or disease progression.
[Mh] Termos MeSH primário: Cardiomiopatias/sangue
Doença de Chagas/fisiopatologia
Fibrose/sangue
Sindecana-4/sangue
[Mh] Termos MeSH secundário: Idoso
Cardiomiopatias/complicações
Doença de Chagas/sangue
Doença Crônica
Feminino
Seres Humanos
Masculino
Meia-Idade
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Syndecan-4)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180104
[Lr] Data última revisão:
180104
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171213
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0189408


  2 / 478 MEDLINE  
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[PMID]:28208699
[Au] Autor:Hara T; Kojima T; Matsuzaki H; Nakamura T; Yoshida E; Fujiwara Y; Yamamoto C; Saito S; Kaji T
[Ad] Endereço:Department of Environmental Health, Faculty of Pharmaceutical Sciences, Tokyo University of Science, Noda 278-8510, Japan. 3b13669@ed.tus.ac.jp.
[Ti] Título:Induction of Syndecan-4 by Organic-Inorganic Hybrid Molecules with a 1,10-Phenanthroline Structure in Cultured Vascular Endothelial Cells.
[So] Source:Int J Mol Sci;18(2), 2017 Feb 08.
[Is] ISSN:1422-0067
[Cp] País de publicação:Switzerland
[La] Idioma:eng
[Ab] Resumo:Organic-inorganic hybrid molecules constitute analytical tools used in biological systems. Vascular endothelial cells synthesize and secrete proteoglycans, which are macromolecules consisting of a core protein and glycosaminoglycan side chains. Although the expression of endothelial proteoglycans is regulated by several cytokines/growth factors, there may be alternative pathways for proteoglycan synthesis aside from downstream pathways activated by these cytokines/growth factors. Here, we investigated organic-inorganic hybrid molecules to determine a variant capable of analyzing the expression of syndecan-4, a transmembrane heparan-sulfate proteoglycan, and identified 1,10-phenanthroline ( -Phen) with or without zinc (Zn-Phen) or rhodium (Rh-Phen). Bovine aortic endothelial cells in culture were treated with these compounds, and the expression of mRNA and core proteins was determined by real-time reverse transcription polymerase chain reaction and Western blot analysis, respectively. Our findings indicated that -Phen and Zn-Phen specifically and strongly induced syndecan-4 expression in cultured vascular endothelial cells through activation of the hypoxia-inducible factor-1α/ß pathway via inhibition of prolyl hydroxylase-domain-containing protein 2. These results demonstrated an alternative pathway involved in mediating induction of endothelial syndecan-4 expression and revealed organic-inorganic hybrid molecules as effective tools for analyzing biological systems.
[Mh] Termos MeSH primário: Células Endoteliais/efeitos dos fármacos
Células Endoteliais/metabolismo
Fenantrolinas/farmacologia
Sindecana-4/biossíntese
[Mh] Termos MeSH secundário: Animais
Aorta
Bovinos
Células Cultivadas
Ativação Enzimática/efeitos dos fármacos
Subunidade alfa do Fator 1 Induzível por Hipóxia/metabolismo
Prolina Dioxigenases do Fator Induzível por Hipóxia/metabolismo
Fenantrolinas/química
Proteoglicanas/biossíntese
Transdução de Sinais/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Hypoxia-Inducible Factor 1, alpha Subunit); 0 (Phenanthrolines); 0 (Proteoglycans); 0 (Syndecan-4); EC 1.14.11.29 (Hypoxia-Inducible Factor-Proline Dioxygenases); W4X6ZO7939 (1,10-phenanthroline)
[Em] Mês de entrada:1704
[Cu] Atualização por classe:170428
[Lr] Data última revisão:
170428
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170218
[St] Status:MEDLINE


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[PMID]:28167607
[Au] Autor:Hang Q; Isaji T; Hou S; Wang Y; Fukuda T; Gu J
[Ad] Endereço:Division of Regulatory Glycobiology, Institute of Molecular Biomembrane and Glycobiology, Tohoku Medical and Pharmaceutical University, Sendai, Miyagi, Japan.
[Ti] Título:A Key Regulator of Cell Adhesion: Identification and Characterization of Important -Glycosylation Sites on Integrin α5 for Cell Migration.
[So] Source:Mol Cell Biol;37(9), 2017 May 01.
[Is] ISSN:1098-5549
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The -glycosylation of integrin α5ß1 is thought to control many fundamental aspects of cell behavior, including cell adhesion and migration. However, the mechanism of how -glycans function remains largely obscure. Here, we used a loss-of-function approach. Wild-type (WT) integrin α5 and -glycosylation mutant S3-5 (sites 3 to 5) integrin α5, which contains fewer -glycans, were stably reconstituted in α5 knockout cancer cells. We found that the migration ability of S3-5 cells was decreased in comparison with that of the WT. Interestingly, the levels of phosphorylated focal adhesion kinase and actin stress fiber formation were greatly enhanced in the S3-5 mutant. In a mechanistic manner, the internalization of active but not total integrin α5ß1 was inhibited in S3-5 cells, which is a process that is related to the enhanced expression of active integrin α5ß1 on the cell surface. Importantly, restoration of -glycosylation on the ß-propeller domain of α5 reinstated the cell migration ability, active α5ß1 expression, and internalization. Moreover, these -glycans are critical for α5-syndecan-4 complex formation. These findings indicate that -glycosylation on the ß-propeller domain functions as a molecular switch to control the dynamics of α5ß1 on the cell surface that in turn is required for optimum adhesion for cell migration.
[Mh] Termos MeSH primário: Adesão Celular/fisiologia
Membrana Celular/metabolismo
Movimento Celular/fisiologia
Integrina alfa5beta1/metabolismo
[Mh] Termos MeSH secundário: Linhagem Celular Tumoral
Quinase 1 de Adesão Focal/metabolismo
Glicosilação
Células HEK293
Células HeLa
Seres Humanos
Complexos Multiproteicos/metabolismo
Fosforilação
Estrutura Terciária de Proteína
Sindecana-4/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Integrin alpha5beta1); 0 (Multiprotein Complexes); 0 (SDC4 protein, human); 0 (Syndecan-4); EC 2.7.10.2 (Focal Adhesion Kinase 1); EC 2.7.10.2 (PTK2 protein, human)
[Em] Mês de entrada:1705
[Cu] Atualização por classe:171014
[Lr] Data última revisão:
171014
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170208
[St] Status:MEDLINE


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[PMID]:28019669
[Au] Autor:Hara T; Yoshida E; Fujiwara Y; Yamamoto C; Kaji T
[Ad] Endereço:Faculty of Pharmaceutical Sciences, Department of Environmental Health, Tokyo University of Science, Noda 278-8510, Japan.
[Ti] Título:Transforming Growth Factor-ß Modulates the Expression of Syndecan-4 in Cultured Vascular Endothelial Cells in a Biphasic Manner.
[So] Source:J Cell Biochem;118(8):2009-2017, 2017 Aug.
[Is] ISSN:1097-4644
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Proteoglycans are macromolecules that consist of a core protein and one or more glycosaminoglycan side chains. Previously, we reported that transforming growth factor-ß (TGF-ß ) regulates the synthesis of a large heparan sulfate proteoglycan, perlecan, and a small leucine-rich dermatan sulfate proteoglycan, biglycan, in vascular endothelial cells depending on cell density. Recently, we found that TGF-ß first upregulates and then downregulates the expression of syndecan-4, a transmembrane heparan sulfate proteoglycan, via the TGF-ß receptor ALK5 in the cells. In order to identify the intracellular signal transduction pathway that mediates this modulation, bovine aortic endothelial cells were cultured and treated with TGF-ß . Involvement of the downstream signaling pathways of ALK5-the Smad and MAPK pathways-in syndecan-4 expression was examined using specific siRNAs and inhibitors. The data indicate that the Smad3-p38 MAPK pathway mediates the early upregulation of syndecan-4 by TGF-ß , whereas the late downregulation is mediated by the Smad2/3 pathway. Multiple modulations of proteoglycan synthesis may be involved in the regulation of vascular endothelial cell functions by TGF-ß . J. Cell. Biochem. 118: 2009-2017,2017. © 2016 The Authors. Journal of Cellular Biochemistry Published by Wiley Periodicals, Inc.
[Mh] Termos MeSH primário: Células Endoteliais/efeitos dos fármacos
Proteína Smad2/genética
Proteína Smad3/genética
Sindecana-4/genética
Fator de Crescimento Transformador beta1/farmacologia
Proteínas Quinases p38 Ativadas por Mitógeno/genética
[Mh] Termos MeSH secundário: Animais
Aorta/citologia
Aorta/efeitos dos fármacos
Aorta/metabolismo
Bovinos
Células Endoteliais/citologia
Células Endoteliais/metabolismo
Regulação da Expressão Gênica
Cultura Primária de Células
Proteínas Serina-Treonina Quinases/genética
Proteínas Serina-Treonina Quinases/metabolismo
RNA Interferente Pequeno/genética
RNA Interferente Pequeno/metabolismo
Receptores de Fatores de Crescimento Transformadores beta/genética
Receptores de Fatores de Crescimento Transformadores beta/metabolismo
Transdução de Sinais
Proteína Smad2/antagonistas & inibidores
Proteína Smad2/metabolismo
Proteína Smad3/antagonistas & inibidores
Proteína Smad3/metabolismo
Sindecana-4/antagonistas & inibidores
Sindecana-4/metabolismo
Fatores de Tempo
Fator de Crescimento Transformador beta1/metabolismo
Proteínas Quinases p38 Ativadas por Mitógeno/antagonistas & inibidores
Proteínas Quinases p38 Ativadas por Mitógeno/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (RNA, Small Interfering); 0 (Receptors, Transforming Growth Factor beta); 0 (Smad2 Protein); 0 (Smad3 Protein); 0 (Syndecan-4); 0 (Transforming Growth Factor beta1); EC 2.7.1.11 (TGF-beta type I receptor); EC 2.7.11.1 (Protein-Serine-Threonine Kinases); EC 2.7.11.24 (p38 Mitogen-Activated Protein Kinases)
[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:161227
[St] Status:MEDLINE
[do] DOI:10.1002/jcb.25861


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[PMID]:27789626
[Au] Autor:Wang Y; Baeyens N; Corti F; Tanaka K; Fang JS; Zhang J; Jin Y; Coon B; Hirschi KK; Schwartz MA; Simons M
[Ad] Endereço:Yale Cardiovascular Research Center, Department of Internal Medicine, Yale University School of Medicine, New Haven, CT 06511, USA.
[Ti] Título:Syndecan 4 controls lymphatic vasculature remodeling during mouse embryonic development.
[So] Source:Development;143(23):4441-4451, 2016 12 01.
[Is] ISSN:1477-9129
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:The role of fluid shear stress in vasculature development and remodeling is well appreciated. However, the mechanisms regulating these effects remain elusive. We show that abnormal flow sensing in lymphatic endothelial cells (LECs) caused by Sdc4 or Pecam1 deletion in mice results in impaired lymphatic vessel remodeling, including abnormal valve morphogenesis. Ablation of either gene leads to the formation of irregular, enlarged and excessively branched lymphatic vessels. In both cases, lymphatic valve-forming endothelial cells are randomly oriented, resulting in the formation of abnormal valves. These abnormalities are much more pronounced in Sdc4 ; Pecam1 double-knockout mice, which develop severe edema. In vitro, SDC4 knockdown human LECs fail to align under flow and exhibit high expression of the planar cell polarity protein VANGL2. Reducing VANGL2 levels in SDC4 knockdown LECs restores their alignment under flow, while VANGL2 overexpression in wild-type LECs mimics the flow alignment abnormalities seen in SDC4 knockdown LECs. SDC4 thus controls flow-induced LEC polarization via regulation of VANGL2 expression.
[Mh] Termos MeSH primário: Linfangiogênese/genética
Vasos Linfáticos/embriologia
Proteínas do Tecido Nervoso/metabolismo
Molécula-1 de Adesão Celular Endotelial de Plaquetas/genética
Sindecana-4/genética
[Mh] Termos MeSH secundário: Animais
Linhagem Celular
Desenvolvimento Embrionário/genética
Seres Humanos
Camundongos
Camundongos Endogâmicos C57BL
Camundongos Knockout
Proteínas do Tecido Nervoso/genética
Interferência de RNA
RNA Interferente Pequeno/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Ltap protein, mouse); 0 (Nerve Tissue Proteins); 0 (Platelet Endothelial Cell Adhesion Molecule-1); 0 (RNA, Small Interfering); 0 (Sdc4 protein, mouse); 0 (Syndecan-4)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:171125
[Lr] Data última revisão:
171125
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161102
[St] Status:MEDLINE


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[PMID]:27591995
[Au] Autor:Nakao M; Sugaya M; Takahashi N; Otobe S; Nakajima R; Oka T; Kabasawa M; Suga H; Morimura S; Miyagaki T; Fujita H; Asano Y; Sato S
[Ad] Endereço:Department of Dermatology, University of Tokyo Graduate School of Medicine, 7-3-1 Hongo, Bunkyo-ku, Tokyo, 113-8655, Japan.
[Ti] Título:Increased syndecan-4 expression in sera and skin of patients with atopic dermatitis.
[So] Source:Arch Dermatol Res;308(9):655-660, 2016 Nov.
[Is] ISSN:1432-069X
[Cp] País de publicação:Germany
[La] Idioma:eng
[Ab] Resumo:Syndecan-4 (SDC-4) is a cell surface proteoglycan, which participates in signaling during cell adhesion, migration, proliferation, endocytosis, and mechanotransduction, and is expressed on various cells, including endothelial cells, epithelial cells, T cells, and eosinophils. Emerging evidences have suggested that SDC-4 might contribute to Th2-driven allergic immune responses. Here, we examined the role of SDC-4 in patients with atopic dermatitis (AD). Serum SDC-4 levels in AD patients were significantly higher than in healthy individuals, and they increased according to the disease severity. Importantly, they positively correlated with Eczema Area and Severity Index and itch visual analogue scale scores. Furthermore, serum SDC-4 levels decreased after treatment. We also analyzed SDC-4 expression in AD lesional skin. SDC-4 mRNA levels in AD skin were significantly higher than those of normal skin. Immunohistochemical staining revealed that SDC-4 was highly expressed in the epidermis and endothelial cells in AD lesional skin. Taken together, our study has demonstrated that SDC-4 expression was increased in sera and skin of AD patients, suggesting that SDC-4 may contribute to the development of AD.
[Mh] Termos MeSH primário: Dermatite Atópica/metabolismo
Epiderme/metabolismo
Prurido/metabolismo
Sindecana-4/metabolismo
[Mh] Termos MeSH secundário: Adulto
Dermatite Atópica/sangue
Dermatite Atópica/tratamento farmacológico
Células Endoteliais/metabolismo
Epiderme/citologia
Epiderme/patologia
Feminino
Voluntários Saudáveis
Seres Humanos
Masculino
Meia-Idade
RNA Mensageiro/metabolismo
Índice de Gravidade de Doença
Sindecana-4/sangue
Adulto Jovem
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (RNA, Messenger); 0 (SDC4 protein, human); 0 (Syndecan-4)
[Em] Mês de entrada:1702
[Cu] Atualização por classe:170217
[Lr] Data última revisão:
170217
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160905
[St] Status:MEDLINE


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[PMID]:27565712
[Au] Autor:Hou S; Hang Q; Isaji T; Lu J; Fukuda T; Gu J
[Ad] Endereço:Division of Regulatory Glycobiology, Institute of Molecular Biomembrane and Glycobiology, Tohoku Medical and Pharmaceutical University, Miyagi, Japan.
[Ti] Título:Importance of membrane-proximal N-glycosylation on integrin ß1 in its activation and complex formation.
[So] Source:FASEB J;30(12):4120-4131, 2016 Dec.
[Is] ISSN:1530-6860
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:N-Glycosylation of integrin α5ß1 plays important roles in cell biologic functions; however, the mechanisms that underlie those roles remain poorly understood. Here, we present evidence that the membrane-proximal N-glycosylation on integrin ß1 could positively regulate cell migration by promoting ß1 activation. The S4-6 ß1 mutant contains only 3 N-glycosylation sites, which are essential for α5 and ß1 heterodimer formation, and despite only a small difference in expression levels of α5ß1 between wild-type and S4-6 mutant, cell spreading and migration of the S4-6 mutant was significantly decreased compared with that of control. Consistent with these phenotypes, ß1-mediated cellular signaling and its activation were clearly suppressed in the S4-6 mutant. Of note, these developments could be rescued by restoration of N-glycosylation sites in the membrane-proximal domain. Further study on the regulatory mechanisms suggested that membrane-proximal N-glycosylation is critical for intermolecular interactions between integrin ß1 and other cell membrane proteins, such as syndecan-4 and epidermal growth factor receptor. Moreover, α2,6-sialylation is required for ß1 activation. These data suggest a novel regulatory mechanism wherein N-glycosylation near the cell membrane on ß1 may serve as a platform that facilitates its complex formation on the cell membrane, thereby affecting integrin-mediated functions.-Hou, S., Hang, Q., Isaji, T., Lu, J., Fukuda, T., Gu, J. Importance of membrane-proximal N-glycosylation on integrin ß1 in its activation and complex formation.
[Mh] Termos MeSH primário: Membrana Celular/metabolismo
Movimento Celular/fisiologia
Integrina beta1/metabolismo
[Mh] Termos MeSH secundário: Animais
Adesão Celular
Cricetulus
Glicosilação
Seres Humanos
Integrina alfa5beta1/metabolismo
Receptor do Fator de Crescimento Epidérmico/metabolismo
Sindecana-4/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Integrin alpha5beta1); 0 (Integrin beta1); 0 (SDC4 protein, human); 0 (Syndecan-4); EC 2.7.10.1 (EGFR protein, human); EC 2.7.10.1 (Receptor, Epidermal Growth Factor)
[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:160828
[St] Status:MEDLINE


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[PMID]:27541034
[Au] Autor:Li R; Wu H; Xie J; Li G; Gu R; Kang L; Wang L; Xu B
[Ad] Endereço:Department of Cardiology, Drum Tower Hospital, Nanjing University Medical School, Zhongyang Road, Nanjing, 210008, China.
[Ti] Título:Syndecan-4 regulates the bFGF-induced chemotactic migration of endothelial cells.
[So] Source:J Mol Histol;47(5):503-9, 2016 Oct.
[Is] ISSN:1567-2387
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Chemotactic migration of endothelial cells (ECs) guided by extracellular attractants is essential for blood vessel formation. Synd4 is a ubiquitous heparin sulfate proteoglycan receptor on the cell surface that has been identified to promote angiogenesis during tissue repair. Here, the role synd4 played in chemotactic migration of ECs was investigated in vitro and in vivo. Human umbilical vein endothelial cells (HUVECs) were transfected with Lenti-synd4-RNAi or Lenti-null. Cell migration was observed in a 2D-chemotaxis slide with a stable gradient of basic fibroblast growth factor (bFGF) for 18 h using time-lapse microscopy. Synd4 knockdown HUVECs showed reduced mobility compared with the control. In animal studies, Matrigel premixed with bFGF was used to induce the migration of ECs. The cells migrated less distance from the skin in the Matrigel plugs of synd4 null mice compared with the control mice. Then recombinant adenoviruses containing the synd4 gene (Ad-synd4) or null (Ad-null) were constructed to enhance the synd4 expression of migratory cells in Matrigel plugs of wild-type mice. Migratory cells with synd4 overexpression did not invade further in the Matrigel plugs of wild-type mice, but showed a high ability to proliferate.
[Mh] Termos MeSH primário: Movimento Celular/genética
Células Endoteliais/metabolismo
Fator 2 de Crescimento de Fibroblastos/metabolismo
Sindecana-4/genética
[Mh] Termos MeSH secundário: Animais
Linhagem Celular Tumoral
Movimento Celular/efeitos dos fármacos
Movimento Celular/imunologia
Quimiotaxia/genética
Quimiotaxia/imunologia
Células Endoteliais/efeitos dos fármacos
Células Endoteliais/imunologia
Fator 2 de Crescimento de Fibroblastos/farmacologia
Expressão Gênica
Técnicas de Silenciamento de Genes
Inativação Gênica
Seres Humanos
Masculino
Camundongos
Camundongos Knockout
Transporte Proteico
RNA Interferente Pequeno/genética
Sindecana-4/metabolismo
Proteínas rac1 de Ligação ao GTP/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (RNA, Small Interfering); 0 (Syndecan-4); 103107-01-3 (Fibroblast Growth Factor 2); EC 3.6.5.2 (rac1 GTP-Binding Protein)
[Em] Mês de entrada:1702
[Cu] Atualização por classe:171020
[Lr] Data última revisão:
171020
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160820
[St] Status:MEDLINE
[do] DOI:10.1007/s10735-016-9693-0


  9 / 478 MEDLINE  
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[PMID]:27448535
[Au] Autor:Bielecka-Dabrowa A; Sakowicz A; Misztal M; von Haehling S; Ahmed A; Pietrucha T; Rysz J; Banach M
[Ad] Endereço:Department of Hypertension, Chair of Nephrology and Hypertension, Medical University of Lodz, Poland. Electronic address: agatbiel7@poczta.onet.pl.
[Ti] Título:Differences in biochemical and genetic biomarkers in patients with heart failure of various etiologies.
[So] Source:Int J Cardiol;221:1073-80, 2016 Oct 15.
[Is] ISSN:1874-1754
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:BACKGROUND/OBJECTIVES: To evaluate whether biomarkers reflecting pathophysiological pathways and selected single nucleotide polymorphisms differ between patients (pts) with heart failure (HF). METHODS: 110 pts with were involved, including HF pts with preserved ejection fraction (HFpEF, n=51) with hypertensive origin, HF pts with reduced ejection fraction (HFrEF) with ischemic aetiology (ICM) (n=32) and HFrEF with dilated cardiomyopathy (DCM) (n=27). We assessed selected HF biomarkers, echocardiographic examinations and functional polymorphisms selected from six candidate genes: CYP27B1, NOS3, IL-6, TGF beta, TNF alpha, and PPAR gamma. RESULTS: Higher concentrations of TNF alpha were observed in pts with hypertensive HFpEF compared to pts with DCM (p=0.008). Pts with HFpEF had higher concentrations of TGF beta 1 compared to DCM and ICM (p=0.0001 and p=0.0003, respectively). For the NOS3 -786 C/T rs2070744 polymorphism in DCM there were significantly more CT heterozygotes than in ICM and HFpEF. In multivariate analysis TGF beta 1 (p=0.001) and syndecan 4 (p=0.001) were the only factors distinguishing HFrEF pts with DCM vs HFpEF and also TGF beta 1 (p=0.001) and syndecan 4 (p=0.023) were the only factors distinguishing HFrEF pts with ICM vs HFpEF pts. CONCLUSIONS: Inflammation mediated through TNF alpha and TGF beta 1 may represent an important component of an inflammatory response that partially drives the pathophysiology of HFpEF. NOS3 -786 C/T rs2070744 polymorphism in DCM may serve as a marker for more rapid progression of heart failure. The only biomarkers independently distinguishing HFpEF and HFrEF are syndecan 4 and TGF beta 1.
[Mh] Termos MeSH primário: Insuficiência Cardíaca
Isquemia Miocárdica/complicações
Óxido Nítrico Sintase Tipo III/genética
Volume Sistólico
Sindecana-4/genética
Fator de Crescimento Transformador beta1/genética
[Mh] Termos MeSH secundário: Idoso
Aminobutiratos/farmacologia
Antagonistas de Receptores de Angiotensina/farmacologia
Cardiomiopatia Dilatada/complicações
Feminino
Marcadores Genéticos
Predisposição Genética para Doença
Insuficiência Cardíaca/diagnóstico
Insuficiência Cardíaca/etiologia
Insuficiência Cardíaca/genética
Insuficiência Cardíaca/fisiopatologia
Seres Humanos
Masculino
Meia-Idade
Peptídeo Natriurético Encefálico/análise
Polimorfismo de Nucleotídeo Único
Volume Sistólico/efeitos dos fármacos
Volume Sistólico/fisiologia
Tetrazóis/farmacologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Aminobutyrates); 0 (Angiotensin Receptor Antagonists); 0 (Genetic Markers); 0 (LCZ 696); 0 (SDC4 protein, human); 0 (Syndecan-4); 0 (TGFB1 protein, human); 0 (Tetrazoles); 0 (Transforming Growth Factor beta1); 114471-18-0 (Natriuretic Peptide, Brain); EC 1.14.13.39 (NOS3 protein, human); EC 1.14.13.39 (Nitric Oxide Synthase Type III)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170927
[Lr] Data última revisão:
170927
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160725
[St] Status:MEDLINE


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[PMID]:27439403
[Au] Autor:Esposito S; Bianchini S; Gambino M; Madini B; Di Pietro G; Umbrello G; Presicce ML; Ruggiero L; Terranova L; Principi N
[Ad] Endereço:Pediatric Highly Intensive Care Unit, Department of Pathophysiology and Transplantation, Università degli Studi di Milano, Fondazione IRCCS Ca' Granda Ospedale Maggiore Policlinico, Via Commenda 9, 20122, Milan, Italy. susanna.esposito@unimi.it.
[Ti] Título:Measurement of lipocalin-2 and syndecan-4 levels to differentiate bacterial from viral infection in children with community-acquired pneumonia.
[So] Source:BMC Pulm Med;16(1):103, 2016 Jul 20.
[Is] ISSN:1471-2466
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: In this study, we evaluated the lipocalin-2 (LIP2) and syndecan-4 (SYN4) levels in children who were hospitalized for radiologically confirmed CAP in order to differentiate bacterial from viral infection. The results regarding the LIP2 and SYN4 diagnostic outcomes were compared with the white blood cell (WBC) count and C reactive protein (CRP) levels. METHODS: A total of 110 children <14 years old who were hospitalized for radiologically confirmed CAP were enrolled. Serum samples were obtained upon admission and on day 5 to measure the levels of LIP2, SYN4, and CRP as well as the WBC. Polymerase chain reaction of the respiratory secretions and tests on blood samples were performed to detect respiratory viruses, Streptococcus pneumoniae, and Mycoplasma pneumoniae. RESULTS: CAP was considered to be due to a probable bacterial infection in 74 children (67.3 %) and due to a probable viral infection in 16 children (14.5 %). Overall, 84 children (76.4 %) were diagnosed with severe CAP. The mean values of the WBC count and the LIP2 and SYN4 levels did not differ among the probable bacterial, probable viral, and undetermined cases. However, the CRP serum concentrations were significantly higher in children with probable bacterial CAP than in those with probable viral disease (32.2 ± 55.5 mg/L vs 9.4 ± 17.0 mg/L, p < 0.05). The WBC count was the best predictor of severe CAP, but the differences among the studied variables were marginal. The WBC count was significantly lower on day 5 in children with probable bacterial CAP (p < 0.01) and in those with an undetermined etiology (p < 0.01). The CRP and LIP2 levels were significantly lower 5 days after enrollment in all of the studied groups, independent of the supposed etiology of CAP (p < 0.01 for all comparisons). No statistically significant variation was observed for SYN4. CONCLUSIONS: Measuring the LIP2 and SYN4 levels does not appear to solve the problem of the poor reliability of routine laboratory tests in defining the etiology and severity of pediatric CAP. Currently, the CRP levels and WBC, when combined with evaluation of clinical data, can be used to limit the overuse of antibiotics as much as possible and to provide the best treatment to the patient.
[Mh] Termos MeSH primário: Infecções Comunitárias Adquiridas/sangue
Lipocalina-2/sangue
Pneumonia Bacteriana/sangue
Pneumonia Viral/sangue
Sindecana-4/sangue
[Mh] Termos MeSH secundário: Biomarcadores/sangue
Proteína C-Reativa/análise
Criança
Pré-Escolar
Infecções Comunitárias Adquiridas/diagnóstico
Diagnóstico Diferencial
Feminino
Seres Humanos
Lactente
Itália
Contagem de Leucócitos
Modelos Logísticos
Masculino
Mycoplasma pneumoniae/isolamento & purificação
Pneumonia Bacteriana/diagnóstico
Pneumonia Viral/diagnóstico
Curva ROC
Reprodutibilidade dos Testes
Respirovirus/isolamento & purificação
Streptococcus pneumoniae/isolamento & purificação
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Biomarkers); 0 (Lipocalin-2); 0 (Syndecan-4); 9007-41-4 (C-Reactive Protein)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171019
[Lr] Data última revisão:
171019
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160722
[St] Status:MEDLINE
[do] DOI:10.1186/s12890-016-0267-4



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