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Pesquisa : D09.698.735.700.500 [Categoria DeCS]
Referências encontradas : 721 [refinar]
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[PMID]:29331373
[Au] Autor:Kwack MH; Yang JM; Won GH; Kim MK; Kim JC; Sung YK
[Ad] Endereço:Department of Immunology, School of Medicine, Kyungpook National University, Daegu, South Korea.
[Ti] Título:Establishment and characterization of five immortalized human scalp dermal papilla cell lines.
[So] Source:Biochem Biophys Res Commun;496(2):346-351, 2018 02 05.
[Is] ISSN:1090-2104
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Dermal papilla (DP) regulates the growth and cycling of hair follicles. Cultured DP cells are useful for the study of their role in relation to hair growth and regeneration. However, cultivation of human DP cells is tedious and difficult. In addition, cultured DP cells possess a relatively short replicative life span, requiring immortalized human DP cell lines. We previously established an immortalized human DP cell line, SV40T-hTERT-DPC, by introducing human telomerase reverse transcriptase (hTERT) gene into the transformed cell line, SV40T-DPC. In this study, we co-transfected the simian virus 40 large T antigen (SV40T-Ag) and hTERT into DP cells from scalp hair follicles from a male with androgenetic alopecia and established five immortalized DP cell lines and named KNU-101, KNU-102, KNU-103, KNU-201 and KNU-202. We then evaluated tumorigenicity, expression of DP markers, responses to androgen, Wnt3a and BMP4, and expression of DP signature genes. These cell lines displayed early passage morphology and maintained responses to androgen, Wnt and BMP. Furthermore, these cell lines expressed DP markers and DP signature genes. KNU cell lines established in this study are potentially useful sources for hair research.
[Mh] Termos MeSH primário: Alopecia/genética
Derme/metabolismo
Efeito Fundador
Folículo Piloso/metabolismo
[Mh] Termos MeSH secundário: Células A549
Alopecia/metabolismo
Alopecia/patologia
Animais
Biglicano/genética
Biglicano/metabolismo
Biomarcadores/metabolismo
Proteína Morfogenética Óssea 4/farmacologia
Carcinogênese/genética
Carcinogênese/metabolismo
Carcinogênese/patologia
Linhagem Celular Transformada
Derme/patologia
Di-Hidrotestosterona/farmacologia
Feminino
Expressão Gênica
Folículo Piloso/efeitos dos fármacos
Folículo Piloso/patologia
Seres Humanos
Queratina-8/genética
Queratina-8/metabolismo
Masculino
Camundongos
Camundongos Endogâmicos BALB C
Camundongos Nus
Receptores Androgênicos/genética
Receptores Androgênicos/metabolismo
Couro Cabeludo/metabolismo
Couro Cabeludo/patologia
Versicanas/genética
Versicanas/metabolismo
Proteína Wnt3A/farmacologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (BGN protein, human); 0 (BMP4 protein, human); 0 (Biglycan); 0 (Biomarkers); 0 (Bone Morphogenetic Protein 4); 0 (KRT8 protein, human); 0 (Keratin-8); 0 (Receptors, Androgen); 0 (VCAN protein, human); 0 (WNT3A protein, human); 0 (Wnt3A Protein); 08J2K08A3Y (Dihydrotestosterone); 126968-45-4 (Versicans)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180214
[Lr] Data última revisão:
180214
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180115
[St] Status:MEDLINE


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[PMID]:28859141
[Au] Autor:Maccarana M; Svensson RB; Knutsson A; Giannopoulos A; Pelkonen M; Weis M; Eyre D; Warman M; Kalamajski S
[Ad] Endereço:Department of Experimental Medical Sciences, Lund University, Lund, Sweden.
[Ti] Título:Asporin-deficient mice have tougher skin and altered skin glycosaminoglycan content and structure.
[So] Source:PLoS One;12(8):e0184028, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The main structural component of connective tissues is fibrillar, cross-linked collagen whose fibrillogenesis can be modulated by Small Leucine-Rich Proteins/Proteoglycans (SLRPs). Not all SLRPs' effects on collagen and extracellular matrix in vivo have been elucidated; one of the less investigated SLRPs is asporin. Here we describe the successful generation of an Aspn-/- mouse model and the investigation of the Aspn-/- skin phenotype. Functionally, Aspn-/- mice had an increased skin mechanical toughness, although there were no structural changes present on histology or immunohistochemistry. Electron microscopy analyses showed 7% thinner collagen fibrils in Aspn-/- mice (not statistically significant). Several matrix genes were upregulated, including collagens (Col1a1, Col1a2, Col3a1), matrix metalloproteinases (Mmp2, Mmp3) and lysyl oxidases (Lox, Loxl2), while lysyl hydroxylase (Plod2) was downregulated. Intriguingly no differences were observed in collagen protein content or in collagen cross-linking-related lysine oxidation or hydroxylation. The glycosaminoglycan content and structure in Aspn-/- skin was profoundly altered: chondroitin/dermatan sulfate was more than doubled and had an altered composition, while heparan sulfate was halved and had a decreased sulfation. Also, decorin and biglycan were doubled in Aspn-/- skin. Overall, asporin deficiency changes skin glycosaminoglycan composition, and decorin and biglycan content, which may explain the changes in skin mechanical properties.
[Mh] Termos MeSH primário: Biglicano/genética
Decorina/genética
Proteínas da Matriz Extracelular/deficiência
Efeito Fundador
Regulação da Expressão Gênica
Pele/metabolismo
[Mh] Termos MeSH secundário: Aminoácido Oxirredutases/genética
Aminoácido Oxirredutases/metabolismo
Animais
Biglicano/metabolismo
Sulfatos de Condroitina/genética
Sulfatos de Condroitina/metabolismo
Colágeno Tipo I/genética
Colágeno Tipo I/metabolismo
Colágeno Tipo III/genética
Colágeno Tipo III/metabolismo
Decorina/metabolismo
Dermatan Sulfato/análogos & derivados
Dermatan Sulfato/genética
Dermatan Sulfato/metabolismo
Matriz Extracelular/genética
Matriz Extracelular/metabolismo
Proteínas da Matriz Extracelular/genética
Feminino
Heparitina Sulfato/genética
Heparitina Sulfato/metabolismo
Sulfato de Ceratano/genética
Sulfato de Ceratano/metabolismo
Masculino
Metaloproteinase 2 da Matriz/genética
Metaloproteinase 2 da Matriz/metabolismo
Metaloproteinase 3 da Matriz/genética
Metaloproteinase 3 da Matriz/metabolismo
Camundongos
Camundongos Knockout
Fenótipo
Pró-Colágeno-Lisina 2-Oxoglutarato 5-Dioxigenase/genética
Pró-Colágeno-Lisina 2-Oxoglutarato 5-Dioxigenase/metabolismo
Pele/ultraestrutura
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Aspn protein, mouse); 0 (Biglycan); 0 (COL3A1 protein, mouse); 0 (Col1a2 protein, mouse); 0 (Collagen Type I); 0 (Collagen Type III); 0 (Dcn protein, mouse); 0 (Decorin); 0 (Extracellular Matrix Proteins); 0 (collagen type I, alpha 1 chain); 0 (dermatan sulfate chondroitin sulfate); 24967-94-0 (Dermatan Sulfate); 9007-28-7 (Chondroitin Sulfates); 9050-30-0 (Heparitin Sulfate); 9056-36-4 (Keratan Sulfate); EC 1.14.11.4 (Procollagen-Lysine, 2-Oxoglutarate 5-Dioxygenase); EC 1.14.11.4 (lysyl hydroxylase 2, mouse); EC 1.4.- (Amino Acid Oxidoreductases); EC 1.4.3.- (Loxl2 protein, mouse); EC 3.4.24.17 (Matrix Metalloproteinase 3); EC 3.4.24.17 (Mmp3 protein, mouse); EC 3.4.24.24 (Matrix Metalloproteinase 2); EC 3.4.24.24 (Mmp2 protein, mouse)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171016
[Lr] Data última revisão:
171016
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170901
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0184028


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[PMID]:28763139
[Au] Autor:Maishi N; Hida K
[Ad] Endereço:Vascular Biology, Frontier Research Unit, Institute for Genetic Medicine, Hokkaido University, Sapporo, Japan.
[Ti] Título:Tumor endothelial cells accelerate tumor metastasis.
[So] Source:Cancer Sci;108(10):1921-1926, 2017 Oct.
[Is] ISSN:1349-7006
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Tumor metastasis is the main cause of cancer-related death. Understanding the molecular mechanisms underlying tumor metastasis is crucial to control this fatal disease. Several molecular pathways orchestrate the complex biological cell events during a metastatic cascade. It is now well known that bidirectional interaction between tumor cells and their microenvironment, including tumor stroma, is important for tumor progression and metastasis. Tumor stromal cells, which acquire their specific characteristics in the tumor microenvironment, accelerate tumor malignancy. The formation of new blood vessels, termed as tumor angiogenesis, is a requirement for tumor progression. Tumor blood vessels supply nutrients and oxygen and also provide the route for metastasis. Tumor endothelial cells, which line tumor blood vessels, also exhibit several altered phenotypes compared with those of their normal counterparts. Recent studies have emphasized "angiocrine factors" that are released from tumor endothelial cells and promote tumor progression. During intravasation, tumor cells physically contact tumor endothelial cells and interact with them by juxtacrine and paracrine signaling. Recently, we observed that in highly metastatic tumors, tumor endothelial cells interact with tumor cells by secretion of a small leucine-rich repeat proteoglycan known as biglycan. Biglycan from tumor endothelial cells stimulates the tumor cells to metastasize. In the present review, we highlight the role of tumor stromal cells, particularly endothelial cells, in the initial steps of tumor metastasis.
[Mh] Termos MeSH primário: Biglicano/secreção
Células Endoteliais/patologia
Neoplasias/irrigação sanguínea
Neovascularização Patológica/patologia
[Mh] Termos MeSH secundário: Animais
Progressão da Doença
Células Endoteliais/metabolismo
Seres Humanos
Metástase Neoplásica
Neoplasias/metabolismo
Neoplasias/patologia
Neovascularização Patológica/metabolismo
Comunicação Parácrina
Transdução de Sinais
Microambiente Tumoral
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (BGN protein, human); 0 (Biglycan)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171005
[Lr] Data última revisão:
171005
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170802
[St] Status:MEDLINE
[do] DOI:10.1111/cas.13336


  4 / 721 MEDLINE  
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[PMID]:28759311
[Au] Autor:Ibrahim I; Serrano MJ; Ruest LB; Svoboda KKH
[Ad] Endereço:1 Department of Biomedical Sciences, Texas A&M University College of Dentistry, Dallas, TX, USA.
[Ti] Título:Biglycan and Decorin Expression and Distribution in Palatal Adhesion.
[So] Source:J Dent Res;96(12):1445-1450, 2017 Nov.
[Is] ISSN:1544-0591
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Previous studies demonstrated that chondroitin sulfate proteoglycans (CSPGs) on apical surfaces of palatal medial edge epithelial (MEE) cells were necessary for palatal adhesion. In this study, we identified 2 proteoglycans, biglycan and decorin, that were expressed in the palatal shelves prior to adhesion. In addition, we established that these proteoglycans were dependent on transforming growth factor ß (TGFß) signaling. Laser capture microdissection was used to collect selected palatal epithelial cells from embryonic mouse embryos at various palate development stages. The expression of specific messenger RNA (mRNA) for biglycan and decorin was determined with quantitative real-time polymerase chain reaction. The TGFßrI kinase inhibitor (SB431542) was used in palatal organ cultures to determine if blocking TFGß signaling changed biglycan and decorin distribution. Immunohistochemistry of both biglycan and decorin revealed expression on the apical and lateral surfaces of MEE cells. Biglycan protein and mRNA levels peaked as the palatal shelves adhered. Decorin was less abundant on the apical epithelial surface and also had reduced mRNA levels compared to biglycan. Their proteins were not expressed on MEE cells of palates treated with SB431542, an inhibitor of TGFß signaling. The temporal expression of biglycan and decorin on the apical surface of MEE, combined with the evidence that these proteins were regulated through the TGFß pathway, indicated that they may be important for adhesion.
[Mh] Termos MeSH primário: Biglicano/metabolismo
Adesão Celular/fisiologia
Decorina/metabolismo
Palato/citologia
[Mh] Termos MeSH secundário: Animais
Benzamidas/farmacologia
Dioxóis/farmacologia
Imuno-Histoquímica
Microdissecção e Captura a Laser
Camundongos
Palato/embriologia
RNA Mensageiro/metabolismo
Reação em Cadeia da Polimerase em Tempo Real
Transdução de Sinais
Fator de Crescimento Transformador beta/farmacologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (4-(5-benzo(1,3)dioxol-5-yl-4-pyridin-2-yl-1H-imidazol-2-yl)benzamide); 0 (Benzamides); 0 (Biglycan); 0 (Decorin); 0 (Dioxoles); 0 (RNA, Messenger); 0 (Transforming Growth Factor beta)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171101
[Lr] Data última revisão:
171101
[Sb] Subgrupo de revista:D; IM
[Da] Data de entrada para processamento:170801
[St] Status:MEDLINE
[do] DOI:10.1177/0022034517722783


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[PMID]:28601321
[Au] Autor:Cheng H; Yao Q; Song R; Zhai Y; Wang W; Fullerton DA; Meng X
[Ad] Endereço:Department of Surgery, University of Colorado Denver, Aurora, Colorado; Department of Cardiology, Shantou University Medical College, Shantou, China.
[Ti] Título:Lysophosphatidylcholine activates the Akt pathway to upregulate extracellular matrix protein production in human aortic valve cells.
[So] Source:J Surg Res;213:243-250, 2017 Jun 01.
[Is] ISSN:1095-8673
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Overproduction of extracellular matrix (ECM) protein by aortic valve interstitial cells (AVICs) plays an important role in valvular sclerosis (thickening) associated with the early pathobiology of aortic stenosis. Accumulation of oxidized low-density lipoprotein (oxLDL) is observed in sclerotic aortic valve and may have a mechanistic role in valvular disease progression. Lysophosphatidylcholine (LysoPC) is a component of oxLDL and has multiple biological activities. This study was to test the hypothesis that oxLDL and LysoPC upregulate ECM protein production in human AVICs. METHODS AND RESULTS: AVICs were isolated from normal human aortic valves. Cells were treated with oxLDL (40 µg/mL) or LysoPC (40 µmol/L). Immunoblotting was applied to analyze ECM proteins (collagens I and III and biglycan) in cell lysate and Picrosirius red staining was used to examine collagen deposition. Both oxLDL and LysoPC upregulated the production of biglycan and collagen I. The upregulation of ECM proteins by LysoPC was preceded by the phosphorylation of Akt and ERK1/2. Inhibition of Akt markedly reduced the effect of LysoPC on ECM protein production and collagen deposition. However, inhibition of ERK1/2 had no effect. CONCLUSIONS: LysoPC upregulates the production of biglycan and collagen I in human AVICs and may mediate the effect of oxLDL on ECM protein production. The Akt pathway appears to be critical in mediating the effect of LysoPC. oxLDL accumulation and generation of LysoPC in the aortic valve tissue may contribute to the mechanism of valvular sclerosis associated with the development and progression of aortic stenosis.
[Mh] Termos MeSH primário: Estenose da Valva Aórtica/metabolismo
Valva Aórtica/metabolismo
Proteínas da Matriz Extracelular/metabolismo
Lipoproteínas LDL/metabolismo
Lisofosfatidilcolinas/metabolismo
Proteínas Proto-Oncogênicas c-akt/metabolismo
Regulação para Cima
[Mh] Termos MeSH secundário: Idoso
Valva Aórtica/citologia
Biglicano/metabolismo
Biomarcadores/metabolismo
Células Cultivadas
Colágeno Tipo I/metabolismo
Colágeno Tipo III/metabolismo
Feminino
Seres Humanos
Masculino
Meia-Idade
Transdução de Sinais
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Biglycan); 0 (Biomarkers); 0 (Collagen Type I); 0 (Collagen Type III); 0 (Extracellular Matrix Proteins); 0 (Lipoproteins, LDL); 0 (Lysophosphatidylcholines); 0 (oxidized low density lipoprotein); EC 2.7.11.1 (Proto-Oncogene Proteins c-akt)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170919
[Lr] Data última revisão:
170919
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170612
[St] Status:MEDLINE


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[PMID]:28408374
[Au] Autor:Chui A; Gunatillake T; Brennecke SP; Ignjatovic V; Monagle PT; Whitelock JM; van Zanten DE; Eijsink J; Wang Y; Deane J; Borg AJ; Stevenson J; Erwich JJ; Said JM; Murthi P
[Ad] Endereço:From the Department of Obstetrics and Gynaecology, The University of Melbourne, Parkville, Victoria, Australia (A.C., T.G., S.P.B., P.M.); Sunshine Hospital, St Albans, Victoria, Australia (A.C., T.G., S.P.B., P.M.); Department of Maternal-Fetal Medicine Pregnancy Research Centre, The Royal Women's
[Ti] Título:Expression of Biglycan in First Trimester Chorionic Villous Sampling Placental Samples and Altered Function in Telomerase-Immortalized Microvascular Endothelial Cells.
[So] Source:Arterioscler Thromb Vasc Biol;37(6):1168-1179, 2017 Jun.
[Is] ISSN:1524-4636
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:OBJECTIVE: Biglycan (BGN) has reduced expression in placentae from pregnancies complicated by fetal growth restriction (FGR). We used first trimester placental samples from pregnancies with later small for gestational age (SGA) infants as a surrogate for FGR. The functional consequences of reduced BGN and the downstream targets of were determined. Furthermore, the expression of targets was validated in primary placental endothelial cells isolated from FGR or control pregnancies. APPROACH AND RESULTS: expression was determined using real-time polymerase chain reaction in placental tissues collected during chorionic villous sampling performed at 10 to 12 weeks' gestation from pregnancies that had known clinical outcomes, including SGA. Short-interference RNA reduced expression in telomerase-immortalized microvascular endothelial cells, and the effect on proliferation, angiogenesis, and thrombin generation was determined. An angiogenesis array identified downstream targets of BGN, and their expression in control and FGR primary placental endothelial cells was validated using real-time polymerase chain reaction. Reduced expression was observed in SGA placental tissues. reduction decreased network formation of telomerase-immortalized microvascular endothelial cells but did not affect thrombin generation or cellular proliferation. The array identified target genes, which were further validated: angiopoetin 4 ( ), platelet-derived growth factor receptor α ( ), tumor necrosis factor superfamily member 15 ( ), angiogenin ( ), serpin family C member 1 ( ), angiopoietin 2 ( ), and CXC motif chemokine 12 ( ) in telomerase-immortalized microvascular endothelial cells and primary placental endothelial cells obtained from control and FGR pregnancies. CONCLUSIONS: This study reports a temporal relationship between altered placental expression and subsequent development of SGA. Reduction of in vascular endothelial cells leads to disrupted network formation and alterations in the expression of genes involved in angiogenesis. Therefore, differential expression of these may contribute to aberrant angiogenesis in SGA pregnancies.
[Mh] Termos MeSH primário: Biglicano/metabolismo
Vilosidades Coriônicas/irrigação sanguínea
Vilosidades Coriônicas/metabolismo
Células Endoteliais/metabolismo
Retardo do Crescimento Fetal/metabolismo
Microvasos/metabolismo
Neovascularização Fisiológica
Primeiro Trimestre da Gravidez/metabolismo
Telomerase/metabolismo
[Mh] Termos MeSH secundário: Animais
Biglicano/genética
Estudos de Casos e Controles
Linhagem Celular
Amostra da Vilosidade Coriônica
Feminino
Retardo do Crescimento Fetal/genética
Retardo do Crescimento Fetal/fisiopatologia
Perfilação da Expressão Gênica
Regulação da Expressão Gênica no Desenvolvimento
Seres Humanos
Recém-Nascido
Recém-Nascido Pequeno para a Idade Gestacional
Masculino
Camundongos Endogâmicos C57BL
Neovascularização Fisiológica/genética
Gravidez
Primeiro Trimestre da Gravidez/genética
Interferência de RNA
Transdução de Sinais
Telomerase/genética
Trombina/metabolismo
Fatores de Tempo
Técnicas de Cultura de Tecidos
Transfecção
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (BGN protein, human); 0 (Biglycan); EC 2.7.7.49 (Telomerase); EC 3.4.21.5 (Thrombin)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:170620
[Lr] Data última revisão:
170620
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170415
[St] Status:MEDLINE
[do] DOI:10.1161/ATVBAHA.117.309422


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[PMID]:28282921
[Au] Autor:Hsieh LT; Nastase MV; Roedig H; Zeng-Brouwers J; Poluzzi C; Schwalm S; Fork C; Tredup C; Brandes RP; Wygrecka M; Huwiler A; Pfeilschifter J; Schaefer L
[Ad] Endereço:Pharmazentrum Frankfurt, Institut für Allgemeine Pharmakologie und Toxikologie, Klinikum der Goethe Universität, Theodor-Stern-Kai 7, Frankfurt am Main 60590, Germany. hsiehlouise@gmail.com.
[Ti] Título:Biglycan- and Sphingosine Kinase-1 Signaling Crosstalk Regulates the Synthesis of Macrophage Chemoattractants.
[So] Source:Int J Mol Sci;18(3), 2017 Mar 09.
[Is] ISSN:1422-0067
[Cp] País de publicação:Switzerland
[La] Idioma:eng
[Ab] Resumo:In its soluble form, the extracellular matrix proteoglycan biglycan triggers the synthesis of the macrophage chemoattractants, chemokine (C-C motif) ligand CCL2 and CCL5 through selective utilization of Toll-like receptors (TLRs) and their adaptor molecules. However, the respective downstream signaling events resulting in biglycan-induced CCL2 and CCL5 production have not yet been defined. Here, we show that biglycan stimulates the production and activation of sphingosine kinase 1 (SphK1) in a TLR4- and Toll/interleukin (IL)-1R domain-containing adaptor inducing interferon (IFN)-ß (TRIF)-dependent manner in murine primary macrophages. We provide genetic and pharmacological proof that SphK1 is a crucial downstream mediator of biglycan-triggered CCL2 and CCL5 mRNA and protein expression. This is selectively driven by biglycan/SphK1-dependent phosphorylation of the nuclear factor NF-κB p65 subunit, extracellular signal-regulated kinase (Erk)1/2 and p38 mitogen-activated protein kinases. Importantly, in vivo overexpression of soluble biglycan causes Sphk1-dependent enhancement of renal CCL2 and CCL5 and macrophage recruitment into the kidney. Our findings describe the crosstalk between biglycan- and SphK1-driven extracellular matrix- and lipid-signaling. Thus, SphK1 may represent a new target for therapeutic intervention in biglycan-evoked inflammatory conditions.
[Mh] Termos MeSH primário: Biglicano/metabolismo
Quimiocina CCL2/metabolismo
Quimiocina CCL5/metabolismo
Sistema de Sinalização das MAP Quinases
Macrófagos/metabolismo
Fosfotransferases (Aceptor do Grupo Álcool)/metabolismo
[Mh] Termos MeSH secundário: Proteínas Adaptadoras de Transporte Vesicular/metabolismo
Animais
Células Cultivadas
Matriz Extracelular/metabolismo
Células HEK293
Seres Humanos
Masculino
Camundongos
Camundongos Endogâmicos C57BL
Proteína Quinase 1 Ativada por Mitógeno/metabolismo
Proteína Quinase 3 Ativada por Mitógeno/metabolismo
Receptor 4 Toll-Like/metabolismo
Fator de Transcrição RelA/metabolismo
Proteínas Quinases p38 Ativadas por Mitógeno/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Adaptor Proteins, Vesicular Transport); 0 (Biglycan); 0 (Chemokine CCL2); 0 (Chemokine CCL5); 0 (TICAM-1 protein, mouse); 0 (Tlr4 protein, mouse); 0 (Toll-Like Receptor 4); 0 (Transcription Factor RelA); EC 2.7.1.- (Phosphotransferases (Alcohol Group Acceptor)); EC 2.7.1.- (sphingosine kinase); EC 2.7.11.24 (Mitogen-Activated Protein Kinase 1); EC 2.7.11.24 (Mitogen-Activated Protein Kinase 3); EC 2.7.11.24 (p38 Mitogen-Activated Protein Kinases)
[Em] Mês de entrada:1704
[Cu] Atualização por classe:170420
[Lr] Data última revisão:
170420
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170312
[St] Status:MEDLINE


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[PMID]:28189483
[Au] Autor:Dodel M; Hemmati Nejad N; Bahrami SH; Soleimani M; Mohammadi Amirabad L; Hanaee-Ahvaz H; Atashi A
[Ad] Endereço:Textile Engineering Department, Amirkabir University of Technology, Tehran, Iran.
[Ti] Título:Electrical stimulation of somatic human stem cells mediated by composite containing conductive nanofibers for ligament regeneration.
[So] Source:Biologicals;46:99-107, 2017 Mar.
[Is] ISSN:1095-8320
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:One of the advances in the field of biomedical nanotechnology, is conductive nanofiber fabrication and the discovery of its applications. Biocompatible flexible nanofibers that have a good biocompatibility, mechanical properties and morphology. Poly (3, 4-ethylene dioxythiophene) (PEDOT) is a conductive polymer that has recently been used in medical applications. In this study, the electrospinning technique and vapor phase polymerization combination method with freeze drying was used to produce Silk fibroin/PEDOT/Chitosan nanocomposite scaffold. The aim of our study was to develop a ligament construct of PEDOT/Silk bilayer nanofibrous scaffold, to mimic the aligned collagen fiber bundles and Chitosan sponge coating was done on these fibrous scaffolds, to mimic the glycosaminoglycans of ECM sheath. The developed constructs were characterized. The unrestricted somatic human stem cells (USSC), were cultured on the scaffold. Then, the effect of applying DC electric pulses to cells cultured on polymer was assessed. Cellular function was actively exhibited in scaffold with electrical induction, as evident by the high expression of collagen I, collagen III, decorin, biglycan and aggrecan genes. Novel scaffold plus electrical stimulation shows facilitating cell seeding and promoting cell proliferation, differentiation. This composites can be used in this new field for stem cells differentiation to target tissues.
[Mh] Termos MeSH primário: Células-Tronco Hematopoéticas/fisiologia
Ligamentos/fisiologia
Nanofibras/química
Regeneração
Engenharia Tecidual/métodos
[Mh] Termos MeSH secundário: Biglicano/genética
Compostos Bicíclicos Heterocíclicos com Pontes/química
Técnicas de Cultura de Células/métodos
Diferenciação Celular/genética
Proliferação Celular/genética
Células Cultivadas
Quitosana/química
Colágeno Tipo I/genética
Colágeno Tipo III/genética
Decorina/genética
Estimulação Elétrica
Técnicas Eletroquímicas
Sangue Fetal/citologia
Fibroínas/química
Expressão Gênica
Células-Tronco Hematopoéticas/citologia
Células-Tronco Hematopoéticas/metabolismo
Seres Humanos
Microscopia Eletrônica de Varredura
Nanocompostos/química
Nanocompostos/ultraestrutura
Nanofibras/ultraestrutura
Polímeros/química
Reprodutibilidade dos Testes
Reação em Cadeia da Polimerase Via Transcriptase Reversa
Tecidos Suporte/química
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Biglycan); 0 (Bridged Bicyclo Compounds, Heterocyclic); 0 (Collagen Type I); 0 (Collagen Type III); 0 (Decorin); 0 (Polymers); 0 (poly(3,4-ethylene dioxythiophene)); 9007-76-5 (Fibroins); 9012-76-4 (Chitosan)
[Em] Mês de entrada:1704
[Cu] Atualização por classe:170418
[Lr] Data última revisão:
170418
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170213
[St] Status:MEDLINE


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[PMID]:28131044
[Au] Autor:Mandraffino G; Aragona CO; Scuruchi M; Mamone F; D'Ascola A; Alibrandi A; Cinquegrani M; Morace C; Oreto L; Saitta C; Mormina E; Carerj S; Saitta A; Imbalzano E
[Ad] Endereço:Department of Clinical and Experimental Medicine, Internal Medicine Unit, University of Messina, Messina, Italy. Electronic address: gmandraffino@unime.it.
[Ti] Título:Biglycan expression, earlier vascular damage and pro-atherogenic profile improvement after smoke cessation in young people.
[So] Source:Atherosclerosis;257:109-115, 2017 Feb.
[Is] ISSN:1879-1484
[Cp] País de publicação:Ireland
[La] Idioma:eng
[Ab] Resumo:BACKGROUND AND AIMS: Young cigarette smokers may already present with early signs of vascular inflammation and damage; biglycan (BGN) has been shown to play a critical role in the initiation and progression of vascular lesions, also in young smokers. We investigated whether after smoke cessation, monocyte BGN expression is reduced; moreover, we evaluated any improvement of pro-atherogenic profile and arterial stiffness (AS), and their relationship with BGN in abstinent smokers. METHODS: Two-hundred-fifty-one young people who had decided to quit smoking were enrolled; of these, 71 had completed the 12-month observation period maintaining smoking abstinence. At enrollment and 12 months later, we evaluated anthropometrics, laboratory profile, carotid-femoral pulse wave velocity (cf-PWV), carotid intima-media thickness (cIMT), BGN expression. RESULTS: After 12-month smoke abstinence, we found a significant decrease in inflammatory markers (Hs-CRP: -23.3%; fibrinogen: -11.8%; IL-6: -9.2%), and increased HDL-C levels (+9.3%); blood pressure values were also slightly reduced. cf-PWV (-8.9%) appeared to be improved; cIMT remained unchanged. BGN expression appeared to be reduced (-42.8% relative reduction). BGN reduction appeared to be associated with fibrinogen reduction, and smoking burden. Reduced cf-PWV appeared to be dependent on change in fibrinogen, SBP, IL-6, and BGN by multiple regression analysis. CONCLUSIONS: After the first year of smoke abstinence, the levels of IL-6, CRP, fibrinogen, HDL-C, and BGN expression, as well cf-PWV, are significantly improved as compared to baseline. This is the first evidence that removing exposure to a well-known cardiovascular risk factor, such as cigarette smoking, leads to significant reduction of BGN expression.
[Mh] Termos MeSH primário: Aterosclerose/sangue
Biglicano/sangue
Endotélio Vascular/fisiopatologia
Inflamação/sangue
Abandono do Hábito de Fumar
Prevenção do Hábito de Fumar
[Mh] Termos MeSH secundário: Adolescente
Adulto
Fatores Etários
Aterosclerose/diagnóstico
Aterosclerose/etiologia
Aterosclerose/fisiopatologia
Biomarcadores/sangue
Pressão Sanguínea
HDL-Colesterol/sangue
Regulação para Baixo
Endotélio Vascular/metabolismo
Endotélio Vascular/patologia
Feminino
Seres Humanos
Inflamação/diagnóstico
Inflamação/etiologia
Inflamação/fisiopatologia
Mediadores da Inflamação/sangue
Masculino
Análise de Onda de Pulso
Recuperação de Função Fisiológica
Fatores de Risco
Fumar/efeitos adversos
Fumar/sangue
Fatores de Tempo
Adulto Jovem
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (BGN protein, human); 0 (Biglycan); 0 (Biomarkers); 0 (Cholesterol, HDL); 0 (Inflammation Mediators)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170129
[St] Status:MEDLINE


  10 / 721 MEDLINE  
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[PMID]:28075546
[Au] Autor:Karamanos NK
[Ad] Endereço:Biochemistry Laboratory, Biochemistry, Biochemical Analysis & Matrix Pathobiology Research Group, Department of Chemistry, University of Patras, Greece.
[Ti] Título:Matrix pathobiology-central roles for proteoglycans and heparanase in health and disease.
[So] Source:FEBS J;284(1):7-9, 2017 Jan.
[Is] ISSN:1742-4658
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:This thematic minireview series highlights new concepts in matrix pathobiology. The reviews in this series cover the roles of the two matrix proteoglycans, decorin and biglycan, in inflammation and autophagy, the various functions of syndecans in cancer development and prognosis and the recently discovered mechanisms underlying the multiple roles of heparanase in cancer progression, inflammation, and autophagy.
[Mh] Termos MeSH primário: Biglicano/metabolismo
Decorina/metabolismo
Matriz Extracelular/metabolismo
Neoplasias/metabolismo
[Mh] Termos MeSH secundário: Glucuronidase/metabolismo
Seres Humanos
Neoplasias/patologia
Sindecanas/metabolismo
[Pt] Tipo de publicação:INTRODUCTORY JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Biglycan); 0 (DCN protein, human); 0 (Decorin); 0 (Syndecans); EC 3.2.1.- (heparanase); EC 3.2.1.31 (Glucuronidase)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:170622
[Lr] Data última revisão:
170622
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170112
[St] Status:MEDLINE
[do] DOI:10.1111/febs.13945



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