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[PMID]:28463693
[Au] Autor:Jeon EY; Choi BH; Jung D; Hwang BH; Cha HJ
[Ad] Endereço:Department of Chemical Engineering, Pohang University of Science and Technology, Pohang 790-784, South Korea.
[Ti] Título:Natural healing-inspired collagen-targeting surgical protein glue for accelerated scarless skin regeneration.
[So] Source:Biomaterials;134:154-165, 2017 Jul.
[Is] ISSN:1878-5905
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Skin scarring after deep dermal injuries is a major clinical problem due to the current therapies limited to established scars with poor understanding of healing mechanisms. From investigation of aberrations within the extracellular matrix involved in pathophysiologic scarring, it was revealed that one of the main factors responsible for impaired healing is abnormal collagen reorganization. Here, inspired by the fundamental roles of decorin, a collagen-targeting proteoglycan, in collagen remodeling, we created a scar-preventive collagen-targeting glue consisting of a newly designed collagen-binding mussel adhesive protein and a specific glycosaminoglycan. The collagen-targeting glue specifically bound to type I collagen in a dose-dependent manner and regulated the rate and the degree of fibrillogenesis. In a rat skin excisional model, the collagen-targeting glue successfully accelerated initial wound regeneration as defined by effective reepithelialization, neovascularization, and rapid collagen synthesis. Moreover, the improved dermal collagen architecture was demonstrated by uniform size of collagen fibrils, their regular packing, and a restoration of healthy tissue component. Collectively, our natural healing-inspired collagen-targeting glue may be a promising therapeutic option for improving the healing rate with high-quality and effective scar inhibition.
[Mh] Termos MeSH primário: Colágeno/química
Hidrogel de Polietilenoglicol-Dimetacrilato/química
Adesivos Teciduais/química
Adesivos Teciduais/uso terapêutico
Cicatrização/efeitos dos fármacos
[Mh] Termos MeSH secundário: Animais
Colágeno Tipo I/química
Colágeno Tipo I/uso terapêutico
Decorina/química
Decorina/uso terapêutico
Eletroforese em Gel de Poliacrilamida
Feminino
Glicosaminoglicanos
Seres Humanos
Camundongos
Microscopia Eletrônica de Transmissão
Células NIH 3T3
Proteínas/química
Proteínas/uso terapêutico
Proteoglicanas/química
Proteoglicanas/uso terapêutico
Ratos
Ratos Sprague-Dawley
Pele/efeitos dos fármacos
Pele/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Collagen Type I); 0 (Decorin); 0 (Glycosaminoglycans); 0 (Proteins); 0 (Proteoglycans); 0 (Tissue Adhesives); 0 (adhesive protein, mussel); 25852-47-5 (Hydrogel, Polyethylene Glycol Dimethacrylate); 9007-34-5 (Collagen)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180228
[Lr] Data última revisão:
180228
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170503
[St] Status:MEDLINE


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[PMID]:28454729
[Au] Autor:Sato E; Zhang LJ; Dorschner RA; Adase CA; Choudhury BP; Gallo RL
[Ad] Endereço:Department of Dermatology, University of California-San Diego, La Jolla, California, USA.
[Ti] Título:Activation of Parathyroid Hormone 2 Receptor Induces Decorin Expression and Promotes Wound Repair.
[So] Source:J Invest Dermatol;137(8):1774-1783, 2017 Aug.
[Is] ISSN:1523-1747
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:In this study, we report that TIP39, a parathyroid hormone ligand family member that was recently identified to be expressed in the skin, can induce decorin expression and enhance wound repair. Topical treatment of mice with TIP39 accelerated wound repair, whereas TIP39-deficient mice had delayed repair that was associated with formation of abnormal collagen bundles. To study the potential mechanism responsible for the action of TIP39 in the dermis, fibroblasts were cultured in three-dimensional collagen gels, a process that results in enhanced decorin expression unless activated to differentiate to adipocytes, whereupon these cells reduce expression of several proteoglycans, including decorin. Small interfering RNA-mediated silencing of parathyroid hormone 2 receptor (PTH2R), the receptor for TIP39, suppressed the expression of extracellular matrix-related genes, including decorin, collagens, fibronectin, and matrix metalloproteases. Skin wounds in TIP39 mice had decreased decorin expression, and addition of TIP39 to cultured fibroblasts induced decorin and increased phosphorylation and nuclear translocation of CREB. Fibroblasts differentiated to adipocytes and treated with TIP39 also showed increased decorin and production of chondroitin sulfate. Furthermore, the skin of PTH2R mice showed abnormal extracellular matrix structure, decreased decorin expression, and skin hardness. Thus, the TIP39-PTH2R system appears to be a previously unrecognized mechanism for regulation of extracellular matrix formation and wound repair.
[Mh] Termos MeSH primário: Decorina/genética
Regulação da Expressão Gênica
Proteínas Nucleares/farmacologia
RNA/genética
Receptor Tipo 2 de Hormônio Paratireóideo/genética
Proteínas de Transporte Vesicular/farmacologia
Cicatrização/fisiologia
Ferimentos e Lesões/genética
[Mh] Termos MeSH secundário: Animais
Diferenciação Celular
Células Cultivadas
Decorina/biossíntese
Modelos Animais de Doenças
Feminino
Immunoblotting
Camundongos
Camundongos Endogâmicos C57BL
Reação em Cadeia da Polimerase em Tempo Real
Receptor Tipo 2 de Hormônio Paratireóideo/biossíntese
Transdução de Sinais
Pele/lesões
Pele/metabolismo
Pele/patologia
Cicatrização/efeitos dos fármacos
Ferimentos e Lesões/metabolismo
Ferimentos e Lesões/patologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Decorin); 0 (Nuclear Proteins); 0 (Receptor, Parathyroid Hormone, Type 2); 0 (Tfip11 protein, mouse); 0 (Vesicular Transport Proteins); 63231-63-0 (RNA)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:180216
[Lr] Data última revisão:
180216
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170430
[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]:28798237
[Au] Autor:Neill T; Sharpe C; Owens RT; Iozzo RV
[Ad] Endereço:From the Department of Pathology, Anatomy, and Cell Biology and the Cancer Cell Biology and Signaling Program, Sidney Kimmel Medical College at Thomas Jefferson University, Philadelphia, Pennsylvania 19107 and.
[Ti] Título:Decorin-evoked paternally expressed gene 3 (PEG3) is an upstream regulator of the transcription factor EB (TFEB) in endothelial cell autophagy.
[So] Source:J Biol Chem;292(39):16211-16220, 2017 Sep 29.
[Is] ISSN:1083-351X
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Macroautophagy is a fundamental and evolutionarily conserved catabolic process that eradicates damaged and aging macromolecules and organelles in eukaryotic cells. Decorin, an archetypical small leucine-rich proteoglycan, initiates a protracted autophagic program downstream of VEGF receptor 2 (VEGFR2) signaling that requires paternally expressed gene 3 (PEG3). We have discovered that PEG3 is an upstream transcriptional regulator of transcription factor EB (TFEB), a master transcription factor of lysosomal biogenesis, for decorin-evoked endothelial cell autophagy. We found a functional requirement of PEG3 for TFEB transcriptional induction and nuclear translocation in human umbilical vein endothelial and PAER2 cells. Mechanistically, inhibiting VEGFR2 or AMP-activated protein kinase (AMPK), a major decorin-activated energy sensor kinase, prevented decorin-evoked TFEB induction and nuclear localization. In conclusion, our findings indicate a non-canonical (nutrient- and energy-independent) mechanism underlying the pro-autophagic bioactivity of decorin via PEG3 and TFEB.
[Mh] Termos MeSH primário: Autofagia
Fatores de Transcrição de Zíper de Leucina e Hélice-Alça-Hélix Básicos/agonistas
Decorina/metabolismo
Endotélio Vascular/metabolismo
Fatores de Transcrição Kruppel-Like/metabolismo
Receptores de Fatores de Crescimento/agonistas
Transdução de Sinais
[Mh] Termos MeSH secundário: Proteínas Quinases Ativadas por AMP/antagonistas & inibidores
Proteínas Quinases Ativadas por AMP/metabolismo
Transporte Ativo do Núcleo Celular/efeitos dos fármacos
Animais
Aorta/citologia
Aorta/efeitos dos fármacos
Aorta/metabolismo
Autofagia/efeitos dos fármacos
Fatores de Transcrição de Zíper de Leucina e Hélice-Alça-Hélix Básicos/genética
Fatores de Transcrição de Zíper de Leucina e Hélice-Alça-Hélix Básicos/metabolismo
Células Cultivadas
Decorina/genética
Endotélio Vascular/citologia
Endotélio Vascular/efeitos dos fármacos
Regulação da Expressão Gênica/efeitos dos fármacos
Células Endoteliais da Veia Umbilical Humana/citologia
Células Endoteliais da Veia Umbilical Humana/efeitos dos fármacos
Células Endoteliais da Veia Umbilical Humana/metabolismo
Seres Humanos
Fatores de Transcrição Kruppel-Like/química
Fatores de Transcrição Kruppel-Like/genética
Fragmentos de Peptídeos/química
Fragmentos de Peptídeos/genética
Fragmentos de Peptídeos/metabolismo
Inibidores de Proteínas Quinases/farmacologia
Interferência de RNA
Receptores de Fatores de Crescimento/metabolismo
Proteínas Recombinantes de Fusão/química
Proteínas Recombinantes de Fusão/metabolismo
Proteínas Recombinantes/química
Proteínas Recombinantes/metabolismo
Transdução de Sinais/efeitos dos fármacos
Sus scrofa
Receptor 2 de Fatores de Crescimento do Endotélio Vascular/antagonistas & inibidores
Receptor 2 de Fatores de Crescimento do Endotélio Vascular/genética
Receptor 2 de Fatores de Crescimento do Endotélio Vascular/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Basic Helix-Loop-Helix Leucine Zipper Transcription Factors); 0 (DCN protein, human); 0 (Decorin); 0 (Kruppel-Like Transcription Factors); 0 (PEG3 protein, human); 0 (Peptide Fragments); 0 (Protein Kinase Inhibitors); 0 (Receptors, Growth Factor); 0 (Recombinant Fusion Proteins); 0 (Recombinant Proteins); 0 (TFEB protein, human); 0 (decorin receptor); EC 2.7.10.1 (KDR protein, human); EC 2.7.10.1 (Vascular Endothelial Growth Factor Receptor-2); EC 2.7.11.31 (AMP-Activated Protein Kinases)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170812
[St] Status:MEDLINE
[do] DOI:10.1074/jbc.M116.769950


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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]: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]:28174297
[Au] Autor:Torres A; Gubbiotti MA; Iozzo RV
[Ad] Endereço:From the Department of Pathology, Anatomy, and Cell Biology and the Cancer Cell Biology and Signaling Program, Kimmel Cancer Center, Sidney Kimmel Medical College, Thomas Jefferson University, Philadelphia, Pennsylvania 19107.
[Ti] Título:Decorin-inducible Peg3 Evokes Beclin 1-mediated Autophagy and Thrombospondin 1-mediated Angiostasis.
[So] Source:J Biol Chem;292(12):5055-5069, 2017 Mar 24.
[Is] ISSN:1083-351X
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:We previously discovered that systemic delivery of decorin for treatment of breast carcinoma xenografts induces paternally expressed gene 3 (Peg3), an imprinted gene encoding a zinc finger transcription factor postulated to function as a tumor suppressor. Here we found that expression of Peg3 increased Beclin 1 promoter activity and protein expression. This process required the full-length Peg3 as truncated mutants lacking either the N-terminal SCAN domain or the zinc fingers failed to translocate to the nucleus and promote Beclin 1 transcription. Importantly, overexpression of Peg3 in endothelial cells stimulated autophagy and concurrently inhibited endothelial cell migration and evasion from a 3D matrix. Mechanistically, we found that Peg3 induced the secretion of the powerful angiostatic glycoprotein Thrombospondin 1 independently of Beclin 1 transcriptional induction. Thus, we provide a new mechanism whereby Peg3 can simultaneously evoke autophagy in endothelial cells and attenuate angiogenesis.
[Mh] Termos MeSH primário: Beclina-1/genética
Decorina/metabolismo
Fatores de Transcrição Kruppel-Like/genética
Trombospondina 1/metabolismo
Regulação para Cima
[Mh] Termos MeSH secundário: Autofagia
Linhagem Celular
Movimento Celular
Células Endoteliais/citologia
Células Endoteliais/metabolismo
Seres Humanos
Fatores de Transcrição Kruppel-Like/metabolismo
Neovascularização Fisiológica
Regiões Promotoras Genéticas
Ativação Transcricional
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (BECN1 protein, human); 0 (Beclin-1); 0 (Decorin); 0 (Kruppel-Like Transcription Factors); 0 (PEG3 protein, human); 0 (Thrombospondin 1)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:170613
[Lr] Data última revisão:
170613
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170209
[St] Status:MEDLINE
[do] DOI:10.1074/jbc.M116.753632


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[PMID]:28138904
[Au] Autor:Kaya E; Kibar Y; Yilmaz S; Ebiloglu T; Ozcan A; Seyrek M; Yildiz O; Ulusoy KG
[Ad] Endereço:Gulhane Military Medical Academy, Ankara, Turkey. drenginkaya@yahoo.com.
[Ti] Título:The histopathological and pharmacodynamic effects of intradetrusor decorin injected in a rabbit partial bladder outlet obstruction model.
[So] Source:Int Urol Nephrol;49(4):607-614, 2017 Apr.
[Is] ISSN:1573-2584
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:PURPOSE: To evaluate whether or not the bladder function can be protected by supporting the detrusor with decorin levels during the fibrotic process. METHODS: Forty-two male rabbits were divided into three main groups, partial bladder outlet obstruction (pBOO) group, pBOO + intradetrusor decorin-injected (IDI) group and control group. Both pBOO and pBOO + IDI groups were divided into three subgroups according to the killing schedule. Histopathological, immunohistochemical and pharmacodynamics studies were performed for the evaluation of fibrotic process and tissue characteristics. RESULTS: Histopathological evaluation revealed statistically significant high fibrosis levels for both pBOO and pBOO + IDI groups when compared with control. Strikingly the antifibrotic effect of decorin was significant on 2nd, 4th and 8th week and increased as time passed. Immunohistochemical analysis was revealed high expressions of anti-TGF-ß1 and decorin levels in all pBOO + IDI groups. Pharmacodynamical results were also revealed better contraction responses in favor of 2nd, 4th and 8th week groups of pBOO + IDI groups, when compared with pBOO groups. In addition, the contraction responses against the depolarizer agent KCl were increased in the three decorin-administrated groups. CONCLUSION: Our study demonstrates the antifibrotic effects of decorin on bladder fibrosis. Strikingly, this antifibrotic effect is shown in histopathological, immunohistochemical and pharmacodynamics studies. Although further studies are warranted to make more decisive inferences regarding its clinical use, our study has the proper pride to be the first step of this time course.
[Mh] Termos MeSH primário: Decorina/farmacologia
Músculo Liso/efeitos dos fármacos
Obstrução do Colo da Bexiga Urinária/tratamento farmacológico
Obstrução do Colo da Bexiga Urinária/patologia
Bexiga Urinária/efeitos dos fármacos
Bexiga Urinária/patologia
[Mh] Termos MeSH secundário: Animais
Carbacol/farmacologia
Decorina/análise
Decorina/uso terapêutico
Modelos Animais de Doenças
Estimulação Elétrica
Fibrose
Injeções Intramusculares
Masculino
Antagonistas Muscarínicos/farmacologia
Contração Muscular/efeitos dos fármacos
Músculo Liso/fisiopatologia
Cloreto de Potássio/farmacologia
Coelhos
Fator de Crescimento Transformador beta1/análise
Bexiga Urinária/química
Bexiga Urinária/fisiopatologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Decorin); 0 (Muscarinic Antagonists); 0 (Transforming Growth Factor beta1); 660YQ98I10 (Potassium Chloride); 8Y164V895Y (Carbachol)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171102
[Lr] Data última revisão:
171102
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170201
[St] Status:MEDLINE
[do] DOI:10.1007/s11255-017-1518-x


  9 / 1428 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


  10 / 1428 MEDLINE  
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[PMID]:28009689
[Au] Autor:Yang SY; Yang JY; Hsiao YC; Chuang SS
[Ad] Endereço:Department of Plastic Surgery, Linkou Burn Center, Chang Gung Memorial Hospital, Chang Gung University, Taipei, Taiwan.
[Ti] Título:A Comparison of Gene Expression of Decorin and MMP13 in Hypertrophic Scars Treated With Calcium Channel Blocker, Steroid, and Interferon: A Human-Scar-Carrying Animal Model Study.
[So] Source:Dermatol Surg;43 Suppl 1:S37-S46, 2017 Jan.
[Is] ISSN:1524-4725
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: The formation of hypertrophic scaring (HSc) is an abnormal wound-healing response. In a previous study, an animal model with human scar tissue implanted into nude mice (BALB/c) has been successfully established. The effects of verapamil as well as combination therapy with verapamil and kenacort have been studied and compared. OBJECTIVE: To treat persistent hypertrophic scars, local injection of drugs composed of steroids, calcium channel blockers (CCBs), and interferon might be a good method. What is the best dose of the regimen and what are the mechanisms are also a worthwhile study. MATERIALS AND METHODS: Scar specimens were harvested from patients with HSc or Keloid resulting from burn injury, and then implanted to BALB/c-nu nude mice for 4 weeks. Before implantation, the specimen was either injected with or without drugs such as steroids (kenacort), CCBs (verapamil), and interferons (INFα2b), respectively. After the removal of implants, quantitative gene expressions of decorin and collagenase (MMP13) were measured using a real-time polymerase chain reaction to detect their mRNAs. Two way-ANOVA and Post Hoc were used for statistical analysis using the software SPSS 15.0. RESULTS: All drug-treated groups increased the expressions of decorin and MMP13 in comparison with those in noninjected group (p < .001) in a dose-dependent manner. Comparing equal amounts of individual drugs, gene expression of decorin was increased with increasing injection amount, and the best result in low amount of injection (0.02 mL of each) was shown in the group injected with INFα2b followed by kenacort and verapamil. However, the results were changed while injection amount was up to 0.04 mL and the strongest decorin gene expression was found in kenacort injection. Regarding MMP-13 expression, low-amount injection (0.02 mL) of INFα2b has strongest gene expression followed by kenacort and verapamil, but in the large-amount regimes (0.04 mL), verapamil had strongest gene expression followed by INFα2b and kenacort. CONCLUSION: This study showed that the kenacort, verapamil, and INFα2b all inhibited HSc in a dose-dependent manner through the evidence of gene expression of decorin and MMP13. In comparison with the injections between small amounts of drugs, INFα2b potentiated the strongest decorin and MMP13 expression. On the contrary, among the large-amount injection regimes, kenacrot was more effective on decorin expression as verapamil to MMP13 expression. To decrease side effects from the drugs and produce promising results for the clinical practice, it is suggested to maintain the dose of INFα2b along with an increased dose of verapamil for HSc improvement.
[Mh] Termos MeSH primário: Bloqueadores dos Canais de Cálcio/administração & dosagem
Cicatriz/tratamento farmacológico
Decorina/genética
Fármacos Dermatológicos/administração & dosagem
Glucocorticoides/administração & dosagem
Interferon-alfa/administração & dosagem
Metaloproteinase 13 da Matriz/genética
[Mh] Termos MeSH secundário: Adolescente
Adulto
Animais
Queimaduras/complicações
Criança
Pré-Escolar
Cicatriz/genética
Cicatriz Hipertrófica/tratamento farmacológico
Cicatriz Hipertrófica/genética
Modelos Animais de Doenças
Relação Dose-Resposta a Droga
Expressão Gênica
Seres Humanos
Injeções Intradérmicas
Injeções Intralesionais
Queloide/tratamento farmacológico
Queloide/genética
Camundongos
Camundongos Endogâmicos BALB C
Camundongos Nus
Triancinolona Acetonida/administração & dosagem
Verapamil/administração & dosagem
Adulto Jovem
[Pt] Tipo de publicação:COMPARATIVE STUDY; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Calcium Channel Blockers); 0 (Decorin); 0 (Dermatologic Agents); 0 (Glucocorticoids); 0 (Interferon-alpha); 0 (Interferon-alpha2b); CJ0O37KU29 (Verapamil); EC 3.4.24.- (MMP13 protein, human); EC 3.4.24.- (Matrix Metalloproteinase 13); F446C597KA (Triamcinolone Acetonide)
[Em] Mês de entrada:1703
[Cu] Atualização por classe:170817
[Lr] Data última revisão:
170817
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161224
[St] Status:MEDLINE
[do] DOI:10.1097/DSS.0000000000000990



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