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[PMID]:29329878
[Au] Autor:Chen Z; Zhao Z; Li Y; Zhang X; Li B; Chen L; Wang H
[Ad] Endereço:Department of Pharmacology, Basic Medical School of Wuhan University, No.185 Donghu Road, Wuhan, Hubei Province, 430071, China.
[Ti] Título:Course-, dose-, and stage-dependent toxic effects of prenatal dexamethasone exposure on fetal articular cartilage development.
[So] Source:Toxicol Lett;286:1-9, 2018 Apr.
[Is] ISSN:1879-3169
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Dexamethasone, a synthetic long-acting glucocorticoid, is routinely used for treating mothers at risk for preterm delivery. However, intrauterine overexposure to glucocorticoids induces low birth weight and cartilage dysplasia in offspring. Also, the "critical window" and safe dose of this treatment are largely unknown. This study investigated the course-, dose-, and stage-dependent toxic effects and the possible mechanisms of prenatal dexamethasone exposure (PDE) on fetal development and articular cartilage development. Pregnant mice (C57BL/6) received subcutaneous injection of dexamethasone (0.8 mg/kg d) once on gestational day (GD) 15 or once a day from GD 15 to 17, or received various doses of dexamethasone (0, 0.2, 0.8, and 1.2 mg/kg d) on GD 15-17, or received dexamethasone (0.8 mg/kg d) at early stage (GD 12-14) or late stage of pregnancy (GD 15-17). Offspring's knee joints were harvested at birth for morphological analyses and detection of gene expression. Repeated PDE significantly suppressed fetal and articular cartilage development, which were characterized by decreased body weight and body length, coarse articular cartilage surfaces, and reduced gene and protein expression of Col2a1 and aggrecan. For those newborns treated with repeated PDE at different doses, the toxic effects on fetal and articular cartilage development were observed at doses of 0.8 and 1.2 mg/kg d, whereas no obvious toxic effects were observed at the dose of 0.2 mg/kg d. Moreover, PDE at 0.8 mg/kg d during the early embryonic stage induced stronger toxic effects on fetal and articular cartilage development, compared with PDE during the late embryonic stage. Detection of gene expression showed that the TGFß signaling pathway in the articular cartilage was down-regulated after PDE. Taken together, PDE induces fetal developmental toxicity and articular cartilage developmental toxicity in a course-, dose-, and stage-dependent manner.
[Mh] Termos MeSH primário: Cartilagem Articular/efeitos dos fármacos
Condrogênese/efeitos dos fármacos
Dexametasona/toxicidade
Feto/efeitos dos fármacos
Glucocorticoides/toxicidade
[Mh] Termos MeSH secundário: Agrecanas/genética
Agrecanas/metabolismo
Animais
Cartilagem Articular/embriologia
Cartilagem Articular/metabolismo
Colágeno Tipo II/genética
Colágeno Tipo II/metabolismo
Dexametasona/administração & dosagem
Relação Dose-Resposta a Droga
Feminino
Feto/metabolismo
Feto/patologia
Regulação da Expressão Gênica no Desenvolvimento/efeitos dos fármacos
Idade Gestacional
Glucocorticoides/administração & dosagem
Exposição Materna
Camundongos Endogâmicos C57BL
Gravidez
Medição de Risco
Transdução de Sinais/efeitos dos fármacos
Fator de Crescimento Transformador beta/genética
Fator de Crescimento Transformador beta/metabolismo
[Pt] Tipo de publicação:COMPARATIVE STUDY; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Aggrecans); 0 (Col2a1 protein, mouse); 0 (Collagen Type II); 0 (Glucocorticoids); 0 (Transforming Growth Factor beta); 7S5I7G3JQL (Dexamethasone)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180220
[Lr] Data última revisão:
180220
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180114
[St] Status:MEDLINE


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[PMID]:28471382
[Au] Autor:Wang Y; Yang T; Liu Y; Zhao W; Zhang Z; Lu M; Zhang W
[Ad] Endereço:Department of Joint Surgery, The First Affiliated Hospital of Dalian Medical University, Dalian 116011, China. WY_landy1116@163.com.
[Ti] Título:Decrease of miR-195 Promotes Chondrocytes Proliferation and Maintenance of Chondrogenic Phenotype via Targeting FGF-18 Pathway.
[So] Source:Int J Mol Sci;18(5), 2017 May 04.
[Is] ISSN:1422-0067
[Cp] País de publicação:Switzerland
[La] Idioma:eng
[Ab] Resumo:Slow growth and rapid loss of chondrogenic phenotypes are the major problems affecting chronic cartilage lesions. The role of microRNA-195 (miR-195) and its detailed working mechanism in the fore-mentioned process remains unknown. Fibroblastic growth factor 18 (FGF-18) plays a key role in cartilage homeostasis; whether miR-195 could regulate FGF-18 and its downstream signal pathway in chondrocyte proliferation and maintenance of chondrogenic phenotypes still remains unclear. The present research shows elevated miR-195 but depressed FGF-18 expressed in joint fluid specimens of 20 patients with chronic cartilage lesions and in CH1M and CH3M chondrocytes when compared with that in joint fluid specimens without cartilage lesions and in CH1W and CH2W chondrocytes, respectively. The following loss of function test revealed that downregulation of miR-195 by transfection of miR-195 inhibitors promoted chondrocyte proliferation and expression of a type II collagen α I chain (Col2a1)/aggrecan. Through the online informatics analysis we theoretically predicted that miR-195 could bind to a FGF-18 3' untranslated region (3'UTR), also, we verified that a miR-195 could regulate the FGF-18 and its downstream pathway. The constructed dual luciferase assay further confirmed that FGF-18 was a direct target of miR-195. The executed anti-sense experiment displayed that miR-195 could regulate chondrocyte proliferation and Col2a1/aggrecan expression via the FGF-18 pathway. Finally, through an in vivo anterior cruciate ligament transection (ACLT) model, downregulation of miR-195 presented a significantly protective effect on chronic cartilage lesions. Evaluating all of the outcomes of the current research revealed that a decrease of miR-195 protected chronic cartilage lesions by promoting chondrocyte proliferation and maintenance of chondrogenic phenotypes via the targeting of the FGF-18 pathway and that the miR-195/FGF-18 axis could be a potential target in the treatment of cartilage lesions.
[Mh] Termos MeSH primário: Proliferação Celular
Condrócitos/metabolismo
Fatores de Crescimento de Fibroblastos/metabolismo
MicroRNAs/genética
Osteocondrite/metabolismo
[Mh] Termos MeSH secundário: Regiões 3' não Traduzidas
Agrecanas/genética
Agrecanas/metabolismo
Animais
Estudos de Casos e Controles
Células Cultivadas
Condrócitos/citologia
Condrócitos/fisiologia
Condrogênese
Colágeno Tipo II/genética
Colágeno Tipo II/metabolismo
Feminino
Fatores de Crescimento de Fibroblastos/genética
Células HEK293
Seres Humanos
MicroRNAs/metabolismo
Osteocondrite/genética
Osteocondrite/patologia
Fenótipo
Ratos
Ratos Sprague-Dawley
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (3' Untranslated Regions); 0 (Aggrecans); 0 (Collagen Type II); 0 (MIRN195 microRNA, human); 0 (MicroRNAs); 0 (fibroblast growth factor 18); 62031-54-3 (Fibroblast Growth Factors)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180212
[Lr] Data última revisão:
180212
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170505
[St] Status:MEDLINE


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[PMID]:28745632
[Au] Autor:Li Y; Hai Y; Chen J; Liu T
[Ad] Endereço:Key Laboratory of Genomic and Precision Medicine, Beijing Institute of Genomics, Chinese Academy of Sciences.
[Ti] Título:Differentiating Chondrocytes from Peripheral Blood-derived Human Induced Pluripotent Stem Cells.
[So] Source:J Vis Exp;(125), 2017 07 18.
[Is] ISSN:1940-087X
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:In this study, we used peripheral blood cells (PBCs) as seed cells to produce chondrocytes via induced pluripotent stem cells (iPSCs) in an integration-free method. Following embryoid body (EB) formation and fibroblastic cell expansion, the iPSCs are induced for chondrogenic differentiation for 21 days under serum-free and xeno-free conditions. After chondrocyte induction, the phenotypes of the cells are evaluated by morphological, immunohistochemical, and biochemical analyses, as well as by the quantitative real-time PCR examination of chondrogenic differentiation markers. The chondrogenic pellets show positive alcian blue and toluidine blue staining. The immunohistochemistry of collagen II and X staining is also positive. The sulfated glycosaminoglycan (sGAG) content and the chondrogenic differentiation markers COLLAGEN 2 (COL2), COLLAGEN 10 (COL10), SOX9, and AGGRECAN are significantly upregulated in chondrogenic pellets compared to hiPSCs and fibroblastic cells. These results suggest that PBCs can be used as seed cells to generate iPSCs for cartilage repair, which is patient-specific and cost-effective.
[Mh] Termos MeSH primário: Células Sanguíneas/citologia
Condrócitos/citologia
Células-Tronco Pluripotentes Induzidas/citologia
[Mh] Termos MeSH secundário: Agrecanas/genética
Agrecanas/metabolismo
Diferenciação Celular
Células Cultivadas
Condrócitos/metabolismo
Condrogênese
Colágeno Tipo II/genética
Colágeno Tipo II/metabolismo
Corpos Embrioides/citologia
Corpos Embrioides/patologia
Seres Humanos
Imuno-Histoquímica
Células-Tronco Pluripotentes Induzidas/metabolismo
Fatores de Transcrição SOX9/genética
Fatores de Transcrição SOX9/metabolismo
Regulação para Cima
Gravação em Vídeo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Aggrecans); 0 (Collagen Type II); 0 (SOX9 Transcription Factor)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180130
[Lr] Data última revisão:
180130
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170727
[St] Status:MEDLINE
[do] DOI:10.3791/55722


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[PMID]:29233086
[Au] Autor:Taipale M; Solovieva S; Leino-Arjas P; Männikkö M
[Ad] Endereço:Center for Life Course Health Research, Faculty of Medicine, University of Oulu, Aapistie 5, 90220, Oulu, Finland.
[Ti] Título:Functional polymorphisms in asporin and CILP together with joint loading predispose to hand osteoarthritis.
[So] Source:BMC Genet;18(1):108, 2017 Dec 12.
[Is] ISSN:1471-2156
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Osteoarthritis (OA) is the most common degenerative joint disease afflicting people in the Western world and has a strong genetic influence. The aim of this study was to examine the association of two known functional polymorphisms in the TGF-ß inhibiting genes, asporin (ASPN) and cartilage intermediate layer protein (CILP), with hand OA and potential gene-occupational hand loading interaction. RESULTS: Statistically significant interaction of the CILP rs2073711 T and ASPN D15 alleles with hand OA was observed (OR = 2.48, 95% CI 1.27-4.85, p = 0.008) in a Finnish hand OA cohort of 543 women (aged 45-63). When stratified by variation in working tasks, low variation of working tasks increased the risk further (OR = 3.00, 95% CI 1.35-6.66, p = 0.007). Based on the analysis of ASPN and CILP protein-coding regions, functional studies were performed with one observed variant, rs41278695 in the ASPN gene. Analyses showed that bone morphogenetic protein 2 (BMP2) mediated expression of aggrecan (Agc1) and type II collagen (Col2a1) was significantly suppressed (p = 0.011 and p = 0.023, respectively) in a murine chondrocytic cell line (ATDC5) with cells stably expressing ASPN rs41278695. CONCLUSIONS: The carriage of either ASPN D15 or CILP rs2073711 TT is associated with increased risk of symmetrical hand OA, particularly in individuals with low variation in work tasks. ASPN rs41278695 SNP had an effect on Agc1 and Col2a1 gene expression when induced with BMP-2 suggesting an effect on the cartilage extracellular matrix composition.
[Mh] Termos MeSH primário: Proteínas da Matriz Extracelular/genética
Predisposição Genética para Doença
Articulação da Mão/fisiopatologia
Doenças Profissionais/genética
Osteoartrite/genética
Pirofosfatases/genética
[Mh] Termos MeSH secundário: Agrecanas/metabolismo
Animais
Células Cultivadas
Condrócitos/citologia
Condrócitos/metabolismo
Estudos de Coortes
Colágeno Tipo II/metabolismo
Feminino
Seres Humanos
Camundongos
Meia-Idade
Doenças Profissionais/patologia
Osteoartrite/patologia
Polimorfismo Genético
[Pt] Tipo de publicação:JOURNAL ARTICLE; RANDOMIZED CONTROLLED TRIAL
[Nm] Nome de substância:
0 (ASPN protein, human); 0 (Aggrecans); 0 (Collagen Type II); 0 (Extracellular Matrix Proteins); EC 3.6.1.- (CILP protein, human); EC 3.6.1.- (Pyrophosphatases)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180118
[Lr] Data última revisão:
180118
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171214
[St] Status:MEDLINE
[do] DOI:10.1186/s12863-017-0585-4


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[PMID]:29197863
[Au] Autor:Xu S; Li Z; Wang Z; Zhai C; Liang W; Zhu C; Fan W
[Ti] Título:Proteomic Analysis Reveals Grb2 as a Key Regulator of Periodic Mechanical Stress Transduction in Chondrocytes.
[So] Source:Cell Physiol Biochem;44(4):1509-1525, 2017.
[Is] ISSN:1421-9778
[Cp] País de publicação:Switzerland
[La] Idioma:eng
[Ab] Resumo:BACKGROUND/AIMS: Periodic mechanical stress could significantly promote chondrocyte proliferation and matrix synthesis. However, the mechanisms underlying the ability of chondrocyte detecting and responding to periodic mechanical stimuli have not been well delineated. METHODS: Quantitative proteomic analysis was performed to construct the differently expressed proteome profiles of chondrocyte under pressure. Then a combination of Western blot, quantitative real-time PCR, lentiviral vector and histological methods were used to confirm the proteomic results and investigate the mechanoseing mechanism. RESULTS: Growth factor receptor-bound protein 2 (Grb2), a component of integrin adhesome, was found a 1.49-fold increase in dynamic stress group. This process was mediated through integrin ß1, leading to increased phosphorylation of focal adhesion kinase (FAK) and extracellular signal-regulated kinase 1/2 (ERK1/2) respectively and then produce the corresponding biological effects. CONCLUSION: This was the first time to demonstrate Grb2 has such an important role in periodic mechanotransduction, and the proteomic data could facilitate the further investigation of chondrocytes mechanosensing.
[Mh] Termos MeSH primário: Proteína Adaptadora GRB2/metabolismo
Proteômica
Estresse Mecânico
[Mh] Termos MeSH secundário: Agrecanas/genética
Agrecanas/metabolismo
Animais
Células Cultivadas
Condrócitos/citologia
Condrócitos/metabolismo
Cromatografia Líquida de Alta Pressão
Colágeno Tipo II/genética
Colágeno Tipo II/metabolismo
Proteína-Tirosina Quinases de Adesão Focal/genética
Proteína-Tirosina Quinases de Adesão Focal/metabolismo
Proteína Adaptadora GRB2/antagonistas & inibidores
Proteína Adaptadora GRB2/genética
Imuno-Histoquímica
Proteína Quinase 1 Ativada por Mitógeno/genética
Proteína Quinase 1 Ativada por Mitógeno/metabolismo
Proteína Quinase 3 Ativada por Mitógeno/genética
Proteína Quinase 3 Ativada por Mitógeno/metabolismo
Fosforilação
Interferência de RNA
RNA Interferente Pequeno/metabolismo
Ratos
Ratos Sprague-Dawley
Reação em Cadeia da Polimerase em Tempo Real
Espectrometria de Massas por Ionização por Electrospray
Engenharia Tecidual
Regulação para Cima
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Aggrecans); 0 (Collagen Type II); 0 (GRB2 Adaptor Protein); 0 (Grb2 protein, rat); 0 (RNA, Small Interfering); EC 2.7.10.2 (Focal Adhesion Protein-Tyrosine Kinases); EC 2.7.11.24 (Mitogen-Activated Protein Kinase 1); EC 2.7.11.24 (Mitogen-Activated Protein Kinase 3)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180118
[Lr] Data última revisão:
180118
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171204
[St] Status:MEDLINE
[do] DOI:10.1159/000485646


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[PMID]:28464560
[Au] Autor:Wilkinson DJ; Habgood A; Lamb HK; Thompson P; Hawkins AR; Désilets A; Leduc R; Steinmetzer T; Hammami M; Lee MS; Craik CS; Watson S; Lin H; Milner JM; Rowan AD
[Ad] Endereço:Newcastle University, Newcastle upon Tyne, UK.
[Ti] Título:Matriptase Induction of Metalloproteinase-Dependent Aggrecanolysis In Vitro and In Vivo: Promotion of Osteoarthritic Cartilage Damage by Multiple Mechanisms.
[So] Source:Arthritis Rheumatol;69(8):1601-1611, 2017 08.
[Is] ISSN:2326-5205
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:OBJECTIVE: To assess the ability of matriptase, a type II transmembrane serine proteinase, to promote aggrecan loss from the cartilage of patients with osteoarthritis (OA) and to determine whether its inhibition can prevent aggrecan loss and cartilage damage in experimental OA. METHODS: Aggrecan release from human OA cartilage explants and human stem cell-derived cartilage discs was evaluated, and cartilage-conditioned media were used for Western blotting. Gene expression was analyzed by real-time polymerase chain reaction. Murine OA was induced by surgical destabilization of the medial meniscus, and matriptase inhibitors were administered via osmotic minipump or intraarticular injection. Cartilage damage was scored histologically and aggrecan cleavage was visualized immunohistochemically using specific neoepitope antibodies. RESULTS: The addition of soluble recombinant matriptase promoted a time-dependent release of aggrecan (and collagen) from OA cartilage, which was sensitive to metalloproteinase inhibition and protease-activated receptor 2 antagonism. Although engineered human (normal) cartilage discs failed to release aggrecan following matriptase addition, both matrix metalloproteinase- and aggrecanase-mediated cleavages of aggrecan were detected in human OA cartilage. Additionally, while matriptase did not directly degrade aggrecan, it promoted the accumulation of low-density lipoprotein receptor-related protein 1 (LRP-1) in conditioned media of the OA cartilage explants. Matriptase inhibition via neutralizing antibody or small molecule inhibitor significantly reduced cartilage damage scores in murine OA, which was associated with reduced generation of metalloproteinase-mediated aggrecan cleavage. CONCLUSION: Matriptase potently induces the release of metalloproteinase-generated aggrecan fragments as well as soluble LRP-1 from OA cartilage. Therapeutic targeting of matriptase proteolytic activity reduces metalloproteinase activity, further suggesting that this serine proteinase may have potential as a disease-modifying therapy in OA.
[Mh] Termos MeSH primário: Agrecanas/efeitos dos fármacos
Cartilagem Articular/efeitos dos fármacos
Osteoartrite do Joelho/metabolismo
Serina Endopeptidases/farmacologia
[Mh] Termos MeSH secundário: Proteína ADAMTS4/efeitos dos fármacos
Proteína ADAMTS4/metabolismo
Proteína ADAMTS5/efeitos dos fármacos
Proteína ADAMTS5/metabolismo
Idoso
Idoso de 80 Anos ou mais
Agrecanas/metabolismo
Animais
Anticorpos Neutralizantes/farmacologia
Western Blotting
Cartilagem Articular/metabolismo
Cartilagem Articular/patologia
Endopeptidases/efeitos dos fármacos
Endopeptidases/metabolismo
Feminino
Perfilação da Expressão Gênica
Seres Humanos
Imuno-Histoquímica
Técnicas In Vitro
Proteína-1 Relacionada a Receptor de Lipoproteína de Baixa Densidade/efeitos dos fármacos
Proteína-1 Relacionada a Receptor de Lipoproteína de Baixa Densidade/metabolismo
Masculino
Metaloproteinases da Matriz/efeitos dos fármacos
Metaloproteinases da Matriz/metabolismo
Proteínas de Membrana/antagonistas & inibidores
Proteínas de Membrana/metabolismo
Meniscos Tibiais/cirurgia
Camundongos
Meia-Idade
Osteoartrite do Joelho/patologia
Reação em Cadeia da Polimerase em Tempo Real
Proteínas Recombinantes/farmacologia
Serina Endopeptidases/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Aggrecans); 0 (Antibodies, Neutralizing); 0 (Low Density Lipoprotein Receptor-Related Protein-1); 0 (Membrane Proteins); 0 (Recombinant Proteins); EC 3.4.- (Endopeptidases); EC 3.4.21.- (Serine Endopeptidases); EC 3.4.21.109 (ST14 protein, human); EC 3.4.21.109 (St14 protein, mouse); EC 3.4.24.- (ADAMTS5 Protein); EC 3.4.24.- (Matrix Metalloproteinases); EC 3.4.24.82 (ADAMTS4 Protein); EC 3.4.99.- (aggrecanase)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:180119
[Lr] Data última revisão:
180119
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170503
[St] Status:MEDLINE
[do] DOI:10.1002/art.40133


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[PMID]:29257018
[Au] Autor:Zhu D; Tapadia MD; Palispis W; Luu M; Wang W; Gupta R
[Ad] Endereço:Peripheral Nerve Research Laboratory, Department of Orthopaedic Surgery, University of California, Irvine, Irvine, California.
[Ti] Título:Attenuation of Robust Glial Scar Formation Facilitates Functional Recovery in Animal Models of Chronic Nerve Compression Injury.
[So] Source:J Bone Joint Surg Am;99(24):e132, 2017 Dec 20.
[Is] ISSN:1535-1386
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Late surgery for chronic nerve compression injuries usually improves sensation but rarely reverses motor atrophy. We hypothesized that a persistent glial scar after chronic nerve compression injury might account for poor motor recovery and that degradation of the glial scar as an adjunct to surgical decompression would improve functional recovery. METHODS: A previously described model of chronic nerve compression injury was created in C57BL/6 mice and Sprague-Dawley rats, and the nerves were harvested early or late after electrophysiological confirmation of the injury. Western blot, polymerase chain reaction, and quantitative immunohistochemical analyses were performed to determine levels of chondroitin sulfate proteoglycans and extracellular matrix molecules. Subsets of mice were treated either with surgical decompression alone or with decompression coupled with intraepineurial injection of a low dose (0.1 µgµL) or a high dose (0.2 µg/µL) of chondroitinase ABC at 6 weeks after injury. RESULTS: Aggrecan showed the greatest change in mRNA and protein levels at the early and late time points following creation of the chronic nerve compression injury. Quantitative immunohistochemical analysis revealed early aggrecan upregulation localized primarily to the endoneurium and late upregulation localized to the perineurium and epineurium (p < 0.0105). Quantitative immunohistochemical analysis for collagen IV, laminin-α2, and fibronectin also showed early upregulation with perineurial scarring. Quantitative immunohistochemical analysis and Western blot analysis for aggrecan demonstrated a marked increase in the endoneurium at the early time points and upregulation of expression in the epineurium and perineurium at the late time points. Decompression along with intraepineurial injection of high-dose chondroitinase ABC at 6 weeks after creation of the compression injury resulted in marked attenuation of decorin and aggrecan expression with functional improvement in nerve conduction velocity. CONCLUSIONS: Significant upregulation of chondroitin sulfate proteoglycans and other extracellular matrix components contributes to the pathogenesis of compression neuropathies in murine models. The administration of chondroitinase ABC degrades these chondroitin sulfate proteoglycans and improves functional recovery after chronic nerve compression injury; thus, it can be considered as a possible therapeutic adjunct.
[Mh] Termos MeSH primário: Condroitina ABC Liase/farmacologia
Cicatriz/prevenção & controle
Descompressão Cirúrgica/métodos
Síndromes de Compressão Nervosa/tratamento farmacológico
Traumatismos dos Nervos Periféricos/tratamento farmacológico
Traumatismos dos Nervos Periféricos/patologia
[Mh] Termos MeSH secundário: Agrecanas/farmacologia
Análise de Variância
Animais
Western Blotting
Doença Crônica
Modelos Animais de Doenças
Injeções Intralesionais
Masculino
Camundongos
Camundongos Endogâmicos C57BL
Síndromes de Compressão Nervosa/patologia
Síndromes de Compressão Nervosa/cirurgia
Condução Nervosa/efeitos dos fármacos
Traumatismos dos Nervos Periféricos/cirurgia
RNA Mensageiro/efeitos dos fármacos
Distribuição Aleatória
Ratos
Ratos Sprague-Dawley
Reação em Cadeia da Polimerase em Tempo Real/métodos
Recuperação de Função Fisiológica/fisiologia
Sensibilidade e Especificidade
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Aggrecans); 0 (RNA, Messenger); EC 4.2.2.20 (Chondroitin ABC Lyase)
[Em] Mês de entrada:1712
[Cu] Atualização por classe:171227
[Lr] Data última revisão:
171227
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:171220
[St] Status:MEDLINE
[do] DOI:10.2106/JBJS.17.00396


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[PMID]:28963928
[Au] Autor:Chang Y; Wang X; Sun Z; Jin Z; Chen M; Wang X; Lammi MJ; Guo X
[Ad] Endereço:Department of Orthopaedics, The Third Affiliated Hospital (Shaanxi Provincial People's Hospital), Health Science Center of Xi'an Jiaotong University, Xi'an 710061, Shaanxi, PR China.
[Ti] Título:Inflammatory cytokine of IL-1ß is involved in T-2 toxin-triggered chondrocyte injury and metabolism imbalance by the activation of Wnt/ß-catenin signaling.
[So] Source:Mol Immunol;91:195-201, 2017 11.
[Is] ISSN:1872-9142
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Mycotoxin T-2 exerts a causative role in Kashin-Beck disease (KBD) suffering chondrocyte apoptosis and cartilage matrix homeostasis disruption. Recent research corroborated the aberrant levels of pro-inflammatory cytokine IL-1ß in KBD patients and mycotoxin environment. In the present study, we investigated the relevance of IL-1ß in T-2 toxin-evoked chondrocyte cytotoxic injury and aberrant catabolism. High levels of IL-1ß were detected in serum and cartilages from KBD patients and in T-2-stimulated chondrocytes. Moreover, knockdown of IL-1ß antagonized the adverse effects of T-2 on cytotoxic injury by enhancing cell viability and inhibiting apoptosis. However, exogenous supplementation of IL-1ß further aggravated cell damage in response to T-2. Additionally, cessation of IL-1ß rescued T-2-elicited tilt of matrix homeostasis toward catabolism by elevating the transcription of collagen II and aggrecan, promoting release of sulphated glycosaminoglycans (sGAG) and TIMP1, and suppressing matrix metalloproteinases production including MMP-1, MMP-3 and MMP-13. Conversely, IL-1ß stimulation deteriorated T-2-induced disruption of matrix metabolism balance toward catabolism. Mechanistic analysis found the high activation of Wnt/ß-catenin in KBD patients and chondrocytes upon T-2. Furthermore, this activation was mitigated after IL-1ß inhibition, but further enhanced following IL-1ß precondition. Importantly, blocking this pathway by transfection with ß-catenin alleviated the adverse roles of IL-1ß on cytotoxic injury and metabolism disorders under T-2 conditioning. Together, this study elucidates a new insight into how T-2 deteriorates the pathological progression of KBD by regulating inflammation-related pathways, indicating a promising anti-inflammation strategy for KBD therapy.
[Mh] Termos MeSH primário: Condrócitos/imunologia
Interleucina-1beta/imunologia
Toxina T-2/toxicidade
Via de Sinalização Wnt/efeitos dos fármacos
beta Catenina/imunologia
[Mh] Termos MeSH secundário: Adulto
Agrecanas/biossíntese
Agrecanas/genética
Agrecanas/imunologia
Animais
Apoptose/genética
Apoptose/imunologia
Condrócitos/metabolismo
Condrócitos/patologia
Colágeno Tipo II/biossíntese
Colágeno Tipo II/genética
Colágeno Tipo II/imunologia
Colagenases/biossíntese
Colagenases/genética
Colagenases/imunologia
Matriz Extracelular/genética
Matriz Extracelular/imunologia
Matriz Extracelular/metabolismo
Matriz Extracelular/patologia
Feminino
Seres Humanos
Interleucina-1beta/genética
Interleucina-1beta/metabolismo
Doença de Kashin-Bek/genética
Doença de Kashin-Bek/imunologia
Doença de Kashin-Bek/metabolismo
Doença de Kashin-Bek/patologia
Masculino
Meia-Idade
Ratos
Ratos Sprague-Dawley
Inibidor Tecidual de Metaloproteinase-1/biossíntese
Inibidor Tecidual de Metaloproteinase-1/genética
Inibidor Tecidual de Metaloproteinase-1/imunologia
Transcrição Genética/efeitos dos fármacos
Transcrição Genética/imunologia
Via de Sinalização Wnt/genética
Via de Sinalização Wnt/imunologia
beta Catenina/genética
beta Catenina/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Aggrecans); 0 (Collagen Type II); 0 (IL1B protein, human); 0 (IL1B protein, rat); 0 (Interleukin-1beta); 0 (TIMP1 protein, human); 0 (Tissue Inhibitor of Metalloproteinase-1); 0 (beta Catenin); 0 (tissue inhibitor of metalloproteinase-1 protein, rat); EC 3.4.24.- (Collagenases); I3FL5NM3MO (T-2 Toxin)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171120
[Lr] Data última revisão:
171120
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171001
[St] Status:MEDLINE


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[PMID]:28942283
[Au] Autor:Lin H; Ma X; Wang BC; Zhao L; Liu JX; Pu FF; Hu YQ; Hu HZ; Shao ZW
[Ad] Endereço:Department of Orthopedic Surgery, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, China.
[Ti] Título:Edaravone ameliorates compression-induced damage in rat nucleus pulposus cells.
[So] Source:Life Sci;189:76-83, 2017 Nov 15.
[Is] ISSN:1879-0631
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:AIMS: Edaravone is a strong free radical scavenger most used for treating acute ischemic stroke. In this study we investigated the protective effects and underlying mechanisms of edaravone on compression-induced damage in rat nucleus pulposus (NP) cells. MATERIALS AND METHODS: Cell viability was determined using MTT assay methods. NP cell apoptosis was measured by Hoechst 33,258 staining and Annexin V/PI double staining. Intracellular reactive oxygen species (ROS), mitochondrial membrane potential (MMP), and intracellular calcium ([Ca ] ) were determined by fluorescent probes DCFH-DA, JC-1 and Fluo-3/AM, respectively. Apoptosis-related proteins (cleaved caspase-3, cytosolic cytochrome c, Bax and Bcl-2) and extracellular matrix proteins (aggrecan and collagen II) were analyzed by western blot. KEY FINDINGS: Edaravone attenuated the compression-induced decrease in viability of NP cells in a dose-dependent manner. 33,258 and Annexin V/PI double staining showed that edaravone protected NP cells from compression-induced apoptosis. Further studies confirmed that edaravone protected NP cells against compression-induced mitochondrial pathway of apoptosis by inhibiting overproduction of ROS, collapse of MMP and overload of [Ca ] . In addition, edaravone promoted the expression of aggrecan and collagen II in compression-treated NP cells. SIGNIFICANCE: These results strongly indicate that edaravone ameliorates compression-induced damage in rat nucleus pulposus cells. Edaravone could be a potential new drug for treatment of IDD.
[Mh] Termos MeSH primário: Antipirina/análogos & derivados
Apoptose/efeitos dos fármacos
Sobrevivência Celular/efeitos dos fármacos
Depuradores de Radicais Livres/farmacologia
Núcleo Pulposo/efeitos dos fármacos
[Mh] Termos MeSH secundário: Agrecanas/genética
Animais
Antipirina/administração & dosagem
Antipirina/farmacologia
Células Cultivadas
Colágeno Tipo II/genética
Relação Dose-Resposta a Droga
Depuradores de Radicais Livres/administração & dosagem
Regulação da Expressão Gênica/efeitos dos fármacos
Degeneração do Disco Intervertebral/tratamento farmacológico
Degeneração do Disco Intervertebral/fisiopatologia
Potencial da Membrana Mitocondrial
Núcleo Pulposo/patologia
Ratos
Ratos Sprague-Dawley
Espécies Reativas de Oxigênio/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Aggrecans); 0 (Collagen Type II); 0 (Free Radical Scavengers); 0 (Reactive Oxygen Species); S798V6YJRP (phenylmethylpyrazolone); T3CHA1B51H (Antipyrine)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171023
[Lr] Data última revisão:
171023
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170925
[St] Status:MEDLINE


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[PMID]:28806939
[Au] Autor:Redeker JI; Schmitt B; Grigull NP; Braun C; Büttner A; Jansson V; Mayer-Wagner S
[Ad] Endereço:Department of Orthopaedic Surgery, Physical Medicine and Rehabilitation, Ludwig-Maximilians-University, Munich, Germany.
[Ti] Título:Effect of electromagnetic fields on human osteoarthritic and non-osteoarthritic chondrocytes.
[So] Source:BMC Complement Altern Med;17(1):402, 2017 Aug 14.
[Is] ISSN:1472-6882
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Studies of the effects of electromagnetic fields (EMFs) on cartilaginous cells show a broad range of outcomes. However EMFs are not yet clinically applied as standard treatment of osteoarthritis, as EMF effects are showing varying outcomes in the literature. The aim of this study was to examine effects of EMFs (5 mT or 8 mT) on osteoarthritic (OA) and non-OA chondrocytes in order to investigate whether EMF effects are related to chondrocyte and EMF quality. METHODS: Pellets of human OA and non-OA chondrocytes were exposed to a sinusoidal 15 Hz EMF produced by a solenoid. Control groups were cultivated without EMF under standard conditions for 7 days. Cultures were examined by staining, immunohistochemistry and quantitative real-time PCR for RNA corresponding to cartilage specific proteins (COL2A1, ACAN, SOX9). RESULTS: OA chondrocytes increased the expression of COL2A1 and ACAN under 5 mT EMF compared to control. In contrast no changes in gene expression were observed in non-OA chondrocytes. OA and non-OA chondrocytes showed no significant changes in gene expression under 8 mT EMF. CONCLUSION: A 5 mT EMF increased the expression of cartilage specific genes in OA chondrocytes whereas in non-OA chondrocytes no changes in gene expression were observed. An 8 mT EMF however showed no effect altogether. This suggests that EMF effects are related to EMF but also to chondrocyte quality. Further studies about the clinical relevance of this effect are necessary.
[Mh] Termos MeSH primário: Agrecanas/metabolismo
Cartilagem Articular/citologia
Condrócitos
Colágeno Tipo II/metabolismo
Campos Eletromagnéticos
Osteoartrite
[Mh] Termos MeSH secundário: Células Cultivadas
Expressão Gênica
Seres Humanos
Imuno-Histoquímica
Terapia de Campo Magnético
Osteoartrite/metabolismo
Osteoartrite/terapia
Reação em Cadeia da Polimerase em Tempo Real
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (ACAN protein, human); 0 (Aggrecans); 0 (COL2A1 protein, human); 0 (Collagen Type II)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170901
[Lr] Data última revisão:
170901
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170816
[St] Status:MEDLINE
[do] DOI:10.1186/s12906-017-1868-z



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