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[PMID]:28467721
[Au] Autor:Sareila O; Hagert C; Kelkka T; Linja M; Xu B; Kihlberg J; Holmdahl R
[Ad] Endereço:1 Medicity Research Laboratory, University of Turku , Turku, Finland .
[Ti] Título:Reactive Oxygen Species Regulate Both Priming and Established Arthritis, but with Different Mechanisms.
[So] Source:Antioxid Redox Signal;27(18):1473-1490, 2017 Dec 20.
[Is] ISSN:1557-7716
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:AIMS: Neutrophil cytosolic factor 1 (NCF1) is a key regulatory component of the phagocytic NOX2 complex, which produces reactive oxygen species (ROS). Polymorphism of the Ncf1 gene is associated with increased arthritis severity. In this study, we generated targeted Ncf1 knock-in mice with inducible Ncf1 expression and determined the critical time window during which the NOX2-derived ROS protect the mice from arthritis. RESULTS: Targeted Ncf1 knock-in mice lacked NOX2-derived ROS, and in vivo allelic conversion of Ncf1 by the CreER recombinase led to full protein expression and ROS production within 10 days. Mice in which Ncf1 had been activated before immunization with type II collagen (CII) developed only mild clinical symptoms of collagen-induced arthritis (CIA), whereas the ROS-deficient littermates had severe arthritis. The functional Ncf1 restricted the expansion of IL-17A-producing T cells specific for the immunodominant CII peptide. When the Ncf1 gene was activated after the priming phase, Ncf1-dependent protection from autoimmune arthritis was still observed, together with a reduced number of splenic monocytes but it was not associated with alterations in peptide-specific T cell response. The Ncf1-deficient mice expressed pronounced interferon signature, which could be normalized by conditional expression of Ncf1 and was also present in the Ncf1-mutated mouse during arthritis. Innovation and Conclusion: Ncf1 deficiency has been known to predispose to autoimmunity in both humans and rodents. Our in vivo results point to a regulatory role of NOX2-derived ROS not only during priming but also during the effector phase of CIA, most likely via different mechanisms. Antioxid. Redox Signal. 27, 1473-1490.
[Mh] Termos MeSH primário: Artrite Experimental/metabolismo
NADPH Oxidases/genética
NADPH Oxidases/metabolismo
Espécies Reativas de Oxigênio/metabolismo
[Mh] Termos MeSH secundário: Animais
Artrite Experimental/induzido quimicamente
Artrite Experimental/genética
Colágeno Tipo II/efeitos adversos
Modelos Animais de Doenças
Técnicas de Introdução de Genes
Seres Humanos
Interleucina-17/metabolismo
Camundongos
Linfócitos T/imunologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Collagen Type II); 0 (Interleukin-17); 0 (Reactive Oxygen Species); EC 1.6.3.- (NADPH Oxidases); EC 1.6.3.1 (neutrophil cytosolic factor 1)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180309
[Lr] Data última revisão:
180309
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170504
[St] Status:MEDLINE
[do] DOI:10.1089/ars.2016.6981


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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]:29287118
[Au] Autor:Daghestani HN; Jordan JM; Renner JB; Doherty M; Wilson AG; Kraus VB
[Ad] Endereço:Duke Molecular Physiology Institute, Duke University School of Medicine, Durham, NC, United States of America.
[Ti] Título:Serum N-propeptide of collagen IIA (PIIANP) as a marker of radiographic osteoarthritis burden.
[So] Source:PLoS One;12(12):e0190251, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:OBJECTIVE: Cartilage homeostasis relies on a balance of catabolism and anabolism of cartilage matrix. Our goal was to evaluate the burden of radiographic osteoarthritis and serum levels of type IIA procollagen amino terminal propeptide (sPIIANP), a biomarker representing type II collagen synthesis, in osteoarthritis. METHODS: OA burden was quantified on the basis of radiographic features as total joint faces with an osteophyte, joint space narrowing, or in the spine, disc space narrowing. sPIIANP was measured in 1,235 participants from the Genetics of Generalized Osteoarthritis study using a competitive enzyme-linked immunosorbent assay. Separate multivariable linear regression models, adjusted for age, sex, and body mass index and additionally for ipsilateral osteophytes or joint/disc space narrowing, were used to assess the independent association of sPIIANP with osteophytes and with joint/disc space narrowing burden in knees, hips, hands and spine, individually and together. RESULTS: After full adjustment, sPIIANP was significantly associated with a lesser burden of hip joint space narrowing and knee osteophytes. sPIIANP was associated with a lesser burden of hand joint space narrowing but a greater burden of hand osteophytes; these results were only evident upon adjustment for osteoarthritic features in all other joints. There were no associations of sPIIANP and features of spine osteoarthritis. CONCLUSIONS: Higher cartilage collagen synthesis, as reflected in systemic PIIANP concentrations, was associated with lesser burden of osteoarthritic features in lower extremity joints (knees and hips), even accounting for osteoarthritis burden in hands and spine, age, sex and body mass index. These results suggest that pro-anabolic agents may be appropriate for early treatment to prevent severe lower extremity large joint osteoarthritis.
[Mh] Termos MeSH primário: Proteínas de Ligação ao Cálcio/sangue
Colágeno Tipo II/sangue
Osteoartrite/diagnóstico por imagem
[Mh] Termos MeSH secundário: Ensaio de Imunoadsorção Enzimática
Feminino
Seres Humanos
Masculino
Osteoartrite/sangue
Osteoartrite/patologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL
[Nm] Nome de substância:
0 (Calcium-Binding Proteins); 0 (Collagen Type II); 0 (chondrocalcin)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180207
[Lr] Data última revisão:
180207
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171230
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0190251


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[PMID]:29305974
[Au] Autor:Zhou ZB; Du D; Huang GX; Chen A; Zhu L
[Ad] Endereço:Department of Orthopaedic Trauma Surgery, Changzheng Hospital, Second Military Medical University, 415 Fengyang Road, Shanghai 200003, China.
[Ti] Título:Circular RNA Atp9b, a competing endogenous RNA, regulates the progression of osteoarthritis by targeting miR-138-5p.
[So] Source:Gene;646:203-209, 2018 Mar 10.
[Is] ISSN:1879-0038
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Osteoarthritis (OA) is the most common joint disease and is mainly characterized by degradation of the articular cartilage. Recently, circular RNAs (circRNAs), novel noncoding RNAs with different biological functions and pathological implications, have been reported to be closely associated with various diseases. Growing evidence indicates that circRNAs act as competing endogenous RNAs (ceRNAs) that bind with microRNAs (miRNAs) and regulate their downstream functions. Here, we identified a new circRNA, circRNA_Atp9b, and further investigated its function in OA using a well-established mouse chondrocyte model. We demonstrated that circRNA_Atp9b expression was significantly up-regulated in mouse chondrocytes after stimulation with interleukin-1 beta (IL-1ß), and that knockdown of circRNA_Atp9b promoted the expression of type II collagen while inhibiting the generation of MMP13, COX-2 and IL-6. Moreover, there was a negative correlation between the expression levels of circRNA_Atp9b and microRNA (miR)-138-5p, indicating that miR-138-5p also played a role in IL-1ß-induced chondrocytes. Bioinformatics analysis predicted circRNA_Atp9b directly target miR-138-5p, which was validated by dual-luciferase assay. Further functional experiments revealed that down-regulation of miR-138-5p partly reversed the effects of circRNA_Atp9b on extracellular matrix (ECM) catabolism and inflammation. Taken together, these results suggest that circRNA_Atp9b regulates OA progression by modulating ECM catabolism and inflammation in chondrocytes via sponging miR-138-5p. Our findings provide novel insight into the regulatory mechanism of circRNA_Atp9b in OA and may contribute to establishing potential therapeutic strategies.
[Mh] Termos MeSH primário: Cartilagem Articular/efeitos dos fármacos
Interleucina-1beta/farmacologia
MicroRNAs/genética
Osteoartrite/genética
RNA/genética
[Mh] Termos MeSH secundário: Animais
Sítios de Ligação
Cartilagem Articular/citologia
Cartilagem Articular/metabolismo
Linhagem Celular
Condrócitos/citologia
Condrócitos/efeitos dos fármacos
Condrócitos/metabolismo
Colágeno Tipo II/metabolismo
Progressão da Doença
Matriz Extracelular/efeitos dos fármacos
Matriz Extracelular/metabolismo
Regulação da Expressão Gênica/efeitos dos fármacos
Seres Humanos
Camundongos
Modelos Biológicos
Osteoartrite/induzido quimicamente
Osteoartrite/metabolismo
Regulação para Cima
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Collagen Type II); 0 (Interleukin-1beta); 0 (MIRN138 microRNA, mouse); 0 (MicroRNAs); 0 (RNA, circular); 63231-63-0 (RNA)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180202
[Lr] Data última revisão:
180202
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180107
[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


  9 / 4205 MEDLINE  
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[PMID]:28466810
[Au] Autor:Phull AR; Eo SH; Kim SJ
[Ad] Endereço:Department of Biological Sciences, College of Natural Sciences, Kongju National University, Gongju, Chungnam 32588, Republic of Korea.
[Ti] Título:Oleanolic acid (OA) regulates inflammation and cellular dedifferentiation of chondrocytes via MAPK signaling pathways.
[So] Source:Cell Mol Biol (Noisy-le-grand);63(3):12-17, 2017 Mar 31.
[Is] ISSN:1165-158X
[Cp] País de publicação:France
[La] Idioma:eng
[Ab] Resumo:Oleanolic acid (OA) is a bioactive triterpenoid in medicinal plants. It possesses various pharmacological properties, including analgesic, anti-inflammatory, and antitumor effects. The effects of OA in chondrocytes, however, are not well characterized. Here, we used rabbit articular chondrocytes as a cellular model to investigate the effects and regulatory mechanisms of OA on dedifferentiation and pro-inflammation. OA promoted dedifferentiation of chondrocytes by inhibiting type II collagen and pro-inflammatory activity by increasing cyclooxygenase-2 (COX-2) expression. Furthermore increased phosphorylation of p38 kinases and down-regulated phosphorylation of ERK was observed. Inhibition of p38 with SB203580 in OA-treated cells rescued the expression of type II collagen and suppressed the expression of COX-2. However, ERK inhibition with PD98059 accelerated the OA-induced inflammatory responses. These results suggest that OA induces loss of type II collagen expression via the p38 pathway and induces inflammation through the p38 and ERK pathways in rabbit articular chondrocytes.
[Mh] Termos MeSH primário: Condrócitos/enzimologia
Condrócitos/patologia
Inflamação/patologia
Sistema de Sinalização das MAP Quinases/efeitos dos fármacos
Ácido Oleanólico/farmacologia
[Mh] Termos MeSH secundário: Animais
Diferenciação Celular/efeitos dos fármacos
Proliferação Celular/efeitos dos fármacos
Condrócitos/efeitos dos fármacos
Condrócitos/metabolismo
Colágeno Tipo II/metabolismo
Ciclo-Oxigenase 2/metabolismo
Regulação para Baixo/efeitos dos fármacos
MAP Quinases Reguladas por Sinal Extracelular/metabolismo
Fluorescência
Modelos Biológicos
Ácido Oleanólico/química
Coelhos
Regulação para Cima/efeitos dos fármacos
Proteínas Quinases p38 Ativadas por Mitógeno/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Collagen Type II); 6SMK8R7TGJ (Oleanolic Acid); EC 1.14.99.1 (Cyclooxygenase 2); EC 2.7.11.24 (Extracellular Signal-Regulated MAP Kinases); EC 2.7.11.24 (p38 Mitogen-Activated Protein Kinases)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180115
[Lr] Data última revisão:
180115
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170504
[St] Status:MEDLINE
[do] DOI:10.14715/cmb/2017.63.3.3


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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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