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Condition: Osteoarthritis

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Total 352 results found since Jan 2013.

MicroRNA-320c inhibits development of osteoarthritis through downregulation of canonical Wnt signaling pathway
Publication date: Available online 8 May 2019Source: Life SciencesAuthor(s): Shu Hu, Guping Mao, Ziji Zhang, Peihui Wu, Xingzhao Wen, Weiming Liao, Zhiqi ZhangAbstractAimsOsteoarthritis (OA) is a leading cause of deformity in aging people. Emerging evidence suggests that microRNAs and Wnt signaling pathway are associated with its pathogenesis. We aimed to determine whether microRNA-320c inhibits the development of osteoarthritis by suppressing Wnt signaling pathway.Materials and methodsMiR-320c and β-catenin expression was assessed in human adipose derived stem cells (hADSCs) model of chondrogenesis and in normal and OA p...
Source: Life Sciences - May 8, 2019 Category: Biology Source Type: research

SOX11 promotes osteoarthritis through induction of TNF- α.
CONCLUSION: Inhibition of SOX11 could improve IL-1β-induced OA like phenomenon in CHON-001 cells, which suggesting SOX11 played an important role during the pathogenesis of OA. Thus, we hypothesized that SOX11 could be a potential target for the treatment of patients with OA. PMID: 31078342 [PubMed - as supplied by publisher]
Source: Pathology, Research and Practice - May 5, 2019 Category: Pathology Authors: Xu S, Yu J, Wang Z, Ni C, Xia L, Tang T Tags: Pathol Res Pract Source Type: research

TNF- α/calreticulin dual signaling induced NLRP3 inflammasome activation associated with HuR nucleocytoplasmic shuttling in rheumatoid arthritis
ConclusionsTNF- α/CRT dual signaling induced NLRP3 inflammasome activation, which could be suppressed by HuR knockdown presumably due to the block of HuR translocating from nucleus to cytoplasma.
Source: Inflammation Research - May 21, 2019 Category: Research Source Type: research

Cyclin D1 regulates osteoarthritis chondrocyte apoptosis via WNT3/ β-catenin signalling.
Conclusions: Cyclin D1 regulated chondrocyte proliferation and apoptosis through Wnt3/β-catenin instead of Wnt10a/β-catenin signalling pathway. PMID: 31155960 [PubMed - in process]
Source: Artificial Cells, Nanomedicine and Biotechnology - June 4, 2019 Category: Biotechnology Tags: Artif Cells Nanomed Biotechnol Source Type: research

Dihydroartemisinin derivative DC32 inhibits inflammatory response in osteoarthritic synovium through regulating Nrf2/NF- κB pathway.
In conclusion, DC32 inhibited the inflammatory response in osteoarthritic synovium through regulating Nrf2/NF-κB pathway and attenuated OA. In this way, DC32 may be a potential agent in the treatment of OA. PMID: 31228817 [PubMed - as supplied by publisher]
Source: International Immunopharmacology - June 18, 2019 Category: Allergy & Immunology Authors: Li YN, Fan ML, Liu HQ, Ma B, Dai WL, Yu BY, Liu JH Tags: Int Immunopharmacol Source Type: research

Directed elimination of senescent cells attenuates development of osteoarthritis by inhibition of c-IAP and XIAP
Publication date: Available online 26 June 2019Source: Biochimica et Biophysica Acta (BBA) - Molecular Basis of DiseaseAuthor(s): Wang Peilin, Teng Songsong, Zhuang Chengyu, Cui Zhi, Ma Chunhui, Yu Yinxian, Zhou Lei, Mao Min, Wang Zongyi, Yang Mengkai, Xu Jing, Zhang Tao, Wang Zhuoying, Yin Fei, Yi ChengqingAbstractAging drives the accumulation of senescent cells (SnCs) by secreting factors that cause the senescence-associated secretory phenotype (SASP), including stem cells in the bone marrow, which contribute to aging-related bone degradation. Osteoarthritis (OA) is a serious chronic injury disease, and increasing age is...
Source: Biochimica et Biophysica Acta (BBA) Molecular Basis of Disease - June 27, 2019 Category: Molecular Biology Source Type: research

Eupatilin protects chondrocytes from apoptosis via activating sestrin2-dependent autophagy.
Abstract Cartilage degradation is the main characterization of osteoarthritis (OA). Accumulating evidence suggests that chondrocyte apoptosis and autophagy are associated with cartilage degradation. Thus, we investigated the protective effect and underlying mechanism of eupatilin for treating OA. IL-1β was used to simulate OA in vitro. Data show that eupatilin treatment attenuated IL-1β-induced apoptosis of chondrocytes. Autophagy was also activated by eupatilin in a dose-dependent manner. Then, pretreatment with chloroquine (CQ), an autophagic inhibitor, decreased eupatilin-induced autophagy and increased apopt...
Source: International Immunopharmacology - July 11, 2019 Category: Allergy & Immunology Authors: Lou Y, Wu J, Liang J, Yang C, Wang K, Wang J, Guo X Tags: Int Immunopharmacol Source Type: research

miR-940 regulates the inflammatory response of chondrocytes by targeting MyD88 in osteoarthritis.
In conclusion, the pathogenesis of OA can be regulated by miR-940/MyD88 axis, which can be achieved through the combined signaling mechanism of MyD88/NF-κB signaling, induced with the help of IL-1β. PMID: 31435813 [PubMed - as supplied by publisher]
Source: Molecular and Cellular Biochemistry - August 20, 2019 Category: Biochemistry Authors: Cao J, Liu Z, Zhang L, Li J Tags: Mol Cell Biochem Source Type: research

Down-regulation of MiR-138-5p Protects Chondrocytes ATDC5 and CHON-001 from IL-1 β-induced Inflammation Via Up-regulating SOX9.
CONCLUSION: miR-138-5p can arrest the proliferation and migration of CHON-001 and ATDC5 via restraining SOX9, and facilitate the apoptosis and inflammation. This study revealed the protective effect of down-regulated miR-138-5p on inflammatory injury of chondrocytes caused by IL-1β. PMID: 31486753 [PubMed - as supplied by publisher]
Source: Current Pharmaceutical Design - September 4, 2019 Category: Drugs & Pharmacology Authors: Chunlei H, Chang Z, Sheng L, Yanchun Z, Lulin L, Daozhang C Tags: Curr Pharm Des Source Type: research

15-Lipoxygenase-1 in osteoblasts promotes TGF-β1 expression via inhibiting autophagy in human osteoarthritis
ConclusionIn the present study, our findings suggested that 15-Lipoxygenase-1 in Osteoblasts Promotes TGF-β1 expression via inhibiting autophagy in human Osteoarthritis. These novel results suggested that 15-Lipoxygenase-1 expressed by subchondral bone osteoblasts might be a promising therapeutic target in human OA.Graphical abstract
Source: Biomedicine and Pharmacotherapy - November 5, 2019 Category: Drugs & Pharmacology Source Type: research

Elevated levels of 15-lipoxygenase-1 contribute to the abnormal phenotypes of osteoblasts in human osteoarthritis
In conclusion, our results suggested that the expression of 15-LOX-1 on osteoblasts from the subchondral bone increased in OA. 15-LOX-1 inhibited autophagy by activated mTORC1, which in turn upregulated the markers of abnormal osteoblast phenotypes RUNX2, COL1, and OCN.
Source: Life Sciences - November 6, 2019 Category: Biology Source Type: research

The pro-inflammatory effect of NR4A3 in osteoarthritis.
In this study, high expression of NR4A3 in human osteoarthritis (OA) cartilage was firstly observed. To explore the relationship between NR4A3 and OA, we used a lentivirus overexpression system to simulate its high expression and study its role in OA. Additionally, siRNA-mediated knockdown of NR4A3 was used to confirm the findings of overexpression experiments. The results showed the stimulatory effect of IL-1β on cartilage matrix-degrading enzyme expression such as MMP-3, 9, INOS and COX-2 was enhanced in NR4A3-overexpressed chondrocytes and decreased in NR4A3-knockdown chondrocytes at both mRNA and protein levels, while...
Source: J Cell Mol Med - November 6, 2019 Category: Molecular Biology Authors: Ma C, Wu L, Song L, He Y, Adel Abdo Moqbel S, Yan S, Sheng K, Wu H, Ran J, Wu L Tags: J Cell Mol Med Source Type: research

15-Lipoxygenase-1 in osteoblasts promotes TGF- β1 expression via inhibiting autophagy in human osteoarthritis.
CONCLUSION: In the present study, our findings suggested that 15-Lipoxygenase-1 in Osteoblasts Promotes TGF-β1 expression via inhibiting autophagy in human Osteoarthritis. These novel results suggested that 15-Lipoxygenase-1 expressed by subchondral bone osteoblasts might be a promising therapeutic target in human OA. PMID: 31704612 [PubMed - as supplied by publisher]
Source: Biomedicine and pharmacotherapy = Biomedecine and pharmacotherapie - November 4, 2019 Category: Drugs & Pharmacology Authors: Wan Y, Lv Y, Li L, Yin Z Tags: Biomed Pharmacother Source Type: research

MiR-203 regulates estrogen receptor α and cartilage degradation in IL-1β-stimulated chondrocytes
ConclusionsMiR-203 is critical in the onset and progression of OA, at least in part, caused by estrogen deficiency and ER α instability in OA patients, providing a novel therapeutic target for the treatment of OA.
Source: Journal of Bone and Mineral Metabolism - December 31, 2019 Category: Orthopaedics Source Type: research

AMD3100 Attenuates Post-Traumatic Osteoarthritis by Maintaining Transforming Growth Factor- β1-Induced Expression of Tissue Inhibitor of Metalloproteinase-3 via the Phosphatidylinositol 3-Kinase/Akt Pathway
In conclusion, inhibition of the CXCL12a/CXCR4 signaling axis maintained TIMP-3 expression via the PI3K/Akt pathway. Our findings provide insight into the mechanism by which AMD3100 prevents OA.
Source: Frontiers in Pharmacology - January 21, 2020 Category: Drugs & Pharmacology Source Type: research