scholarly journals IL-1β impedes the chondrogenic differentiation of synovial fluid mesenchymal stem cells in the human temporomandibular joint

2016 ◽  
Vol 39 (2) ◽  
pp. 317-326 ◽  
Author(s):  
Wenjing Liu ◽  
Yangpeng Sun ◽  
Yiqing He ◽  
Hong Zhang ◽  
Youhua Zheng ◽  
...  
Keyword(s):  
Stem Cells ◽  
Mesenchymal Stem Cells ◽  
Synovial Fluid ◽  
Temporomandibular Joint ◽  
Chondrogenic Differentiation

scholarly journals Effects of Interleukin-1β on Long Noncoding RNA and mRNA Expression Profiles of Human Synovial Fluid-derived Mesenchymal Stem Cells

2021 ◽  
Author(s):  
Yang-peng Sun ◽  
Yun-yang Lu ◽  
Jianyu Chen ◽  
Jia-hao Bao ◽  
Hong Zhang ◽  
...  
Keyword(s):  
Stem Cells ◽  
Mesenchymal Stem Cells ◽  
Synovial Fluid ◽  
Mrna Expression ◽  
Temporomandibular Joint ◽  
Long Noncoding Rna ◽  
Noncoding Rna ◽  
Expression Profiles ◽  
Biological Behavior ◽  
Antisense Lncrnas

Abstract Synovial fluid-derived mesenchymal stem cells (SFMSCs) play important regulatory roles in the physiological balance of the temporomandibular joint. Interleukin (IL)-1β regulates the biological behavior of SFMSCs; however, the effects of IL-1β on long noncoding RNA (lncRNA) and mRNA expression in SFMSCs in the temporomandibular joint are unclear. Here, we evaluated the lncRNA and mRNA expression profiles of IL-1β-stimulated SFMSCs. Using microarrays, we identified 286 lncRNAs (222 upregulated, 64 downregulated) and 304 mRNAs (242 upregulated, 62 downregulated) that were differentially expressed after treatment with IL-1β (fold change ≥ 2, P < 0.05). Kyoto Encyclopedia of Genes and Genomes pathway analysis found that one of the most significantly enriched pathways was the NF-κB pathway. Five paired antisense lncRNAs and mRNAs, eight paired enhancer lncRNAs and mRNAs, and nine paired long intergenic noncoding RNAs and mRNAs were predicted to be co-expressed. A network constructed by the top 30 k-score genes was visualized and evaluated. We found a co-expression relationship between ENST00000427824 and ENST00000307407 and between LOC541472 and IL6, which are related to NF-κB pathway activation. Overall, our results provide important insights into changes in lncRNA and mRNA expression in IL-1β-stimulated SFMSCs, which can facilitate the identification of potential therapeutic targets.

scholarly journals Indoleamine 2, 3 Dioxygenase 1 Impairs Chondrogenic Differentiation of Mesenchymal Stem Cells in the Joint of Osteoarthritis Mice Model

2021 ◽  
Vol 12 ◽  
Author(s):  
Murad Alahdal ◽  
Rongxiang Huang ◽  
Li Duan ◽  
Deng Zhiqin ◽  
Ouyang Hongwei ◽  
...  
Keyword(s):  
Stem Cells ◽  
Animal Model ◽  
Mesenchymal Stem Cells ◽  
Synovial Fluid ◽  
Transcriptome Sequencing ◽  
Chondrogenic Differentiation ◽  
Cartilage Regeneration ◽  
Mice Model ◽  
Indoleamine 2 ◽  
Cell Based Therapy

Osteoarthritis (OA) is a serious joint inflammation that leads to cartilage degeneration and joint dysfunction. Mesenchymal stem cells (MSCs) are used as a cell-based therapy that showed promising results in promoting cartilage repair. However, recent studies and clinical trials explored unsatisfied outcomes because of slow chondrogenic differentiation and increased calcification without clear reasons. Here, we report that the overexpression of indoleamine 2,3 dioxygenase 1 (IDO1) in the synovial fluid of OA patients impairs chondrogenic differentiation of MSCs in the joint of the OA mice model. The effect of MSCs mixed with IDO1 inhibitor on the cartilage regeneration was tested compared to MSCs mixed with IDO1 in the OA animal model. Further, the mechanism exploring the effect of IDO1 on chondrogenic differentiation was investigated. Subsequently, miRNA transcriptome sequencing was performed for MSCs cocultured with IDO1, and then TargetScan was used to verify the target of miR-122-5p in the SF-MSCs. Interestingly, we found that MSCs mixed with IDO1 inhibitor showed a significant performance to promote cartilage regeneration in the OA animal model, while MSCs mixed with IDO1 failed to stimulate cartilage regeneration. Importantly, the overexpression of IDO1 showed significant inhibition to Sox9 and Collagen type II (COL2A1) through activating the expression of β-catenin, since inhibiting of IDO1 significantly promoted chondrogenic signaling of MSCs (Sox9, COL2A1, Aggrecan). Further, miRNA transcriptome sequencing of SF-MSCs that treated with IDO1 showed significant downregulation of miR-122-5p which perfectly targets Wnt1. The expression of Wnt1 was noticed high when IDO1 was overexpressed. In summary, our results suggest that IDO1 overexpression in the synovial fluid of OA patients impairs chondrogenic differentiation of MSCs and cartilage regeneration through downregulation of miR-122-5p that activates the Wnt1/β-catenin pathway.

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