Journal
BONE & JOINT RESEARCH
Volume 9, Issue 10, Pages 689-700Publisher
BRITISH EDITORIAL SOC BONE & JOINT SURGERY
DOI: 10.1302/2046-3758.910.BJR-2020-0140.R1
Keywords
Temporomandibular jiont; Osteoarthritis; miR-21-5p; Growth differentiation factor 5; Interleukin-6
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Funding
- National Natural Science Foundation of China [61771290, 61871393]
- Science and Technology Development Plans of Shandong province [2018GSF118196]
- Natural Science Foundation of Shandong Province [ZR2018PH022, ZR2019PH015]
- China Postdoctoral Science Foundation [2019M652408]
- Jinan Science and Technology Plan [201907098]
- Fundamental Research Funds of Shandong University [2019GN091]
- [tsqn201812137]
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Aims The study aimed to determine whether the microRNA miR21-5p (MiR21) mediates temporo mandibular joint osteoarthritis (TMJ-OA) by targeting growth differentiation factor 5 (Gdf5). Methods TMJ-OA was induced in MiR21 knockout (KO) mice and wild-type (WT) mice by a unilateral anterior crossbite (UAC) procedure. Mouse tissues exhibited histopathological changes, as assessed by: Safranin O, toluidine blue, and immunohistochemistry staining; western blotting (WB); and quantitative real-time polymerase chain reaction (RT-qPCR). Mouse condylar chondrocytes were transfected with a series of MiR21 mimic, MiR21 inhibitor, Gdf5 siRNA (si-GDF5), and flag-GDF5 constructs. The effects of MiR-21 and Gdf5 on the expression of OA related molecules were evaluated by immunofluorescence, alcian blue staining, WB, and RT-qPCR. Results UAC altered the histological structure and extracellular matrix content of cartilage in the temporomandibular joint (TMJ), and KO of MiR21 alleviated this effect (p < 0.05). Upregulation of MiR21 influenced the expression of TMJ-OA related molecules in mandibular condylar chondrocytes via targeting Gdf5 (p < 0.05). Gdf5 overexpression significantly decreased matrix metalloproteinase 13 (MMP13) expression (p < 0.05) and reversed the effects of MiR21 (p < 0.05). Conclusion MiR21, which acts as a critical regulator of Gdf5 in chondrocytes, regulates TMJ-OA related molecules and is involved in cartilage matrix degradation, contributing to the progression of TMJ-OA.
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