Abstract:
AIMS:The study aimed to determine whether the microRNA miR21-5p (MiR21) mediates temporomandibular 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. Cite this article: Bone Joint Res 2020;9(10):689-700.
journal_name
Bone Joint Resjournal_title
Bone & joint researchauthors
Zhang A,Ma S,Yuan L,Wu S,Liu S,Wei X,Chen L,Ma C,Zhao Hdoi
10.1302/2046-3758.910.BJR-2020-0140.R1subject
Has Abstractpub_date
2020-10-01 00:00:00pages
689-700issue
10issn
2046-3758journal_volume
9pub_type
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journal_title:Bone & joint research
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journal_title:Bone & joint research
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journal_title:Bone & joint research
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更新日期:2018-05-05 00:00:00
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更新日期:2015-10-01 00:00:00