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MicroRNA-101a-3p could be involved in the pathogenesis of temporomandibular joint osteoarthritis by mediating UBE2D1 and FZD4.
Mao, Dan; Wu, Mingsong; Wei, Jiying; Zhou, Xiangwen; Yang, Lan; Chen, Fang.
Afiliación
  • Mao D; Department of Prosthetics, The Affiliated Stomatology Hospital of Zunyi Medical University, Zunyi Medical University, Zunyi, China.
  • Wu M; Key Laboratory of Oral Disease Research in General Colleges and Universities of Guizhou Province, Zunyi Medical University, Zunyi, China.
  • Wei J; Department of Prosthetics, The Affiliated Stomatology Hospital of Zunyi Medical University, Zunyi Medical University, Zunyi, China.
  • Zhou X; Department of Prosthetics, The Affiliated Stomatology Hospital of Zunyi Medical University, Zunyi Medical University, Zunyi, China.
  • Yang L; Department of Prosthetics, The Affiliated Stomatology Hospital of Zunyi Medical University, Zunyi Medical University, Zunyi, China.
  • Chen F; Department of Prosthetics, The Affiliated Stomatology Hospital of Zunyi Medical University, Zunyi Medical University, Zunyi, China.
J Oral Pathol Med ; 50(2): 236-243, 2021 Feb.
Article en En | MEDLINE | ID: mdl-33187014
BACKGROUND: Temporomandibular joint osteoarthritis (TMJOA) is a degenerative disease that gradually affects the articular cartilage, synovium, and bone structure. To date, the molecular mechanism of TMJOA pathogenesis remains unclear. The aim of this study was to explore the biological function of the micro-ribonucleic acid 101a-3p (miR-101a-3p) and its role in TMJOA. METHODS: We detected the effect of interleukin-1ß (IL-1ß) on chondrocyte proliferation using Cell Counting Kit-8 (CCK-8) technology. Using quantitative polymerase chain reaction (qPCR), we detected transcription levels of miR-101a-3p in a rat model with TMJOA and inflamed chondrocytes, as well as in a group of normal rats. The effect of miR-101a-3p on apoptosis was examined in vitro using flow cytometry (FCM). We then analyzed the target of miR-101a-3p via bioinformatics and confirmed it using a luciferase reporter assay (LRA). RESULTS: We showed that IL-1ß could inhibit proliferation of chondrocytes. We found that miR-101a-3p levels were significantly lower in the rat inflammation model with TMJOA and inflamed chondrocytes than in the normal group. Additionally, miR-101a-3p substantially promoted apoptosis of chondrocytes, and both bioinformatic analyses and LRA found that this miRNA targeted the genes ubiquitin-conjugating enzyme 2D1 (UBE2D1) and Frizzled class receptor 4 (FZD4). CONCLUSION: Our results suggested that miR-101a-3p was involved in the pathogenesis of TMJOA and that its mechanism was probably interaction with its target genes UBE2D1 and FZD4.
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Osteoartritis / Cartílago Articular / MicroARNs Tipo de estudio: Etiology_studies Límite: Animals Idioma: En Revista: J Oral Pathol Med Asunto de la revista: ODONTOLOGIA / PATOLOGIA Año: 2021 Tipo del documento: Article País de afiliación: China Pais de publicación: Dinamarca
Texto completo
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Osteoartritis / Cartílago Articular / MicroARNs Tipo de estudio: Etiology_studies Límite: Animals Idioma: En Revista: J Oral Pathol Med Asunto de la revista: ODONTOLOGIA / PATOLOGIA Año: 2021 Tipo del documento: Article País de afiliación: China Pais de publicación: Dinamarca