Long Non-coding RNA DLEU1 Promotes Progression of Osteoarthritis via miR-492/TLR8 Axis
- Авторы: Ni C.1, Zhang W.2, Qiu S.1, Cheng H.1, Ma C.3
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Учреждения:
- Department of Orthopedic Surgery, Qidong Peoples Hospital, Nantong University
- Department of Orthopaedics, Shanghai Childrens Medical Center, Shanghai Jiaotong University School of Medicine
- Department of Orthopedic Surgery, Shanghai General Hospital, Shanghai Jiao Tong University
- Выпуск: Том 25, № 16 (2024)
- Страницы: 2166-2181
- Раздел: Biotechnology
- URL: https://gynecology.orscience.ru/1389-2010/article/view/645302
- DOI: https://doi.org/10.2174/0113892010275579240116061104
- ID: 645302
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Аннотация
Background:Long non-coding RNAs (LncRNAs) are generally reported to participate in the development of Osteoarthritis (OA) by acting as competing endogenous RNAs (ceRNAs). However, the molecular mechanism is largely unknown. This study aimed to investigate the possible mechanisms contributing to osteoarthritis (OA).
Methods:Four gene expression profiles from patients with OA were downloaded from a public database and integrated to screen important RNAs associated with OA. Differentially expressed (DE) lncRNAs, microRNAs (miRNAs), and mRNAs were filtered, and a ceRNA network was constructed. An in vitro OA model was established by treating chondrocytes with IL-1β. The expression levels of MMP-13, COL2A1, aggrecan, and RUNX2 were detected by qRT-PCR and western blot. Cell proliferation ability was detected by CCK-8 assay. Flow cytometry was used for apoptosis assay. A dual luciferase reporter gene was used to confirm the relationship between DLEU1, miR-492, and TLR8
Results:An OA-related ceRNA network, including 11 pathways, 3 miRNAs, 7 lncRNAs, and 16 mRNAs, was constructed. DLEU1 and TLR8 were upregulated, and miR-492 was downregulated in IL-1β-induced chondrocytes. Overexpression of DLEU1 suppressed viability and promoted apoptosis and extracellular matrix (ECM) degradation in IL-1β induced chondrocytes. Luciferase reporter assay validated the regulatory relations among DLEU1, miR-492, and TLR8. Further study revealed that the effects of DLEU1 on chondrocytes could be reversed by miR-492.
Conclusion:DLEU1 may be responsible for the viability, apoptosis, and ECM degradation in OA via miR-492/TLR8 axis
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Об авторах
Chenzhe Ni
Department of Orthopedic Surgery, Qidong Peoples Hospital, Nantong University
Email: info@benthamscience.net
Wanglin Zhang
Department of Orthopaedics, Shanghai Childrens Medical Center, Shanghai Jiaotong University School of Medicine
Email: info@benthamscience.net
Sai Qiu
Department of Orthopedic Surgery, Qidong Peoples Hospital, Nantong University
Автор, ответственный за переписку.
Email: info@benthamscience.net
Hao Cheng
Department of Orthopedic Surgery, Qidong Peoples Hospital, Nantong University
Автор, ответственный за переписку.
Email: info@benthamscience.net
Chunhui Ma
Department of Orthopedic Surgery, Shanghai General Hospital, Shanghai Jiao Tong University
Автор, ответственный за переписку.
Email: info@benthamscience.net
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