长链非编码 RNA FOXD2-AS1 通过海绵吸附 miR-27a-3p 诱导骨关节炎软骨细胞增殖。
LncRNA FOXD2-AS1 induces chondrocyte proliferation through sponging miR-27a-3p in osteoarthritis.
机构信息
a Department of Emergency, Changhai Hospital , Second Military Medical University , Shanghai , China.
b Department of Orthopedics, Changhai Hospital , Second Military Medical University , Shanghai , China.
出版信息
Artif Cells Nanomed Biotechnol. 2019 Dec;47(1):1241-1247. doi: 10.1080/21691401.2019.1596940.
Osteoarthritis (OA) is a common degenerative joint disease worldwide. Long non-coding RNAs (lncRNAs) have been widely confirmed to involve in the modulation of OA progression. However, the underlying mechanisms of lncRNA FOXD2-AS1 in OA remain unclear. In the present study, we showed FOXD2-AS1 expression was upregulated and positively associated with the severity of OA patients. IL-1β and/or TNF-α treatment could increase FOXD2-AS1 expression in chondrocytes. FOXD2-AS1 overexpression induced cell proliferation, inflammation and extracellular matrix (ECM) degradation in chondrocytes. Mechanistically, we found that FOXD2-AS1 upregulated the expression level of TLR4 by sponging miR-27a-3p. In addition, we revealed that miR-27a-3p mimics could abolish the effects of FOXD2-AS1 overexpression on cell proliferation, inflammation, and ECM degradation in chondrocytes. Therefore, we demonstrated that FOXD2-AS1 could play a crucial role in the progression of OA, at least partially, by regulating miR-27a-3p/TLR4 axis.
骨关节炎（OA）是一种全球范围内常见的退行性关节疾病。长链非编码 RNA（lncRNA）已被广泛证实参与 OA 进展的调控。然而，lncRNA FOXD2-AS1 在 OA 中的潜在机制尚不清楚。在本研究中，我们发现 FOXD2-AS1 的表达上调，并与 OA 患者的严重程度呈正相关。IL-1β和/或 TNF-α处理可增加软骨细胞中 FOXD2-AS1 的表达。FOXD2-AS1 的过表达可诱导软骨细胞增殖、炎症和细胞外基质（ECM）降解。机制上，我们发现 FOXD2-AS1 通过海绵吸附 miR-27a-3p 而上调 TLR4 的表达水平。此外，我们还揭示了 miR-27a-3p 模拟物可消除 FOXD2-AS1 过表达对软骨细胞增殖、炎症和 ECM 降解的影响。因此，我们证明 FOXD2-AS1 至少部分通过调节 miR-27a-3p/TLR4 轴在 OA 的进展中发挥关键作用。
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