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长链非编码RNA SNHG14的抑制通过吸附miR-137保护骨关节炎中的软骨细胞免受损伤。

Inhibition of LncRNA SNHG14 protects chondrocyte from injury in osteoarthritis via sponging miR-137.

作者信息

Zheng Dong, Yang Kaiyuan, Chen Tong, Lv Songwei, Wang Liangliang, Gui Jianchao, Xu Chao

机构信息

Department of Orthopedics, The Affiliated Changzhou No.2 People's Hospital with Nanjing Medical University, Changzhou, China.

Department of Orthopedics, The Nanjing First Hospital, Nanjing Medical University, Nanjing, China.

出版信息

Autoimmunity. 2023 Dec;56(1):2270185. doi: 10.1080/08916934.2023.2270185. Epub 2023 Oct 17.

DOI:10.1080/08916934.2023.2270185
PMID:37849308
Abstract

Long-chain noncoding small nucleolar RNA host gene 14 (LncRNA SNHG14) is highly expressed in various diseases and promotes diseases progression, but the role and mechanism of LncRNA SNHG14 on targeting miR-137 in promoting osteoarthritis (OA) chondrocyte injury remains unclear. To measure the expression of the LncRNAs SNHG14 and miR-137, cell survival, inflammatory response, chondrocyte apoptosis, and extracellular matrix (ECM) levels, we subjected human chondrocytes to a variety of lipopolysaccharide (LPS) concentrations. To measure the luciferase activity of SNHG14-WT and SNHG14-MUT transfected with miR-137 mimic or miR-NC mimic, luciferase reporter genes were utilized. The results showed that chondrocyte viability was significantly inhibited with LPS treatment and chondrocyte inflammatory response, apoptosis and extracellular matrix degradation were significantly increased. However, the above results were significantly reversed after LncRNA SNHG14 inhibition. The luciferase activity bound to miR-137 was decreased in SNHG14-WT group, but there was no change in SNHG14-mut group, which indicated that LncRNA SNHG14 inhibited miR-137 expression as a miRNA sponge. In conclusion, inhibition of LncRNA SNHG14 attenuates chondrocyte inflammatory response, apoptosis and extracellular matrix degradation by targeting miR-137 in LPS induced chondrocytes.

摘要

长链非编码小核仁RNA宿主基因14(LncRNA SNHG14)在多种疾病中高表达并促进疾病进展,但LncRNA SNHG14靶向miR - 137在促进骨关节炎(OA)软骨细胞损伤中的作用及机制尚不清楚。为了检测LncRNAs SNHG14和miR - 137的表达、细胞存活率、炎症反应、软骨细胞凋亡及细胞外基质(ECM)水平,我们将人软骨细胞置于多种脂多糖(LPS)浓度环境中。为了检测转染了miR - 137模拟物或miR - NC模拟物的SNHG14 - WT和SNHG14 - MUT的荧光素酶活性,我们利用了荧光素酶报告基因。结果显示,LPS处理显著抑制了软骨细胞活力,且软骨细胞炎症反应、凋亡及细胞外基质降解均显著增加。然而,抑制LncRNA SNHG14后,上述结果得到显著逆转。SNHG14 - WT组中与miR - 137结合的荧光素酶活性降低,但SNHG14 - mut组无变化,这表明LncRNA SNHG14作为一种miRNA海绵抑制了miR - 137的表达。总之,抑制LncRNA SNHG14可通过靶向LPS诱导的软骨细胞中的miR - 137减轻软骨细胞炎症反应、凋亡及细胞外基质降解。

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