长链非编码 RNA PRNCR1 通过海绵吸附 miR-377-3p 调控骨关节炎滑膜细胞的增殖和凋亡。
Long non-coding PRNCR1 regulates the proliferation and apoptosis of synoviocytes in osteoarthritis by sponging miR-377-3p.
机构信息
Department of Orthopaedics, The Affiliated Hospital of Southwest Medical University, Sichuan Provincial Laboratory of Orthopaedic Engineering, Luzhou City, Sichuan Province, 646000, People's Republic of China.
School of Pharmacy, Southwest Medical University, No. 319, Section 3, Zhongshan Road, Luzhou City, Sichuan Province, 646000, People's Republic of China.
出版信息
J Orthop Surg Res. 2022 Apr 14;17(1):238. doi: 10.1186/s13018-022-03035-2.
BACKGROUND
LncRNA PRNCR1 has been reported to be involved in LPS-induced inflammation, which contributes to osteoarthritis (OA). We predicted that miR-377-3p could bind to PRNCR1.MiR-377-3p can suppress OA development. We therefore analyzed the potential interaction between them in OA.
METHODS
Expression of miR-377-3p and PRNCR1 in both OA (n = 40) and control (n = 40) samples were analyzed by RT-qPCR. MiR-377-3p or PRNCR1 were overexpressed in synoviocytes to explore their potential interaction. The subcellular location of PRNCR1 was analyzed by nuclear fractionation assay. The direct interaction between miR-377-3p and PRNCR1 was analyzed by RNA-pull down assay. The proliferation and apoptosis of synoviocytes were analyzed by BrdU and apoptosis assay, respectively.
RESULTS
PRNCR1 was overexpressed in OA, while miR-377-3p was downexpressed in OA. PRNCR1 was detected in the cytoplasm and directly interacted with miR-377-3p. Interestingly, overexpression of PRNCR1 and miR-377-3p showed no regulatory role in each other's expression. LPS treatment increased PRNCR1 expression and decreased miR-377-3p expression. PRNCR1 overexpression decreased LPS-induced synoviocyte proliferation and increased LPS-induced synoviocyte apoptosis. MiR-377-3p played opposite roles in cell proliferation and apoptosis. Moreover, PRNCR1 suppressed the role of miR-377-3p.
CONCLUSIONS
Therefore, PRNCR1 is was detected in cytoplasm and regulates synoviocyte proliferation and apoptosis in OA by sponging miR-377-3p.
背景
长链非编码 RNA（lncRNA）PRNCR1 已被报道参与 LPS 诱导的炎症，这有助于骨关节炎（OA）的发生。我们预测 miR-377-3p 可以与 PRNCR1 结合。miR-377-3p 可以抑制 OA 的发展。因此，我们分析了它们在 OA 中的潜在相互作用。
方法
通过 RT-qPCR 分析 OA（n=40）和对照（n=40）样本中 miR-377-3p 和 PRNCR1 的表达。在滑膜细胞中过表达 miR-377-3p 或 PRNCR1 以探索它们的潜在相互作用。通过核分馏测定分析 PRNCR1 的亚细胞定位。通过 RNA 下拉测定分析 miR-377-3p 和 PRNCR1 之间的直接相互作用。通过 BrdU 和凋亡测定分别分析滑膜细胞的增殖和凋亡。
结果
PRNCR1 在 OA 中过表达，而 miR-377-3p 在 OA 中下调。PRNCR1 检测到在细胞质中，并与 miR-377-3p 直接相互作用。有趣的是，PRNCR1 和 miR-377-3p 的过表达彼此之间没有调节作用。LPS 处理增加了 PRNCR1 的表达，降低了 miR-377-3p 的表达。PRNCR1 的过表达降低了 LPS 诱导的滑膜细胞增殖，并增加了 LPS 诱导的滑膜细胞凋亡。miR-377-3p 在细胞增殖和凋亡中起相反的作用。此外，PRNCR1 抑制了 miR-377-3p 的作用。
结论
因此，PRNCR1 被检测到在细胞质中，并通过海绵 miR-377-3p 调节 OA 中的滑膜细胞增殖和凋亡。
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