LncRNA MALAT1靶向miR-106a-5p/Smad7对IL-1β诱导的软骨细胞损伤的影响

doi:10.3969/j.issn.1006-6233.2025.07.09

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Abstract Objective: To investigate the impact of long non-coding RNA (LncRNA) metastasis associated lung adenocarcinoma transcript 1 (MALAT1) on interleukin-1β (IL-1β) -induced chondrocyte injury, and to determine whether it is related to microRNA-106a-5p (miR-106a-5p)/mother against decapentaplegic homolog 7 (Smad7). Methods: The human chondrocyte line C20/A4 was used as the research subject, and a chondrocyte injury model was induced by IL-1β. The cells were assigned into IL-1β group, IL-1β+sh-NC group, IL-1β+sh-MALAT1 group, IL-1β+sh-MALAT1+inhibitor NC group, and IL-1β+sh-MALAT1+miR-106a-5p inhibitor group. The control group was C20/A4 without IL-1β induction. QRT-PCR was performed to detect the mRNA expression of LncRNA MALAT1, miR-106a-5p, and Smad7. MTT and flow cytometry were performed to detect cell proliferation and apoptosis. ELISA was performed to detect IL-6, IL-8, and IL-10. Dual luciferase reporter assay was used to validate the targeting relationship between miR-106a-5p with LncRNA MALAT1 and Smad7. In addition, Western blot was used to detect apoptosis related proteins. Results: Compared with the control group, the IL-1β group showed increased LncRNA MALAT1, Smad7 mRNA expression, cell proliferation inhibition rate, apoptosis rate, IL-6, IL-8 levels, and Bax protein expression, and decreased miR-106a-5p expression, IL-10 level, and Bcl-2 protein expression (P<0.05). Compared with the IL-1β group and the IL-1β+sh-NC group, the IL-1β+sh-MALAT1 group had reduction in LncRNA MALAT1, Smad7 mRNA expression, cell proliferation inhibition rate, apoptosis rate, IL-6, IL-8 levels, and Bax protein expression, and elevation in miR-106a-5p expression, IL-10 level, and Bcl-2 protein expression (P<0.05). Compared with the IL-1β+sh-MALAT1 group and the IL-1β+sh-MALAT1+inhibitor NC group, the IL-1β+sh-MALAT1+miR-106a-5p inhibitor group showed no significant difference in LncRNA MALAT1 expression (P>0.05), reduced miR-106a-5p expression, IL-10 level, and Bcl-2 protein expression, and elevated Smad7 mRNA expression, cell proliferation inhibition rate, apoptosis rate, IL-6, IL-8 levels, and Bax protein expression (P<0.05). MALAT1 targeted the regulation of miR-106a-5p/Smad7 axis. Conclusion: Silencing MALAT1 can upregulate miR-106a-5p and inhibit Smad7, thereby promoting cell proliferation, inhibiting cell apoptosis and inflammatory response, and alleviating IL-1β - induced chondrocyte injury.

Key words： LncRNA MALAT1 miR-106a-5p/Smad7 IL-1β Chondrocyte

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http://www.hbyxzzs.cn/EN/10.3969/j.issn.1006-6233.2025.07.09 OR http://www.hbyxzzs.cn/EN/Y2025/V31/I7/1102

[1] Lu J,Bian J,Wang Y,et al.Oxymatrine protects articular chondrocytes from IL-1β-induced damage through autophagy activation via AKT/mTOR signaling pathway inhibition[J].Orthop Surg Res,2024,19(1):178-183.
[2] 宋超,王冶,蒲劲松,等.MALAT1通过调控miR-146a减轻关节软骨细胞凋亡和基质降解的研究[J].现代免疫学,2021,41(2):111-117.
[3] Tian F,Wang J,Zhang Z,et al.LncRNA SNHG7/miR-34a-5p/SYVN1 axis plays a vital role in proliferaton,apoptosis and autophagy in osteoarthritis[J].Biol Res,2020,53(1):9-19.
[4] Xu J,Xu Y.LncRNA MEG3 downregulation leads to osteoarthritis progression via miR-16/SMAD7 axis[J].Cell Biosci,2017,13(7):69-75.
[5] Chen W,Zheng H,Zhang X,et al.Columbianetin alleviates lipopolysaccharides(LPS)-induced inflammation and apoptosis in chondrocyte through activation of autophagy by inhibiting serum and glucocorticoid-induced protein kinase 1(SGK1) expression[J].Bioengineered,2022,13(2):4051-4062.
[6] 李伟,黄耀凯,王洪林,等.槲皮素通过下调MALAT1抑制膝骨关节炎小鼠软骨损伤及软骨细胞凋亡的相关机制[J].中华骨质疏松和骨矿盐疾病杂志,2023,16(1):33-40.
[7] Li H,Xie S,Li H,et al.LncRNA MALAT1 mediates proliferation of LPS treated-articular chondrocytes by targeting the miR-146a-PI3K/Akt/mTOR axis[J].Life Sci,2020,254(1):116801-116806.
[8] Danial NN.BCL-2 family proteins:critical checkpoints of apoptotic cell death[J].Clin Cancer Res,2007,13(24):7254-7263.
[9] Jiang L,Zhou X,Huang C,et al.The elevated expression of IL-38 serves as an anti-inflammatory factor in osteoarthritis and its protective effect in osteoarthritic chondrocytes[J].Int Immunopharmacol,2021,94(1):107489-107499.
[10] 杨利斌,杨林,赵恩典,等.miR-106a-5p过表达对ACLT诱导的骨关节炎大鼠软骨退变和细胞外基质降解的修复及血清炎症因子的影响[J].中国免疫学杂志,2021,37(13):1553-1557.
[11] Xiang Q,Wang J,Wang T,et al.Combination of baicalein and miR-106a-5p mimics significantly alleviates IL-1β-induced inflammatory injury in CHON-001 cells[J].Exp Ther Med,2021,21(4):345-352.
[12] Zheng C,Hoshi K,Hikita A.miR-92a-3p-inspired shRNA exhibits pro-chondrogenic and chondrocyte protective effects in osteoarthritis treatment through targeting SMAD6/7[J].Bone Miner Metab,2024,42(1):1-16.