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微小 RNA-122-3p 在作为长链非编码 RNA LINC00665 的靶标抑制关节炎进展中发挥作用。

MicroRNA-122-3p plays as the target of long non-coding RNA LINC00665 in repressing the progress of arthritis.

机构信息

Department of Rheumatology, Shouguang People's Hospital, Shouguang, Shandong, P.R. China.

Trauma orthopedics, The No. 4 hospital of Jinan, Jinan, Shandong, P.R. China.

出版信息

Bioengineered. 2022 May;13(5):13328-13340. doi: 10.1080/21655979.2022.2081757.

DOI:10.1080/21655979.2022.2081757
PMID:35635065
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9275898/
Abstract

MicroRNAs (miRNAs) play important roles in many diseases, including rheumatoid arthritis (RA). However, the mechanisms underlying the effects of miR-122-3p-3p on RA are not distinct and require further investigation. Patients with RA and healthy controls were recruited to analyze the miR-122-3p levels. The MH7A cells were stimulated with interleukin (IL)-1β to mimic the local inflammation of RA. Cell Counting Kit-8 (CCK-8) and flow cytometry were performed to measure the viability and apoptosis of MH7A cells. Diana tools and TargetScan were used to predict the target relationships. Luciferase reporter assay was used to validate the target relationship. miR-122-3p is downregulated in RA patients and IL-1β-stimulated MH7A cells. miR-122-3p suppresses MH7A cell viability and promotes MH7A cell apoptosis. miR-122-3p targets LINC00665. LINC00665 eliminates the inhibitory effect of miR-122-3p on IL-1β-stimulated MH7A cells. Eukaryotic translation initiation factor 2 alpha kinase 1 (EIF2AK1) targets miR-122-3p. In addition, EIF2AK1 is highly expressed in patients with RA. In addition, EIF2AK1 activates the mTOR signaling pathway. miR-122-3p represses RA progression by reducing cell viability and increasing synoviocyte apoptosis.

摘要

微小 RNA(miRNA)在许多疾病中发挥着重要作用,包括类风湿关节炎(RA)。然而,miR-122-3p-3p 对 RA 的影响机制尚不清楚,需要进一步研究。招募 RA 患者和健康对照者分析 miR-122-3p 水平。用白细胞介素(IL)-1β刺激 MH7A 细胞模拟 RA 的局部炎症。通过细胞计数试剂盒-8(CCK-8)和流式细胞术测量 MH7A 细胞的活力和凋亡。使用 Diana 工具和 TargetScan 预测靶关系。使用荧光素酶报告基因检测验证靶关系。miR-122-3p 在 RA 患者和 IL-1β 刺激的 MH7A 细胞中下调。miR-122-3p 抑制 MH7A 细胞活力并促进 MH7A 细胞凋亡。miR-122-3p 靶向 LINC00665。LINC00665 消除了 miR-122-3p 对 IL-1β 刺激的 MH7A 细胞的抑制作用。真核翻译起始因子 2α 激酶 1(EIF2AK1)靶向 miR-122-3p。此外,EIF2AK1 在 RA 患者中高表达。此外,EIF2AK1 激活 mTOR 信号通路。miR-122-3p 通过减少细胞活力和增加滑膜细胞凋亡来抑制 RA 进展。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c8c9/9275898/ffa593c162ad/KBIE_A_2081757_F0007_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c8c9/9275898/bd9c251123f7/KBIE_A_2081757_UF0001_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c8c9/9275898/0765f8905199/KBIE_A_2081757_F0001_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c8c9/9275898/fb9b4fcd2feb/KBIE_A_2081757_F0002_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c8c9/9275898/6a9b19b5700d/KBIE_A_2081757_F0003_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c8c9/9275898/1a5873ce5694/KBIE_A_2081757_F0004_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c8c9/9275898/90c9677a1e2c/KBIE_A_2081757_F0005_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c8c9/9275898/6200c565692d/KBIE_A_2081757_F0006_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c8c9/9275898/ffa593c162ad/KBIE_A_2081757_F0007_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c8c9/9275898/bd9c251123f7/KBIE_A_2081757_UF0001_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c8c9/9275898/0765f8905199/KBIE_A_2081757_F0001_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c8c9/9275898/fb9b4fcd2feb/KBIE_A_2081757_F0002_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c8c9/9275898/6a9b19b5700d/KBIE_A_2081757_F0003_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c8c9/9275898/1a5873ce5694/KBIE_A_2081757_F0004_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c8c9/9275898/90c9677a1e2c/KBIE_A_2081757_F0005_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c8c9/9275898/6200c565692d/KBIE_A_2081757_F0006_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c8c9/9275898/ffa593c162ad/KBIE_A_2081757_F0007_OC.jpg

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