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长非编码RNADLEU1通过miR-492/TLR8轴促进骨关节炎的进展

Chenzhe Ni¹, Wanglin Zhang², Sai Qiu¹

¹Department of Orthopaedics, Qidong People's Hospital, Nantong University, Jiangsu, 226200, China.

Current pharmaceutical biotechnology

|February 7, 2024

概括

长非编码RNA DLEU1通过通过miR-492/TLR8轴影响细胞活力,细胞亡和细胞外基质降解来促进骨关节炎. 这项研究阐明了OA发展中的关键分子机制.

科学领域:

分子生物学分子生物学
遗传学是一个遗传学.
生物化学生化学

背景情况:

骨关节炎 (OA) 的发病包括长非编码RNAs (lncRNAs),作为竞争的内源RNAs (ceRNAs).
在OA中 lncRNA参与的精确分子机制在很大程度上仍未被阐明.
这项研究研究了 lncRNAs 在OA发展中的作用.

研究的目的:

探索骨关节炎 (OA) 发展的分子机制.
构建与OA相关的竞争性内源RNA (ceRNA) 网络.
为了研究DLEU1在OA病变发生过程中的功能.

主要方法:

整合了OA患者的基因表达特征,以确定关键的RNA.
使用IL-1β治疗的红细胞构建了一个ceRNA网络和一个体外OA模型.
评估了细胞活力,细胞亡,细胞外矩阵 (ECM) 降解,并使用qRT-PCR,西斑,CCK-8,流细胞计和双光酶记者测定验证了分子相互作用.

主要成果:

建立了一个与OA相关的ceRNA网络,包括11个途径,3个miRNA,7个lncRNA和16个mRNA.
在IL-1β诱导的冠状细胞中,DLEU1和TLR8的调节上升,而miR-492的调节下降.
DLEU1过度表达损害了冠状细胞活力,增加了细胞亡,并促进了ECM降解,miR-492可逆效应,证实了DLEU1/miR-492/TLR8调节轴.

结论:

DLEU1在调节冠状细胞活力,细胞亡和OCM降解方面发挥着重要作用.
miR-492/TLR8轴是DLEU1在OA中发挥作用的关键途径.
DLEU1代表了骨关节炎的潜在治疗标.

关键词:

DLEU1 欧盟法令第1号骨关节炎是一种骨关节炎.在TLR8中,竞争的内源RNA. 竞争的内源RNA.在 miR-492 里,权重的基因共同表达网络分析.

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