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hsa_circ_0095812通过吸附miR-485-3p介导THBS1表达来加速牙周炎的进展

XiaoTing Xie¹, RuiTing Li¹, FangLin Mi¹

¹North Sichuan Medical College, Nanchong City, Sichuan Province, PR China.

Clinics (Sao Paulo, Brazil)

|April 12, 2025

概括

循环RNA circLRRC4C通过海绵化miR-485-3p促进牙周炎,导致血栓蛋白-1 (THBS1) 表达和炎症的增加. 抑制circLRRC4C可以缓解小鼠牙周炎.

科学领域:

口腔生物学口腔生物学
分子生物学分子生物学
免疫学免疫学免疫学

背景情况:

牙周炎是一种普遍的炎症性疾病,影响牙支结构.
循环RNAs (circRNAs) 正在成为各种疾病的关键调节者,包括炎症状况.
在牙周炎病原体中circLRRC4C的特定作用仍然在很大程度上未被探索.

研究的目的:

研究hsa_circ_0095812 (circLRRC4C) 在牙周炎中的作用.
阐明涉及miR-485-3p和Thrombospondin-1 (THBS1) 的潜在分子机制.

主要方法:

在人类牙周炎组织和由脂聚糖 (LPS) 刺激的牙周带细胞 (PDLCs) 中分析circLRRC4C表达.
在体外研究评估细胞活力,炎症,细胞亡和火细胞亡后circLRRC4C操纵.
在活体研究中,使用鼠标模式的牙周炎与有针对性的circLRRC4C干预.
分子分析包括qRT-PCR,西部斑点和miRNA-海绵测试,以确定调节关系.

主要成果:

在牙周炎组织和用LPS治疗的PDLC中,CircLRRC4C被显著上调.
循环LRRC4C的下调降低了LPS诱导的炎症,亡和烧亡,同时改善了细胞活力.
循环LRRC4C作为miR-485-3p的分子海绵,THBS1被确定为miR-485-3p的基因.
发现circLRRC4C/miR-485-3p/THBS1轴会加剧牙周炎,其抑制在小鼠模型中改善了病情.

结论:

循环LRRC4C通过海绵化miR-485-3p促进牙周炎的进展,从而调节Thrombospondin-1 (THBS1) 表达.
准circLRRC4C为牙周炎提供了一个潜在的治疗策略.

关键词:

牙周结节细胞牙周结节细胞牙周病是指牙周病的发生.在THBS1中,THBS1是THBS1.这是一个圆圈LRRC4CC.在 miR-485-3p 中使用.

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