Department of Stomatology, The Affiliated Hospital of Qingdao University, No. 16 Jiangsu Road, Shinan District, Qingdao 266000, Shandong, China.
Department of Stomatology, Qingdao Women and Children's Hospital. No. 6 Tongfu Road, Shibei District, Qingdao 266000, Shandong, China.
Biosci Rep. 2021 May 28;41(5). doi: 10.1042/BSR20210138.
MicroRNA-543-3p (miR-543-3p) has been reported to be involved in many human disease's progression, but its role in inflammation is still unclear. After bacterial infection, innate immune cells are activated to trigger inflammation by recognizing lipopolysaccharide (LPS) on the bacterial outer membrane. In our research, it showed that miR-543-3p was down-regulated in LPS-treated periodontal ligament cells (PDLCs). And it mediated the apoptosis of PDLC induced by LPS, which may be involved in periodontitis development. Besides, up-regulation of miR-543-3p alleviated the inflammatory damage induced by LPS. Furthermore, our research demonstrated Kruppel-like factor 6 (KLF6) served as a direct downstream target of miR-543-3p to play a vital role in periodontitis. Simply put, these findings suggest that miR-543-3p could down-regulate inflammation and inhibit periodontitis by targeting KLF6, and it provides a new insight into the molecular mechanism of periodontitis, which may be helpful for the early diagnosis and treatment of this disease.
微小 RNA-543-3p(miR-543-3p)已被报道参与多种人类疾病的进展,但它在炎症中的作用仍不清楚。在细菌感染后,先天免疫细胞通过识别细菌外膜上的脂多糖(LPS)而被激活,从而引发炎症。在我们的研究中,结果表明 miR-543-3p 在 LPS 处理的牙周韧带细胞(PDLCs)中下调。并且它介导 LPS 诱导的 PDLC 凋亡,这可能与牙周炎的发展有关。此外,miR-543-3p 的上调减轻了 LPS 诱导的炎症损伤。此外,我们的研究表明,Krüppel 样因子 6(KLF6)是 miR-543-3p 的直接下游靶标,在牙周炎中发挥重要作用。简而言之,这些发现表明,miR-543-3p 可以通过靶向 KLF6 下调炎症并抑制牙周炎,为牙周炎的分子机制提供了新的见解,这可能有助于该疾病的早期诊断和治疗。