Department of Operative Dentistry and Endodontics, Hospital of Stomatology, Guanghua School of Stomatology, Sun Yat-sen University, 56 Ling yuan Road West, Guangzhou, 510055, China.
Guangdong Provincial Key Laboratory of Stomatology, Guangzhou, China.
J Mol Histol. 2021 Oct;52(5):919-928. doi: 10.1007/s10735-021-10004-2. Epub 2021 Jul 26.
Lipopolysaccharides (LPS), which are components of the cell wall of Gram-negative bacteria, are among the important factors that induce inflammation, including pulpitis. Autophagy in human dental pulp cells (hDPCs) acts as a protective mechanism that promotes cell survival under adverse conditions through different signaling pathways. In this study, we examined whether LPS increases autophagy in hDPCs and investigated the role of mitogen-activated protein kinases signaling and nuclear factor κB (NF-κB) in this process. We found that stimulation of hDPCs with 0.1 µg/mL LPS increased the protein and mRNA levels of autophagy markers, beclin1 and microtubule associated protein light chain 3II (LC3II). In addition, acridine orange staining and transmission electron microscopy demonstrated the induction of autophagy upon the treatment of LPS. Furthermore, LPS affected phosphorylation of p38, extracellular signal-regulated kinase (ERK), and c-Jun N-terminal kinase (JNK), and the nuclear translocation of NF-κB. While p38 inhibitor suppressed the LPS-induced increase in protein levels of beclin1 and LC3-II. Our results suggest that LPS induced autophagy in hDPCs and affected the phosphorylation of p38, ERK, and JNK, as well as the nuclear translocation of NF-κB. Phosphorylation of p38 may be involved in LPS-induced autophagy in hDPCs.
脂多糖（LPS）是革兰氏阴性菌细胞壁的组成部分，是引起炎症的重要因素之一，包括牙髓炎。人牙髓细胞（hDPCs）中的自噬作为一种保护机制，通过不同的信号通路促进细胞在不利条件下的存活。在本研究中，我们研究了 LPS 是否会增加 hDPCs 中的自噬，并探讨了丝裂原活化蛋白激酶信号和核因子 κB（NF-κB）在这一过程中的作用。我们发现，用 0.1μg/mL LPS 刺激 hDPCs 会增加自噬标志物 beclin1 和微管相关蛋白轻链 3II（LC3II）的蛋白和 mRNA 水平。此外，吖啶橙染色和透射电子显微镜显示 LPS 处理后会诱导自噬。此外，LPS 影响 p38、细胞外信号调节激酶（ERK）和 c-Jun N-末端激酶（JNK）的磷酸化以及 NF-κB 的核转位。而 p38 抑制剂抑制了 LPS 诱导的 beclin1 和 LC3-II 蛋白水平的增加。我们的结果表明，LPS 诱导 hDPCs 中的自噬，并影响 p38、ERK 和 JNK 的磷酸化以及 NF-κB 的核转位。p38 的磷酸化可能参与了 LPS 诱导的 hDPCs 中的自噬。
