|
|
|
| Effect of miR-153-3p Targeted Regulation of CHI3L1 on the Inflammatory Response of LPS-Induced Human Periodontal Ligament Stem Cells |
| FAN Jing, et al |
| The Second Affiliated Hospital of Xi'an Medical University, Shaanxi Xi'an 710038, China |
|
|
|
|
Abstract Objective: To explore whether miR-153-3p can improve the inflammatory response of human periodontal ligament stem cells (hPDLSCs) induced by lipopolysaccharide (LPS) by targeting regulates chitinase 3-like protein 1 (CHI3L1). Methods: The hPDLSCs were isolated and cultured, and inflammatory cell models were established using LPS treatment and transfected with miR-NC, miR-153-3p mimics, si-NC, si-CHI3L1, and miR-153-3p mimics+pc-NC, miR-153-3p mimics+pcDNA-CHI3L1. 48 h after transfection, the expressions of miR-153-3p and CHI3L1 mRNA in the cells of each group were detected by qRT-PCR, the levels of IL-6, IL-1β and TNF-α in the cell supernatant were detected by ELISA, cell apoptosis was detected by flow cytometry, the expression of CHI3L1 protein in cells was detected by Western Blot, the targeting relationship between miR-153-3p and CHI3L1 was detected by dual-luciferase reporter gene assay. Results: The expression of miR-153-3p was down-regulated in hPDLSCs after LPS treatment (P<0.05), while the expressions of CHI3L1 mRNA and protein were significantly up-regulated (P<0.05); over-expression of miR-153-3p or inhibition of CHI3L1 expression could reduce the levels of IL-6, IL-1β and TNF-α in LPS-induced hPDLSCs, down-regulate the expressions of CHI3L1 mRNA and protein, and reduce the apoptosis rate, and the differences were statistically significant (P<0.05). The dual-luciferase reporter gene assay confirmed that miR-153-3p could targeting regulates the expression of CHI3L1 (P<0.05). In addition, the over-expression of CHI3L1 could significantly reverse the inhibitory effects of the over-expression of miR-153-3p on LPS-induced apoptosis and inflammatory response of hPDLSCs (P<0.05). Conclusion: MiR-153-3p can reduce the LPS-induced inflammatory response and apoptosis of hPDLSCs by targeting regulates CHI3L1 expression.
|
|
|
|
|
|
[1] Larsson L,Garaicoa-pazmino C,Asa'ad F,et al.Understanding the role of endotoxin tolerance in chronic inflammatory conditions and periodontal disease[J].Clin Periodontol,2022,49(3):270-279.
[2] Liu J,Ruan J,Weir MD,et al.Periodontal bone-ligament-cementum regeneration via scaffolds and stem cells[J].Cells,2019,8(6):537.
[3] Luan W,Shi Y,Zhou Z,et al.Corrigendum to circRNA_0084043 promote malignant melanoma progression via miR-153-3p/Snail axis[J].Biochem Biophys Res Commun,2022,587:168-169.
[4] 李晓文,王后红,黄海,等.CHI3L1通过激活TGF-β信号通路促进肝细胞肝癌进展及分子机制[J].中国现代医生,2019,57(34):31-34.
[5] 高芸,孙斌.血清CHI3L1、CGRP、IL-23在慢性牙周炎患者中的表达及在病情、疗效评价中的作用探讨[J].实用口腔医学杂志,2019,35(6):851-855.
[6] 冯娜,李珂,邵江红.miR-146a在人炎症牙周膜干细胞中的表达及其与TLR4靶向调控作用的研究[J].牙体牙髓牙周病学杂志,2018,28(1):1-5.
[7] 孔晨,李永丽,李思佳,等.牙周炎动物模型的研究进展[J].医学综述,2019,25(17):3344-3349.
[8] Carvalho JS,Ramadan D,De Paiva Gonc Alves V,et al.Impact of citrus flavonoid supplementation on inflammation in lipopolysaccharide-induced periodontal disease in mice[J].Food Funct,2021,12(11):5007-5017.
[9] 吴雪,段少宇,梁萍,等.miR-34a靶向STAT1基因调控牙周膜细胞增殖及凋亡的分子机制[J].中国美容医学,2021,30(4):115-118.
[10] Guo J,LI J,Zhang J,et al.LncRNA PVT1 knockdown alleviated ox-LDL-induced vascular endothelial cell injury and atherosclerosis by miR-153-3p/GRB2 axis via ERK/p38 pathway[J].Nutr Metab Cardiovasc Dis,2021,31(12):3508-3521. |
|
|
|
2023, Vol. 29 
