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微小 RNA-138 对肿瘤坏死因子-α诱导的牙髓干细胞成骨分化抑制作用及其机制。

Effect of MicroRNA-138 on Tumor Necrosis Factor-Alpha-Induced Suppression of Osteogenic Differentiation of Dental Pulp Stem Cells and Underlying Mechanism.

机构信息

Department of Stomatology, The Second Affiliated Hospital of Guangzhou Medical University, Guangzhou, 510260 Guangdong, China.

出版信息

Biomed Res Int. 2022 Jul 8;2022:7230167. doi: 10.1155/2022/7230167. eCollection 2022.

DOI:10.1155/2022/7230167
PMID:35845957
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9286885/
Abstract

High doses of tumor necrosis factor- (TNF-) suppress osteogenic differentiation of human dental pulp stem cells (hDPSCs). In the present study, we aimed to explore the role and potential regulatory mechanism of microRNA-138 (miR-138) in the osteogenic differentiation of hDPSCs after treatment with a high dose of TNF-. The hDPSCs were cultured in osteogenic medium with or without 50 ng/ml TNF-. The miR-138 levels were upregulated during osteogenic differentiation of the hDPSCs following TNF- treatment. The miR-138 overexpression accelerated but miR-138 knockdown alleviated the TNF--induced suppression of the alkaline phosphatase activity, calcium deposition, and protein abundance of dentin sialophosphoprotein, dentin matrix protein 1, bone sialoprotein, and osteopontin during osteogenic differentiation induction of hDPSCs. Additionally, miR-138 overexpression accelerated but miR-138 knockdown alleviated the suppression of the focal adhesion kinase- (FAK-) extracellular signal-regulated kinase 1/2 (ERK1/2) signaling pathway during osteogenic differentiation induction of hDPSCs under TNF- treatment. In conclusion, miR-138 accelerates TNF--induced suppression of osteogenic differentiation of hDPSCs. Inactivation of the FAK-ERK1/2 signaling pathway may be one of the mechanisms underlying the effect of miR-138. Inhibition of miR-138 expression may be a strategy to weaken the inhibitory effect of high-dose TNF- on the osteogenic differentiation of hDPSCs.

摘要

高剂量肿瘤坏死因子- (TNF-) 可抑制人牙髓干细胞 (hDPSCs) 的成骨分化。本研究旨在探讨 microRNA-138 (miR-138) 在 hDPSCs 经高剂量 TNF- 处理后成骨分化中的作用及其潜在调控机制。将 hDPSCs 在成骨培养基中培养，或在含有 50ng/ml TNF- 的成骨培养基中培养。hDPSCs 在 TNF- 处理后成骨分化过程中 miR-138 水平上调。miR-138 过表达加速但 miR-138 敲低减轻了 TNF-诱导的碱性磷酸酶活性、钙沉积和牙本质涎磷蛋白、牙本质基质蛋白 1、骨唾液蛋白和骨桥蛋白的蛋白丰度在 hDPSCs 成骨分化诱导中的抑制作用。此外，miR-138 过表达加速但 miR-138 敲低减轻了 TNF-处理下 hDPSCs 成骨分化诱导中粘着斑激酶- (FAK-) 细胞外信号调节激酶 1/2 (ERK1/2) 信号通路的抑制作用。综上所述，miR-138 加速了 TNF-诱导的 hDPSCs 成骨分化抑制。FAK-ERK1/2 信号通路失活可能是 miR-138 作用的机制之一。抑制 miR-138 表达可能是削弱高剂量 TNF-对 hDPSCs 成骨分化抑制作用的策略。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bd9c/9286885/fec579964c20/BMRI2022-7230167.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bd9c/9286885/3bbfd8f53831/BMRI2022-7230167.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bd9c/9286885/36dc547b68b4/BMRI2022-7230167.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bd9c/9286885/50c0c3f9d197/BMRI2022-7230167.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bd9c/9286885/fec579964c20/BMRI2022-7230167.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bd9c/9286885/3bbfd8f53831/BMRI2022-7230167.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bd9c/9286885/36dc547b68b4/BMRI2022-7230167.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bd9c/9286885/50c0c3f9d197/BMRI2022-7230167.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bd9c/9286885/fec579964c20/BMRI2022-7230167.004.jpg

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