MicroRNA-23a inhibits osteogenesis of periodontal mesenchymal stem cells by targeting bone morphogenetic protein signaling

• Published in: Archives of oral biology Vol. 102; pp. 93 - 100
• Main Authors: Zhang, Yuchen, Li, Shiying, Yuan, Shujing, Zhang, Huifeng, Liu, Jingying
• Format: Journal Article
• Language: English
• Published: England Elsevier Ltd 01.06.2019
• Subjects: Bone Morphogenetic Proteins; Cell Differentiation; Cells, Cultured; Chronic periodontitis; Gingival crevicular fluid; Humans; Mesenchymal Stem Cells; MicroRNAs - genetics; miR-23a; Osteogenesis; Periodontal Ligament; Periodontal mesenchymal stem cells; Stem Cells; Periodontal mesenchymal stem cells; BMP; Chronic periodontitis; miR-23a; BMPR1ABMPR1ABMPR1A; BMPR1B; Smad1/5/9; PDLSCs; Gingival crevicular fluid; Osteogenesis
• ISSN: 0003-9969; 1879-1506; 1879-1506
• DOI: 10.1016/j.archoralbio.2019.04.001

•MiR-23a increased in PDLSCs and gingival crevicular fluid of periodontitis patients.•miR-23a inhibited osteogenesis of PDLSCs.•miR-23a inhibited the phosphorylation of Smad1/5/9 via BMPR1B.•miR-23a may serve as a biomarker and potential target of periodontitis. To investigate the role of microRNA-23a (miR-23a) in the osteogenesis of periodontal mesenchymal stem cells (PDLSCs) in periodontitis. Gingival crevicular fluid samples were collected from 21 control subjects and 29 patients with chronic periodontitis. MiR-23a was determined by quantitative real-time PCR. PDLSCs were transfected with miR-23a overexpressing lentiviruses. Subsequently, PDLSCs were induced with osteogenic differentiation media. Osteogenic differentiation of PDLSCs was assessed by alkaline phosphatase activity assay, Alizarin red staining, and qRT-PCT detection of osteogenic gene expression. Western blot was performed to detect the protein levels of the SMAD family member 1/5/9 (Smad1/5/9) and their phosphorylation level. TargetScan was used to predict the target gene of miR-23a. Cotransfections of bone morphogenetic protein receptor type 1B (BMPR1B) and miR-23a applied to explore the relationship between BMPR1B and miR-23a. MiR-23a was significantly increased in PDLSCs and gingival crevicular fluid of periodontitis patients. Patients with gingival crevicular fluid miR-23a levels above a threshold showed more clinical indicators of periodontitis. After periodontal therapy, miR-23a levels significantly decreased. Overexpression miR-23a inhibited osteogenesis of PDLSCs, which was evidenced by reduced Alizarin Red S and osteogenic gene expressions. In addition, miR-23a inhibited the phosphorylation of Smad1/5/9. TargetScan predicted that BMPR1B is a target gene of miR-23a. Overexpression of BMPR1B abolished the effects caused by overexpression of miR-23a. Our study provides novel evidence that miR-23a acts as a negative regulator of osteogenesis in periodontitis patients’PDLSCs and that miR-23a may serve as a biomarker and potential target of periodontitis.