Yuzhuo Wang,Ying Li,Pu Shao,Liuyi Wang,Xingfu Bao,Min Hu
Cementum regeneration is considered the gold standard for the treatment of periodontitis. As one of the most important primary proinflammatory cytokines, interleukin 1β (IL1β) plays an essential role during the early stage of periodontitis and its amounts simultaneously increase dramatically during this stage. Though promising, the differentiation of cementoblasts upon IL1β-induced inflammation of the microenvironment and the relative interaction mechanism are still unknown. Here, we found that IL1β inhibited cementoblast differentiation and microRNA-325-3p (miR-325-3p) was increased during IL1β-stimulated cementoblasts. Bioinformatics analysis and luciferase reporter assay demonstrated miR-325-3p targeted runt-related transcription factor 2 directly. Transfection of miR-325-3p suppressed cementoblast differentiation in vitro and the formation of cementum-like tissues in vivo. The inhibitor of miR-325-3p could mitigate the above effects induced by IL1β. Accordingly, our finding suggests a critical role of miR-325-3p in linking inflammation to impaired cementum regeneration and provides a potential possibility for applying miR-325-3p inhibitors in the treatment of periodontitis-related bone loss.
Yan Penghui,Wu Xuejian,Liu Xiaokang,Cai Yingchun,Shao Chenglong,Zhu Guangduo
Microglial activation and inflammatory response played an important role in the secondary injury of spinal cord injury (SCI). Several microRNAs were associated with this procedure, but the underlying molecular mechanism was poorly understood. Sprague-Dawley (SD) rats were divided into four groups: SCI group ( n = 7), agomiR-325-3p group ( n = 7), and their control groups. Expression of miR-325-3p and proteins in epidermal growth factor receptor (EGFR)/mitogen-activated protein kinase (MAPK) signaling pathway was evaluated in microglia from SCI rats and primary microglia/BV2 cells activated by lipopolysaccharide (LPS). Concentrations of interleukin-1β (IL-1β) and tumor necrosis factor α (TNF-α) in supernatants were measured by ELISA. Low expression of miR-325-3p and activation of EGFR/MAPK was observed in microglia of SCI and LPS-induced primary microglia. Overexpression of miR-325-3p in LPS-induced BV2 cells inhibited microglial activation and release of TNF-α and IL-1β. Luciferase reporter assay confirmed that miR-325-3p negatively regulated EGFR by targeting its 3′-untranslated regions. Additionally, agomiR-325-3p inhibited the activation of microglia and EGFR/MAPK, alleviating the inflammatory response. These results indicated that miR-325-3p attenuated secondary injury after SCI through inhibition of EGFR/MAPK signaling pathway, the microglial activation, and the release of inflammatory cytokines, suggesting that miR-325-3p may be employed as a therapeutic target for SCI.
危险品化学品经营许可证（带存储）