State Key Laboratory of Medical Proteomics, Beijing Proteome Research Center, National Center for Protein Sciences (Beijing), Beijing Institute of Lifeomics, Beijing, China.
Department of Oral Pathology, Peking University School and Hospital of Stomatology & National Center of Stomatology & National Clinical Research Center for Oral Diseases & National Engineering Research Center of Oral Biomaterials and Digital Medical Devices, Beijing, China.
Oral Dis. 2024 Sep;30(6):3951-3961. doi: 10.1111/odi.14826. Epub 2024 Jan 31.
To explore the effect of protein arginine methyltransferase 5 (PRMT5) on tooth extraction sockets healing, we established an extraction sockets model in osteoblast-conditional Prmt5 knockout mice. The results provided clues for promoting extraction sockets healing in clinical settings.
Maxillary first molars were extracted from 6 to 8-week-old mice to establish an extraction fossa model. Microcomputed tomography (Micro-CT), histology, and immunostaining assays were performed on samples harvested at 3-, 7-, and 14-day post-extraction. Prmt5-silenced cell lines were employed to explore the regulatory mechanisms underlying the osteigenic differentiation.
PRMT5 expression was higher in the early stage of socket healing. Micro-CT analysis showed that the percentage of new bone in the extraction sockets was lower in OC-Cre; Prmt5 mice than in the control group, consistent with Masson staining. We found that, Prmt5 deficiency delayed the osteogenesis during extraction socket healing, which might be achieved through the decrease of H4R3me2s in the Sp7 promoter region.
PRMT5 in osteoblasts may promote the differentiation of osteoblasts by regulating the Sp7 promoter H4R3me2s and participate in the healing of tooth extraction sockets.
为了探索精氨酸甲基转移酶 5(PRMT5)对拔牙窝愈合的影响,我们在成骨细胞条件性 Prmt5 敲除小鼠中建立了拔牙窝模型。结果为临床促进拔牙窝愈合提供了线索。
从 6 至 8 周龄的小鼠中取出上颌第一磨牙,建立拔牙窝模型。在拔牙后 3、7 和 14 天采集样本,进行微计算机断层扫描(Micro-CT)、组织学和免疫染色分析。采用 Prmt5 沉默细胞系探索成骨分化的调控机制。
PRMT5 在牙槽窝愈合的早期表达较高。Micro-CT 分析显示,在 OC-Cre;Prmt5 小鼠中的拔牙窝中,新骨的百分比低于对照组,与 Masson 染色结果一致。我们发现,Prmt5 缺失延迟了拔牙窝愈合过程中的成骨作用,这可能是通过 Sp7 启动子区域 H4R3me2s 的减少来实现的。
成骨细胞中的 PRMT5 可能通过调节 Sp7 启动子 H4R3me2s 促进成骨细胞的分化,并参与牙齿拔牙窝的愈合。