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PTX3 通过 HA/ITGB1/FAK/YAP1 信号通路促进牙骨质形成和牙胚细胞分化。

PTX3 promotes cementum formation and cementoblast differentiation via HA/ITGB1/FAK/YAP1 signaling pathway.

机构信息

State Key Laboratory of Oral & Maxillofacial Reconstruction and Regeneration, Key Laboratory of Oral Biomedicine Ministry of Education, Hubei Key Laboratory of Stomatology, School & Hospital of Stomatology, Wuhan University, Wuhan, Hubei 430079, China.

State Key Laboratory of Oral & Maxillofacial Reconstruction and Regeneration, Key Laboratory of Oral Biomedicine Ministry of Education, Hubei Key Laboratory of Stomatology, School & Hospital of Stomatology, Wuhan University, Wuhan, Hubei 430079, China.

出版信息

Bone. 2024 Oct;187:117199. doi: 10.1016/j.bone.2024.117199. Epub 2024 Jul 9.

DOI:10.1016/j.bone.2024.117199
PMID:38992453
Abstract

Cementum is a vital component of periodontium, yet its regeneration remains a challenge. Pentraxin 3 (PTX3) is a multifunctional glycoprotein involved in extracellular matrix remodeling and bone metabolism regulation. However, the role of PTX3 in cementum formation and cementoblast differentiation has not been elucidated. In this study, we initially observed an increase in PTX3 expression during cementum formation and cementoblast differentiation. Then, overexpression of PTX3 significantly enhanced the differentiation ability of cementoblasts. While conversely, PTX3 knockdown exerted an inhibitory effect. Moreover, in Ptx3-deficient mice, we found that cementum formation was hampered. Furthermore, we confirmed the presence of PTX3 within the hyaluronan (HA) matrix, thereby activating the ITGB1/FAK/YAP1 signaling pathway. Notably, inhibiting any component of this signaling pathway partially reduced the ability of PTX3 to promote cementoblast differentiation. In conclusion, our study indicated that PTX3 promotes cementum formation and cementoblast differentiation, which is partially dependent on the HA/ITGB1/FAK/YAP1 signaling pathway. This research will contribute to our understanding of cementum regeneration after destruction.

摘要

牙骨质是牙周组织的重要组成部分,但牙骨质的再生仍然是一个挑战。五聚素 3(PTX3)是一种多功能糖蛋白,参与细胞外基质重塑和骨代谢调节。然而,PTX3 在牙骨质形成和牙骨质细胞分化中的作用尚未阐明。在本研究中,我们最初观察到在牙骨质形成和牙骨质细胞分化过程中 PTX3 的表达增加。过表达 PTX3 显著增强了牙骨质细胞的分化能力。相反,PTX3 敲低则发挥抑制作用。此外,在 Ptx3 缺陷小鼠中,我们发现牙骨质形成受到阻碍。此外,我们证实了 PTX3 存在于透明质酸(HA)基质中,从而激活了 ITGB1/FAK/YAP1 信号通路。值得注意的是,抑制该信号通路的任何成分都部分降低了 PTX3 促进牙骨质细胞分化的能力。总之,本研究表明 PTX3 促进牙骨质形成和牙骨质细胞分化,部分依赖于 HA/ITGB1/FAK/YAP1 信号通路。这项研究将有助于我们理解破坏后牙骨质的再生。

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