The Shh-p38-NFATc1 signaling pathway is essential for osteoclastogenesis during tooth eruption.

Autor: Liu J; Department of Stomatology, Beijing Friendship Hospital, Capital Medical University, Beijing, China; Immunology Research Center for Oral and Systemic Health, Beijing Friendship Hospital, Capital Medical University, Beijing, China., Wang J; Department of Stomatology, Beijing Friendship Hospital, Capital Medical University, Beijing, China; Immunology Research Center for Oral and Systemic Health, Beijing Friendship Hospital, Capital Medical University, Beijing, China., Huang R; Department of Stomatology, Beijing Friendship Hospital, Capital Medical University, Beijing, China; Immunology Research Center for Oral and Systemic Health, Beijing Friendship Hospital, Capital Medical University, Beijing, China., Jia X; Department of Stomatology, Beijing Friendship Hospital, Capital Medical University, Beijing, China; Immunology Research Center for Oral and Systemic Health, Beijing Friendship Hospital, Capital Medical University, Beijing, China., Huang X; Department of Stomatology, Beijing Friendship Hospital, Capital Medical University, Beijing, China; Immunology Research Center for Oral and Systemic Health, Beijing Friendship Hospital, Capital Medical University, Beijing, China. Electronic address: xiaofengh@ccmu.edu.cn.
Jazyk: angličtina
Zdroj: Tissue & cell [Tissue Cell] 2025 Feb; Vol. 92, pp. 102643. Date of Electronic Publication: 2024 Nov 28.
DOI: 10.1016/j.tice.2024.102643
Abstrakt: Tooth eruption, a critical stage in tooth development, is related to osteoclastogenesis. Intraperitoneal injection of Shh agonists into neonatal mice promoted tooth eruption at postnatal day (PN) 15, whereas treatment with the Shh inhibitor (LDE225) suppressed this process. When RAW264.7 osteoclast precursor cells were treated with RANKL, NFATc1 translocated from the cytoplasm to the nucleus and induced cell differentiation into TRAP + osteoclasts; this process was activated by Shh but inhibited by LDE225. Treating RAW264.7 cells with the p38 inhibitor, BIRB796, also inhibited NFATc1 nuclear localization. p-p38 expression in the alveolar bone of PN3 and PN5 mice was decreased by treatment with LDE225, and RAW264.7 cell differentiation was reduced by BIRB796, regardless of treatment with Shh. Furthermore, Shh activated p38 signaling pathway in RAW264.7 cells, while p38 phosphorylation was reduced by LDE225, which ultimately inhibited osteoclast precursor differentiation. Therefore, we concluded that Shh promotes osteoclast precursor differentiation via the p38-NFATc1 signaling pathway.
Competing Interests: Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.
(Copyright © 2024 Elsevier Ltd. All rights reserved.)
Databáze: MEDLINE
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