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. 2021 Apr 9;12:2136. doi: 10.1038/s41467-021-22402-x

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© The Author(s) 2021

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

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Fig. 5 — Parathyroid hormone (PTH) binding to parathyroid hormone 1 receptor (PTH1R) upregulates SLPI expression via the pathways of adenylyl cyclase (AC)/protein kinase A, and Erk. SLPI directly acts in osteoblasts to enhance bone formation by controlling gene expression. Additionally, SLPI promotes the adhesion of osteoblasts to neighboring osteoclasts, thereby increasing direct cell–cell contact. This indirect effect creates a microenvironment in the reversal phase, leading to stimulation of Slpi and Fgf2 expression in osteoblasts, and inhibition of osteoclastic bone resorption.