Procalcitonin is expressed in osteoblasts and limits bone resorption through inhibition of macrophage migration during intermittent PTH treatment.

Abstract

Intermittent injections of parathyroid hormone (iPTH) are applied clinically to stimulate bone formation by osteoblasts, although continuous elevation of parathyroid hormone (PTH) primarily results in increased bone resorption. Here, we identified Calca, encoding the sepsis biomarker procalcitonin (ProCT), as a novel target gene of PTH in murine osteoblasts that inhibits osteoclast formation. During iPTH treatment, mice lacking ProCT develop increased bone resorption with excessive osteoclast formation in both the long bones and axial skeleton. Mechanistically, ProCT inhibits the expression of key mediators involved in the recruitment of macrophages, representing osteoclast precursors. Accordingly, ProCT arrests macrophage migration and causes inhibition of early but not late osteoclastogenesis. In conclusion, our results reveal a potential role of osteoblast-derived ProCT in the bone microenvironment that is required to limit bone resorption during iPTH.

• Authors: Anke Baranowsky, Denise Jahn, Shan Jiang, Timur Yorgan, Peter Ludewig, Jessika Appelt, Kai K Albrecht, Ellen Otto, Paul Knapstein, Antonia Donat, Jack Winneberger, Lana Rosenthal, Paul Köhli, Cordula Erdmann, Melanie Fuchs, Karl-Heinz Frosch, Serafeim Tsitsilonis, Michael Amling, Thorsten Schinke, Johannes Keller
• Journal: Bone research (Bone Res) Vol. 10 Issue 1 Pg. 9 (Jan 27 2022) ISSN: 2095-4700 [Print] China
• PMID: 35087025 (Publication Type: Journal Article)
• Copyright: © 2022. The Author(s).