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

作     者：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 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 K?hli;Cordula Erdmann;Melanie Fuchs;Karl-Heinz Frosch;Serafeim Tsitsilonis;Michael Amling;Thorsten Schinke;Johannes Keller

作者机构：Department of Trauma and Orthopedic SurgeryUniversity Medical Center Hamburg-EppendorfHamburg 20246Germany Department of Osteology and BiomechanicsUniversity Medical Center Hamburg-EppendorfHamburg 20246Germany Center for Musculoskeletal SurgeryCharité-Universitätsmedizin BerlinBerlin 13353Germany Julius Wolff Institute for Biomechanics and Musculoskeletal RegenerationCharité-Universitätsmedizin BerlinBerlin 13353Germany Department of NeurologyUniversity Medical Center Hamburg-EppendorfHamburg 20251Germany Berlin Institute of HealthBerlin 10178Germany 

出 版 物：《Bone Research》 (骨研究（英文版）)

年 卷 期：2022年第10卷第1期

页      面：107-121页

核心收录：

学科分类：0710[理学-生物学] 1002[医学-临床医学] 1001[医学-基础医学(可授医学、理学学位)] 100210[医学-外科学(含：普外、骨外、泌尿外、胸心外、神外、整形、烧伤、野战外)] 10[医学] 

基　　金：funded by grants from the Else-Kr?ner-Fresenius-Stiftung (EKFS 2017_A22) the German Research Foundation (DFG KE 2179/4-1) the Berlin Institute of Health to JK from the Hertie-Stiftung (Hertie Academy of Clinical Neuroscience) the German Research Foundation (DFG grant numbers: DFG FOR 2879 [project LU 1924/1-]) to PL 

主　　题：treatment representing skeleton 

摘      要：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.