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 

机构地区：[1]Department of Trauma and Orthopedic Surgery,University Medical Center Hamburg-Eppendorf,Hamburg 20246,Germany [2]Department of Osteology and Biomechanics,University Medical Center Hamburg-Eppendorf,Hamburg 20246,Germany [3]Center for Musculoskeletal Surgery,Charité-Universitätsmedizin Berlin,Berlin 13353,Germany [4]Julius Wolff Institute for Biomechanics and Musculoskeletal Regeneration,Charité-Universitätsmedizin Berlin,Berlin 13353,Germany [5]Department of Neurology,University Medical Center Hamburg-Eppendorf,Hamburg 20251,Germany [6]Berlin Institute of Health,Berlin 10178,Germany

出　　处：《Bone Research》2022年第1期107-121,共15页骨研究（英文版）

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.

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.

关 键 词：TREATMENT representing SKELETON 

分 类 号：R68[医药卫生—骨科学]