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

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Procalcitonin is expressed in osteoblasts and limits bone resorption through inhibition of macrophage migration during intermittent PTH treatment. / Baranowsky, Anke; Jahn, Denise; Jiang, Shan; Yorgan, Timur; Ludewig, Peter; Appelt, Jessika; Albrecht, Kai K; Otto, Ellen; Knapstein, Paul; Donat, Antonia; Winneberger, Jack; Rosenthal, Lana; Köhli, Paul; Erdmann, Cordula; Fuchs, Melanie; Frosch, Karl-Heinz; Tsitsilonis, Serafeim; Amling, Michael; Schinke, Thorsten; Keller, Johannes.

in: BONE RES, Jahrgang 10, Nr. 1, 9, 27.01.2022.

Publikationen: SCORING: Beitrag in Fachzeitschrift/ZeitungSCORING: ZeitschriftenaufsatzForschungBegutachtung

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@article{e403b72927a148f8b8c457f66dbd76e8,
title = "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.",
author = "Anke Baranowsky and Denise Jahn and Shan Jiang and Timur Yorgan and Peter Ludewig and Jessika Appelt and Albrecht, {Kai K} and Ellen Otto and Paul Knapstein and Antonia Donat and Jack Winneberger and Lana Rosenthal and Paul K{\"o}hli and Cordula Erdmann and Melanie Fuchs and Karl-Heinz Frosch and Serafeim Tsitsilonis and Michael Amling and Thorsten Schinke and Johannes Keller",
note = "{\textcopyright} 2022. The Author(s).",
year = "2022",
month = jan,
day = "27",
doi = "10.1038/s41413-021-00172-y",
language = "English",
volume = "10",
journal = "BONE RES",
issn = "2095-4700",
publisher = "NATURE PUBLISHING GROUP",
number = "1",

}

RIS

TY - JOUR

T1 - Procalcitonin is expressed in osteoblasts and limits bone resorption through inhibition of macrophage migration during intermittent PTH treatment

AU - Baranowsky, Anke

AU - Jahn, Denise

AU - Jiang, Shan

AU - Yorgan, Timur

AU - Ludewig, Peter

AU - Appelt, Jessika

AU - Albrecht, Kai K

AU - Otto, Ellen

AU - Knapstein, Paul

AU - Donat, Antonia

AU - Winneberger, Jack

AU - Rosenthal, Lana

AU - Köhli, Paul

AU - Erdmann, Cordula

AU - Fuchs, Melanie

AU - Frosch, Karl-Heinz

AU - Tsitsilonis, Serafeim

AU - Amling, Michael

AU - Schinke, Thorsten

AU - Keller, Johannes

N1 - © 2022. The Author(s).

PY - 2022/1/27

Y1 - 2022/1/27

N2 - 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.

AB - 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.

U2 - 10.1038/s41413-021-00172-y

DO - 10.1038/s41413-021-00172-y

M3 - SCORING: Journal article

C2 - 35087025

VL - 10

JO - BONE RES

JF - BONE RES

SN - 2095-4700

IS - 1

M1 - 9

ER -