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The calcitonin receptor protects against bone loss and excessive inflammation in collagen antibody-induced arthritis

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The calcitonin receptor protects against bone loss and excessive inflammation in collagen antibody-induced arthritis. / Maleitzke, Tazio; Hildebrandt, Alexander; Dietrich, Tamara; Appelt, Jessika; Jahn, Denise; Otto, Ellen; Zocholl, Dario; Baranowsky, Anke; Duda, Georg N; Tsitsilonis, Serafeim; Keller, Johannes.

In: ISCIENCE, Vol. 25, No. 1, 103689, 21.01.2022.

Research output: SCORING: Contribution to journal › SCORING: Journal article › Research › peer-review

Harvard

Maleitzke, T, Hildebrandt, A, Dietrich, T, Appelt, J, Jahn, D, Otto, E, Zocholl, D, Baranowsky, A, Duda, GN, Tsitsilonis, S & Keller, J 2022, 'The calcitonin receptor protects against bone loss and excessive inflammation in collagen antibody-induced arthritis', ISCIENCE, vol. 25, no. 1, 103689. https://doi.org/10.1016/j.isci.2021.103689

APA

Maleitzke, T., Hildebrandt, A., Dietrich, T., Appelt, J., Jahn, D., Otto, E., Zocholl, D., Baranowsky, A., Duda, G. N., Tsitsilonis, S., & Keller, J. (2022). The calcitonin receptor protects against bone loss and excessive inflammation in collagen antibody-induced arthritis. ISCIENCE, 25(1), [103689]. https://doi.org/10.1016/j.isci.2021.103689

Vancouver

Maleitzke T, Hildebrandt A, Dietrich T, Appelt J, Jahn D, Otto E et al. The calcitonin receptor protects against bone loss and excessive inflammation in collagen antibody-induced arthritis. ISCIENCE. 2022 Jan 21;25(1). 103689. https://doi.org/10.1016/j.isci.2021.103689

Bibtex

@article{27373b55bde64a7497f12afe5e9d1953,
title = "The calcitonin receptor protects against bone loss and excessive inflammation in collagen antibody-induced arthritis",
abstract = "Pharmacological application of teleost calcitonin (CT) has been shown to exert chondroprotective and anti-resorptive effects in patients with rheumatoid arthritis (RA). However, the role of endogenous CT that signals through the calcitonin receptor (CTR) remains elusive. Collagen II antibody-induced arthritis (CAIA) was stimulated in wild type (WT) and CTR-deficient (Calcr-/-) mice. Animals were monitored over 10 or 48 days. Joint inflammation, cartilage degradation, and bone erosions were assessed by clinical arthritis score, histology, histomorphometry, gene expression analysis, and μ-computed tomography. CAIA was accompanied by elevated systemic CT levels and CTR expression in the articular cartilage. Inflammation, cartilage degradation, and systemic bone loss were more pronounced in Calcr-/- CAIA mice. Expression of various pro-inflammatory, bone resorption, and catabolic cartilage markers were exclusively increased in Calcr-/- CAIA mice. Endogenous CT signaling through the mammalian CTR has the potential to protect against joint inflammation, cartilage degradation, and excessive bone remodeling in experimental RA.",
author = "Tazio Maleitzke and Alexander Hildebrandt and Tamara Dietrich and Jessika Appelt and Denise Jahn and Ellen Otto and Dario Zocholl and Anke Baranowsky and Duda, {Georg N} and Serafeim Tsitsilonis and Johannes Keller",
note = "{\textcopyright} 2021 The Author(s).",
year = "2022",
month = jan,
day = "21",
doi = "10.1016/j.isci.2021.103689",
language = "English",
volume = "25",
journal = "ISCIENCE",
issn = "2589-0042",
publisher = "Elsevier Inc.",
number = "1",

}

RIS

TY - JOUR

T1 - The calcitonin receptor protects against bone loss and excessive inflammation in collagen antibody-induced arthritis

AU - Maleitzke, Tazio

AU - Hildebrandt, Alexander

AU - Dietrich, Tamara

AU - Appelt, Jessika

AU - Jahn, Denise

AU - Otto, Ellen

AU - Zocholl, Dario

AU - Baranowsky, Anke

AU - Duda, Georg N

AU - Tsitsilonis, Serafeim

AU - Keller, Johannes

N1 - © 2021 The Author(s).

PY - 2022/1/21

Y1 - 2022/1/21

N2 - Pharmacological application of teleost calcitonin (CT) has been shown to exert chondroprotective and anti-resorptive effects in patients with rheumatoid arthritis (RA). However, the role of endogenous CT that signals through the calcitonin receptor (CTR) remains elusive. Collagen II antibody-induced arthritis (CAIA) was stimulated in wild type (WT) and CTR-deficient (Calcr-/-) mice. Animals were monitored over 10 or 48 days. Joint inflammation, cartilage degradation, and bone erosions were assessed by clinical arthritis score, histology, histomorphometry, gene expression analysis, and μ-computed tomography. CAIA was accompanied by elevated systemic CT levels and CTR expression in the articular cartilage. Inflammation, cartilage degradation, and systemic bone loss were more pronounced in Calcr-/- CAIA mice. Expression of various pro-inflammatory, bone resorption, and catabolic cartilage markers were exclusively increased in Calcr-/- CAIA mice. Endogenous CT signaling through the mammalian CTR has the potential to protect against joint inflammation, cartilage degradation, and excessive bone remodeling in experimental RA.

AB - Pharmacological application of teleost calcitonin (CT) has been shown to exert chondroprotective and anti-resorptive effects in patients with rheumatoid arthritis (RA). However, the role of endogenous CT that signals through the calcitonin receptor (CTR) remains elusive. Collagen II antibody-induced arthritis (CAIA) was stimulated in wild type (WT) and CTR-deficient (Calcr-/-) mice. Animals were monitored over 10 or 48 days. Joint inflammation, cartilage degradation, and bone erosions were assessed by clinical arthritis score, histology, histomorphometry, gene expression analysis, and μ-computed tomography. CAIA was accompanied by elevated systemic CT levels and CTR expression in the articular cartilage. Inflammation, cartilage degradation, and systemic bone loss were more pronounced in Calcr-/- CAIA mice. Expression of various pro-inflammatory, bone resorption, and catabolic cartilage markers were exclusively increased in Calcr-/- CAIA mice. Endogenous CT signaling through the mammalian CTR has the potential to protect against joint inflammation, cartilage degradation, and excessive bone remodeling in experimental RA.

U2 - 10.1016/j.isci.2021.103689

DO - 10.1016/j.isci.2021.103689

M3 - SCORING: Journal article

C2 - 35036874

VL - 25

JO - ISCIENCE

JF - ISCIENCE

SN - 2589-0042

IS - 1

M1 - 103689

ER -