| First Author | Maleitzke T | Year | 2022 |
| Journal | iScience | Volume | 25 |
| Issue | 1 | Pages | 103689 |
| PubMed ID | 35036874 | Mgi Jnum | J:328682 |
| Mgi Id | MGI:6856478 | Doi | 10.1016/j.isci.2021.103689 |
| Citation | Maleitzke T, et al. (2022) The calcitonin receptor protects against bone loss and excessive inflammation in collagen antibody-induced arthritis. iScience 25(1):103689 |
| abstractText | 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 mu-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. |
