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Mesenchymal cell-derived Wnt1 signaling regulates subchondral bone remodeling but has no effects on the development of growth plate or articular cartilage in mice

Säämänen Anna-Marja; Wang Fan; Kiviranta Riku; Heino Terhi J; Pehkonen Matias; Rummukainen Petri

Mesenchymal cell-derived Wnt1 signaling regulates subchondral bone remodeling but has no effects on the development of growth plate or articular cartilage in mice

Säämänen Anna-Marja
Wang Fan
Kiviranta Riku
Heino Terhi J
Pehkonen Matias
Rummukainen Petri
Katso/Avaa
1-s2.0-S8756328222001740-main.pdf (3.346Mb)
Lataukset: 

Elsevier Science Inc.
doi:10.1016/j.bone.2022.116497
URI
https://doi.org/10.1016/j.bone.2022.116497
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Julkaisun pysyvä osoite on:
https://urn.fi/URN:NBN:fi-fe2022091258719
Tiivistelmä

Chondrocyte differentiation is a principal progress in endochondral ossification and in the formation of secondary ossification center (SOC) during the long bone development. We have previously reported that targeted deletion of Wnt1 in mesenchymal progenitors (Wnt1Prrx-/-) leads to spontaneous fractures and severe osteopenia in mouse long bones, suggesting that Wnt1 is a key regulator of bone metabolism. However, the effect of Wnt1 on the regulation of cartilage development and chondrocyte differentiation remained unknown. In this study, WNT1 protein expression was observed in lateral superficial cartilage and growth plate pre-hypertrophic chondrocytes in mice. Wnt1 mRNA expression was detected in epiphyseal cartilage from E16.5 to 3 month-old mice. Detailed histological analyses revealed that the average thickness and chondrocyte density of proximal tibial articular cartilage and growth plate were unchanged between Wnt1Prrx-/- and control mice. However, mu CT analysis of tibial epiphyses showed that the subchondral bone mass was reduced in Wnt1Prrx-/- mice compared to control mice, as demonstrated by decreased bone volume, trabecular number, trabecular thickness, and increased trabecular separation in Wnt1Prrx-/- mice. Mechanistically, histomorphometric analyses showed that the reduced subchondral bone mass in Wnt1Prrx-/- mice was due to impaired bone formation and enhanced bone resorption. In vitro, exogenous Wntl inhibited chondrogenesis and chondrocyte hypertrophy in both cell autonomous and juxtacrine manners, while matrix mineralization and the expression of Mmp13, Mmp9 and Opn were induced in a juxtacrine manner. Taken together, mesenchymal cell-derived Wntl is an important regulator of subchondral bone remodeling, although it has no effect on the regulation of growth plate or articular cartilage.

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