Cbfβ Is a Novel Modulator Against Osteoarthritis by Maintaining Articular Cartilage Homeostasis Through TGF-Ꞵ Signaling

Xiangguo Che; Xian Jin; Narae Park; Hee-June Kim; Hee-Soo Kyung; Hyun-Ju Kim; Jane B. Lian; Janet L. Stein; And Je-Yong Choi

doi:10.20944/preprints202302.0284.v1

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preprints.org > life sciences > cell & developmental biology > doi: 10.20944/preprints202302.0284.v1

Preprint Article Version 1 Preserved in Portico This version is not peer-reviewed

Cbfβ Is a Novel Modulator Against Osteoarthritis by Maintaining Articular Cartilage Homeostasis Through TGF-Ꞵ Signaling

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These authors contributed equally to this work.

Version 1 : Received: 14 February 2023 / Approved: 16 February 2023 / Online: 16 February 2023 (09:40:30 CET)

How to cite: Che, X.; Jin, X.; Park, N.; Kim, H.; Kyung, H.; Kim, H.; Lian, J.B.; Stein, J.L.; Choi, A.J. Cbfβ Is a Novel Modulator Against Osteoarthritis by Maintaining Articular Cartilage Homeostasis Through TGF-Ꞵ Signaling. Preprints 2023, 2023020284. https://doi.org/10.20944/preprints202302.0284.v1. Che, X.; Jin, X.; Park, N.; Kim, H.; Kyung, H.; Kim, H.; Lian, J.B.; Stein, J.L.; Choi, A.J. Cbfβ Is a Novel Modulator Against Osteoarthritis by Maintaining Articular Cartilage Homeostasis Through TGF-Ꞵ Signaling. Preprints 2023, 2023020284. https://doi.org/10.20944/preprints202302.0284.v1.

Cite as:

Che, X.; Jin, X.; Park, N.; Kim, H.; Kyung, H.; Kim, H.; Lian, J.B.; Stein, J.L.; Choi, A.J. Cbfβ Is a Novel Modulator Against Osteoarthritis by Maintaining Articular Cartilage Homeostasis Through TGF-Ꞵ Signaling. Preprints 2023, 2023020284. https://doi.org/10.20944/preprints202302.0284.v1. Che, X.; Jin, X.; Park, N.; Kim, H.; Kyung, H.; Kim, H.; Lian, J.B.; Stein, J.L.; Choi, A.J. Cbfβ Is a Novel Modulator Against Osteoarthritis by Maintaining Articular Cartilage Homeostasis Through TGF-Ꞵ Signaling. Preprints 2023, 2023020284. https://doi.org/10.20944/preprints202302.0284.v1.

Abstract

TGF-ꞵ signaling is a vital regulator for maintaining articular cartilage homeostasis. Runx transcription factors, downstream targets of TGF-ꞵ signaling, have been studied in the context of osteoarthritis (OA). Although Runx partner core binding factor β (Cbfβ) is known to play a pivotal role in chondrocyte and osteoblast differentiation, the role of Cbfβ in maintaining articular cartilage remains obscure. This study investigated Cbfβ as a novel anabolic modulator of TGF-ꞵsignaling and determined its role in articular cartilage homeostasis. Cbfβ significantly decreased in aged mouse articular cartilage and human OA cartilage. Articular chondrocyte-specific Cbfb-deficient mice (Cbfb△ac/△ac) exhibited early cartilage degeneration at 20 weeks old and developed OA at 12 months old. Cbfb△ac/△ac mice showed enhanced OA progression under the surgical-induced mice OA model. Mechanistically, forced expression of Cbfβ rescued Col2α1 and Runx1 expression in Cbfβ-deficient chondrocytes. TGF-ꞵ1-mediated Col2α1 expression failed despite the pSmad3 activation under TGF-ꞵ1 treatment in Cbfβ-deficient chondrocytes. Cbfβ protected Runx1 from proteasomal degradation through Cbfβ/Runx1 complex formation. These results indicate that Cbfβ is a novel anabolic regulator for cartilage homeostasis, suggesting that Cbfβ could protect OA development by maintaining the integrity of the TGF-ꞵ1 signaling pathway in articular cartilage.

Keywords

articular cartilage; Runx1/Cbfβ complex; Osteoarthritis; TGF-β signaling; proteasomal degradation

Subject

LIFE SCIENCES, Cell & Developmental Biology

Copyright: This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

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