Journal
JOURNAL OF CELLULAR PHYSIOLOGY
Volume 234, Issue 4, Pages 3436-3444Publisher
WILEY
DOI: 10.1002/jcp.26761
Keywords
chondrocyte; hypertrophy; runt-related transcription factor-2 (Runx2); temporomandibular joint
Categories
Funding
- National Natural Science Foundation of China [81700997]
- National Institute of Arthritis and Musculoskeletal and Skin Diseases [R01AR070222, R01AR054465]
- Shenzhen Science and Technology Innovation Committee, China [JCYJ20160331114205502]
- Shenzhen Development and Reform Committee, China
- Fundamental Research Funds for the Central Universities of China [Lxjj2017026]
Ask authors/readers for more resources
Runt-related transcription factor-2 (Runx2) is essential for chondrocyte maturation during cartilage development and embryonic mandibular condylar development. The process that chondrocytes, especially a subgroup of hypertrophic chondrocytes (HC), could transform into bone cells in mandibular condyle growth makes chondrocytes crucially important for normal endochondral bone formation. To determine whether Runx2 regulates postnatal condylar cartilage growth and tissue homeostasis, we deleted Runx2 in chondrocytes in postnatal mice and assessed the consequences on temporomandibular joint (TMJ) cartilage growth and remodeling. The cell lineage tracing data provide information demonstrating the role of chondrocytes in subchondral bone remodeling. The histologic and immunohistochemical data showed that Runx2 deficiency caused condylar tissue disorganization, including loss of HC and reduced hypertrophic zone, reduced proliferative chondrocytes, and decreased cartilage matrix production. Expression of Col10a1, Mmp13, Col2a1, Aggrecan, and Ihh was significantly reduced in Runx2 knockout mice. The findings of this study demonstrate that Runx2 is required for chondrocyte proliferation and hypertrophy in TMJ cartilage and postnatal TMJ cartilage growth and homeostasis, and that Runx2 may play an important role in regulation of chondrocyte-derived subchondral bone remodeling.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available