» Articles » PMID: 28955690

Regulation of Cartilage Development and Diseases by Transcription Factors

Overview
Journal J Bone Metab
Date 2017 Sep 29
PMID 28955690
Citations 20
Authors
Affiliations
Soon will be listed here.
Abstract

Genetic studies and molecular cloning approaches have been successfully used to identify several transcription factors that regulate the numerous stages of cartilage development. Sex-determining region Y (SRY)-box 9 (Sox9) is an essential transcription factor for the initial stage of cartilage development. Sox5 and Sox6 play an important role in the chondrogenic action of Sox9, presumably by defining its cartilage specificity. Several transcription factors have been identified as transcriptional partners for Sox9 during cartilage development. Runt-related transcription factor 2 (Runx2) and Runx3 are necessary for hypertrophy of chondrocytes. CCAAT/enhancer-binding protein β (C/EBPβ) and activating transcription factor 4 (ATF4) function as co-activators for Runx2 during hypertrophy of chondrocytes. In addition, myocyte-enhancer factor 2C (Mef2C) is required for initiation of chondrocyte hypertrophy, presumably by functioning upstream of Runx2. Importantly, the pathogenic roles of several transcription factors in osteoarthritis have been demonstrated based on the similarity of pathological phenomena seen in osteoarthritis with chondrocyte hypertrophy. We discuss the importance of investigating cellular and molecular properties of articular chondrocytes and degradation mechanisms in osteoarthritis, one of the most common cartilage diseases.

Citing Articles

The Therapeutic Potential of Adipose-Derived Mesenchymal Stem Cell Secretome in Osteoarthritis: A Comprehensive Study.

Gonzalez-Cubero E, Gonzalez-Fernandez M, Esteban-Blanco M, Perez-Castrillo S, Perez-Fernandez E, Navasa N Int J Mol Sci. 2024; 25(20).

PMID: 39457070 PMC: 11508730. DOI: 10.3390/ijms252011287.


A Narrative Review of the Roles of Chondromodulin-I (Cnmd) in Adult Cartilage Tissue.

Reyes Alcaraz V, Pattappa G, Miura S, Angele P, Blunk T, Rudert M Int J Mol Sci. 2024; 25(11).

PMID: 38892027 PMC: 11173128. DOI: 10.3390/ijms25115839.


TMF suppresses chondrocyte hypertrophy in osteoarthritic cartilage by mediating the FOXO3a/BMPER pathway.

Huang J, Ren Q, Jiao L, Niu S, Liu C, Zhou J Exp Ther Med. 2024; 28(1):283.

PMID: 38800044 PMC: 11117099. DOI: 10.3892/etm.2024.12571.


Extremely low frequency-electromagnetic fields promote chondrogenic differentiation of adipose-derived mesenchymal stem cells through a conventional genetic program.

Zerillo L, Coletta C, Madera J, Grasso G, Tutela A, Vito P Sci Rep. 2024; 14(1):10182.

PMID: 38702382 PMC: 11068729. DOI: 10.1038/s41598-024-60846-5.


Association of gene polymorphisms with Kashin-Beck disease risk in the Chinese Han population.

He N, Hong A, Zhao K, Zhang Z, Wang S, Jia Y Open Med (Wars). 2024; 19(1):20230883.

PMID: 38205152 PMC: 10775412. DOI: 10.1515/med-2023-0883.


References
1.
Masuda K, Ripley B, Nishimura R, Mino T, Takeuchi O, Shioi G . Arid5a controls IL-6 mRNA stability, which contributes to elevation of IL-6 level in vivo. Proc Natl Acad Sci U S A. 2013; 110(23):9409-14. PMC: 3677444. DOI: 10.1073/pnas.1307419110. View

2.
Saito T, Ikeda T, Nakamura K, Chung U, Kawaguchi H . S100A1 and S100B, transcriptional targets of SOX trio, inhibit terminal differentiation of chondrocytes. EMBO Rep. 2007; 8(5):504-9. PMC: 1866207. DOI: 10.1038/sj.embor.7400934. View

3.
Kawane T, Komori H, Liu W, Moriishi T, Miyazaki T, Mori M . Dlx5 and mef2 regulate a novel runx2 enhancer for osteoblast-specific expression. J Bone Miner Res. 2014; 29(9):1960-9. DOI: 10.1002/jbmr.2240. View

4.
Yoshida M, Hata K, Takashima R, Ono K, Nakamura E, Takahata Y . The transcription factor Foxc1 is necessary for Ihh-Gli2-regulated endochondral ossification. Nat Commun. 2015; 6:6653. DOI: 10.1038/ncomms7653. View

5.
Wagner T, Wirth J, Meyer J, Zabel B, Held M, Zimmer J . Autosomal sex reversal and campomelic dysplasia are caused by mutations in and around the SRY-related gene SOX9. Cell. 1994; 79(6):1111-20. DOI: 10.1016/0092-8674(94)90041-8. View