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Background  Individual skeletal elements of the vertebrate limbs arise through a segmentation process introducing joints in specific locations. However, the molecular pathways controlling joint formation and subsequent joint maintenance are largely unknown. In this study, we focused on  SOX11 , and its contribution to the regulation of  GDF5 , a secreted signal necessary for proper joint formation and postnatal joint homeostasis.    Results   Sox11  is initially expressed broadly in the murine cartilage condensations at early stages of skeletal development, but its expression is specifically increased in the forming joint interzone as is forms.  SOX11  overexpression can directly activate  GDF5  expression both in vitro and in micromass cell cultures prepared from chick limb buds. Conserved  SOX  family binding sites are present in the 5’ UTR region of the  GDF5  gene and we show  SOX11  can specifically bind to one of them. While misexpression of  Sox11  in developing chick limbs through RCAS virus infection does not induce  Gdf5  expression in ectopic locations, it does enhance its expression. To explore the roles of  Sox11  in joint homeostasis, we analyzed adult knee joints in an osteoarthritis mouse model where the medial meniscus and the medial collateral ligament were removed. We also analyzed knee joints from human subjects who underwent total knee replacement surgery. We find that  SOX11  is mainly expressed in the weight-bearing areas of knee joints, and its expression is decreased in degraded cartilage during progression of knee osteoarthritis in both mice and humans.    Conclusions  This work implicates  SOX11  as a potential regulator of  GDF5  expression in joint maintenance and suggests a possible role in the pathogenesis of osteoarthritis.

SOX11 contributes to the regulation of GDF5 in joint maintenance