| First Author | Bradley EW | Year | 2015 |
| Journal | J Biol Chem | Volume | 290 |
| Issue | 1 | Pages | 118-26 |
| PubMed ID | 25389289 | Mgi Jnum | J:218396 |
| Mgi Id | MGI:5617420 | Doi | 10.1074/jbc.M114.596247 |
| Citation | Bradley EW, et al. (2015) Histone deacetylase 7 (Hdac7) suppresses chondrocyte proliferation and beta-catenin activity during endochondral ossification. J Biol Chem 290(1):118-26 |
| abstractText | Histone deacetylases (Hdacs) regulate endochondral ossification by suppressing gene transcription and modulating cellular responses to growth factors and cytokines. We previously showed that Hdac7 suppresses Runx2 activity and osteoblast differentiation. In this study, we examined the role of Hdac7 in postnatal chondrocytes. Hdac7 was highly expressed in proliferating cells within the growth plate. Postnatal tissue-specific ablation of Hdac7 with a tamoxifen-inducible collagen type 2a1-driven Cre recombinase increased proliferation and beta-catenin levels in growth plate chondrocytes and expanded the proliferative zone. Similar results were obtained in primary chondrocyte cultures where Hdac7 was deleted with adenoviral-Cre. Hdac7 bound beta-catenin in proliferating chondrocytes, but stimulation of chondrocyte maturation promoted the translocation of Hdac7 to the cytoplasm where it was degraded by the proteasome. As a result, beta-catenin levels and transcription activity increased in the nucleus. These data demonstrate that Hdac7 suppresses proliferation and beta-catenin activity in chondrocytes. Reducing Hdac7 levels in early chondrocytes may promote the expansion and regeneration of cartilage tissues. |
