Journal
FEBS LETTERS
Volume 587, Issue 24, Pages 3961-3967Publisher
ELSEVIER SCIENCE BV
DOI: 10.1016/j.febslet.2013.10.028
Keywords
Epigenetic regulation; Osteoblast differentiation; Mesenchymal stem cell; Bone development
Funding
- NIH [RO1 AR051455]
- VA Merit Review Award from the U.S. Department of Veterans Affairs, Office of Research and Development Biomedical Laboratory Research Program
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To investigate the effects of histone methyltransferase ESET (also known as SETDB1) on bone metabolism, we analyzed osteoblasts and osteoclasts in ESET knockout animals, and performed osteogenesis assays using ESET-null mesenchymal stem cells. We found that ESET deletion severely impairs osteoblast differentiation but has no effect on osteoclastogenesis, that co-transfection of ESET represses Runx2-mediated luciferase reporter while siRNA knockdown of ESET activates the luciferase reporter in mesenchymal cells, and that ESET is required for postnatal expression of Indian hedgehog protein in the growth plate. As the bone phenotype in ESET-null mice is 100% penetrant, these results support ESET as a critical regulator of osteoblast differentiation during bone development. Published by Elsevier B.V. on behalf of the Federation of European Biochemical Societies.
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