ArticleJournal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research2015
Mesenchymal Deletion of Histone Demethylase NO66 in Mice Promotes Bone Formation.
Article in Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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16 citing papers in PubMed, 21 citations in OpenAlex.
- Histone demethylase KDM7A regulates bone homeostasis through balancing osteoblast and osteoclast differentiation.Cell death & disease · 2024Article
- Roles and Regulation of H3K4 Methylation During Mammalian Early Embryogenesis and Embryonic Stem Cell Differentiation.Advances in experimental medicine and biology · 2024Review
- Dysregulation of histone modifications in bone marrow mesenchymal stem cells during skeletal ageing: roles and therapeutic prospects.Stem cell research & therapy · 2023Review
- Osteoblast-Specific Overexpression of Nucleolar ProteinJournal of osteoporosis · 2023Article
- Comprehensive analysis of epigenetics mechanisms in osteoporosis.Frontiers in genetics · 2023Review
- RIOX1-demethylated cGAS regulates ionizing radiation-elicited DNA repair.Bone research · 2022Article
- Mechanisms Regulating Muscle Protein Synthesis in CKD.Journal of the American Society of Nephrology : JASN · 2020Article
- Epigenetic Regulators of Mesenchymal Stem/Stromal Cell Lineage Determination.Current osteoporosis reports · 2020Review
- Article
- The Roles of Epigenetics Regulation in Bone Metabolism and Osteoporosis.Frontiers in cell and developmental biology · 2020Review
- Bone Remodeling: Histone Modifications as Fate Determinants of Bone Cell Differentiation.International journal of molecular sciences · 2019Review
- The small members of the JMJD protein family: Enzymatic jewels or jinxes?Biochimica et biophysica acta. Reviews on cancer · 2019Review
- HnRNPL inhibits the osteogenic differentiation of PDLCs stimulated by SrClJournal of cellular and molecular medicine · 2019Article
- The emerging roles of ribosomal histidyl hydroxylases in cell biology, physiology and disease.Cellular and molecular life sciences : CMLS · 2018Review
- Phylogenetic and genomic analyses of the ribosomal oxygenases Riox1 (No66) and Riox2 (Mina53) provide new insights into their evolution.BMC evolutionary biology · 2018Article
- The histone methyltransferase DOT1L inhibits osteoclastogenesis and protects against osteoporosis.Cell death & disease · 2018Article
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
Our previous studies indicated that the Jumonji C (JmjC)-domain-containing NO66 is a histone demethylase with specificity for methylated histone H3K4 and H3K36. NO66 binds to the transcription factor Osterix (Osx) and inhibits its transcriptional activity in promoter assays. However, the physiological role of NO66 in formation of mammalian bones is unknown. Here, using a genetically engineered mouse model, we show that during early skeletal development, Prx1-Cre-dependent mesenchymal deletion of NO66 promotes osteogenesis and formation of both endochondral as well as intramembranous skeletal elements, leading to a larger skeleton and a high bone mass phenotype in adult mice. The excess bone formation in mice where NO66 was deleted in cells of mesenchymal origin is associated with an increase in the number of preosteoblasts and osteoblasts. Further analysis revealed that in the embryonic limbs and adult calvaria of mice with deletion of NO66 in cells of mesenchymal origin, expression of several genes including bone morphogenetic protein 2 (Bmp2), insulin-like growth factor 1 (Igf1), and osteoclast inhibitor osteoprotegerin was increased, concurrent with an increase in expression of bone formation markers such as osterix (Osx), type I collagen, and bone sialoprotein (Bsp). Taken together, our results provide the first in vivo evidence that NO66 histone demethylase plays an important role in mammalian osteogenesis during early development as well as in adult bone homeostasis. We postulate that NO66 regulates bone formation, at least in part, via regulating the number of bone-forming cells and expression of multiple genes that are critical for these processes.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.