Journal
NATURE METABOLISM
Volume 1, Issue 4, Pages 485-496Publisher
NATURE RESEARCH
DOI: 10.1038/s42255-019-0053-8
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Funding
- National key research and development program [2016YFC102705/2017YFA0505001/2018YFC0910200]
- National Natural Science Foundation [81822012, 81770873, 81722031, 81470715, 81771043, 31671312, 3137134]
- Guangdong Natural Science Funds [2014A030313358]
- Major Project in Guangdong Province of Science [2014KZDXM011]
- Guangdong Natural Science Funds for Distinguished Young Scholars [S2013050013880]
- [2017BR009]
- [2014BAI04B07]
- [Kx0200020173386]
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Long noncoding RNAs (lncRNAs) have emerged as integral regulators of physiology and disease, but specific roles of lncRNAs in bone disease remain largely unknown. Here, we show that lnc-ob1 regulates osteoblast activity and bone formation in mice by upregulating the osteogenic transcription factor Osterix. Expression of lnc-ob1 is enriched in osteoblasts and upregulated during osteoblastogenesis. We demonstrate that osteoblast-specific knock-in of lnc-ob1 enhances bone formation and increases bone mass. Pharmacological overexpression of lnc-ob1 specifically in osteoblasts confers resistance to ovariectomy-induced osteoporosis in mice. In humans, expression of the homologue, lnc-OB1, decreases with age in osteoblasts of patients with osteoporosis. Mechanistically, lnc-ob1 upregulates the expression of Osterix in mouse and human osteoblasts, probably via inhibition of H3K27me3 methylation. Our data indicate that lnc-OB1 regulates bone formation and might be a drug target for the treatment of osteoporosis.
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