The long noncoding RNA lnc-ob1 facilitates bone formation by upregulating Osterix in osteoblasts
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ABSTRACT:
PROVIDER: PRJNA445648 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR6895900_1.fastq.gz | Fastqsanger.gz | |||
| SRR6895900_2.fastq.gz | Fastqsanger.gz | |||
| SRR6895901_1.fastq.gz | Fastqsanger.gz | |||
| SRR6895901_2.fastq.gz | Fastqsanger.gz | |||
| SRR6895902_1.fastq.gz | Fastqsanger.gz |
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Project description: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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