1. A Novel lncRNA Mediates the Delayed Tooth Eruption of Cleidocranial Dysplasia.
- Author
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Xin Y, Liu Y, Li J, Liu D, Zhang C, Wang Y, and Zheng S
- Subjects
- Animals, Core Binding Factor Alpha 1 Subunit genetics, Epigenesis, Genetic, Mice, RAW 264.7 Cells, Receptors, CXCR3, Tooth Eruption genetics, Bone Resorption, Cleidocranial Dysplasia genetics, MicroRNAs genetics, RNA, Long Noncoding genetics
- Abstract
Delayed eruption of permanent teeth is a common symptom of cleidocranial dysplasia (CCD). Previous studies have focused on the anomaly of osteogenesis resulting from mutations in the Runt-related transcription factor-2 gene (RUNX2). However, deficiencies in osteoclastogenesis and bone resorption, and the epigenetic regulation mediated by long non-coding (lnc)RNAs in CCD remain to be elucidated. Here, a novel osteoclast-specific lncRNA (OC-lncRNA) was identified during the osteoclast differentiation of RAW 264.7 cells transfected with a RUNX2 mutation expression cassette. We further confirmed that OC-lncRNA positively regulated osteoclastogenesis and bone resorption. The OC-lncRNA promoted the expression of CXC chemokine receptor type 3 (CXCR3) by competitively binding to microRNA (miR)-221-5p. The CXCR3-CXC-motif chemokine ligand 10 (CXCL10) interaction and nuclear factor-κB constituted a positive feedback that positively regulated osteoclastogenesis and bone resorption. These results demonstrate that OC-lncRNA-mediated osteoclast dysfunction via the OC-lncRNA-miR-221-5p-CXCR3 axis, which is involved in the process of delayed tooth eruption of CCD.
- Published
- 2022
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