PMID- 35481341 OWN - Quintessence Publishing Company, Ltd. CI - Copyright Quintessence Publishing Company, Ltd. OCI - Copyright Quintessence Publishing Company, Ltd. TA - Oral Health Prev Dent JT - Oral Health and Preventive Dentistry IS - 1757-9996 (Electronic) IP - 1 VI - 20 PST - epublish DP - 2022 PG - 173-184 LA - en TI - Role of LINC01133 in Osteogenic Differentiation of Dental Pulp Stem Cells by Targeting miR-199b-5p LID - 10.3290/j.ohpd.b2960495 [doi] FAU - Shi, Qiaorui AU - Shi Q FAU - Zheng, Ming AU - Zheng M CN - OT - AKT3 OT - DPSCs OT - competitive endogenous RNA OT - LINC01133 OT - miR-199b-5p OT - osteogenic differentiation AB - Purpose: Recently, increasing attention has been paid to the function of long non-coding RNAs (lncRNAs) in osteogenic differentiation (OD) of dental pulp stem cells (DPSCs). LINC01133 was reported to have a close relationship with tumorigenesis for multiple cancers, but no study has yet explored the role of LINC01133 in modulating OD of DPSCs. Materials and Methods: Alizarin red S (ARS) staining and alkaline phosphatase (ALP) staining were perfomed to assess the OD potential of DPSCs. Osteogenic markers including runt-related transcription factor 2 (RUNX2), osterix (OSX) and ALP expression levels in DPSCs were monitored by qRT-PCR and Western blot before and after cell transfection. Luciferase reporter gene assay detected the relationship between LINC01133 and miR-199b-5p. Results: The expression of LINC01133 was low, while miR-199b-5p was increasingly expressed during OD of DPSCs. Overexpression of LINC01133 in DPSCs resulted in decreased expression of RUNX2, OSX, ALP, DSPP and DMP1, whose expression was reversed in DPSCs after transfections of miR-199b-5p overexpression. Co-transfection of pcDNA3.1-LINC01133 and miR-199b-5p mimic led to elevated expression of RUNX2, OSX, ALP, DSPP and DMP1 compared with pcDNA3.1-LINC01133 transfection alone. LINC01133 served as a sponge of miR-199b-5p. AKT3 was verified as a downstream effector of miR-199b-5p in DPSCs. Conclusion: LINC01133 inhibits the OD of DPSCs by upregulating AKT3 via sponging miR-199b-5p, which may act as a potential diagnostic biomarker for dentin regeneration in the dental pulp. AID - 2960495