Abstract
ObjectiveHuman periodontal ligament stem cells (hPDLSCs) refer to one kind of somatic stem cells that are capable of differentiating into multiple cell kinds and undergoing robust clonal self-renewal. This work was unearthed to elucidate the possible molecular mechanism of miR-142–3p in mediating osteogenic differentiation of hPDLSCs by targeting SGK1. MethodsThe hPDLSCs were isolated, cultured, and identified. hPDLSCs were identified by immunofluorescence staining and multiple differentiation ability detection. Cell proliferation ability was assessed by CCK-8 assay. hPDLSCs were induced using osteogenic differentiation medium. ALP activity was detected by alkaline phosphatase (ALP) staining and ALP activity assay, and mineralized nodule formation was determined by alizarin red staining. The expression levels of osteogenic differentiation marker proteins ALP, RUNX2, and OCN were measured by RT-qPCR. miR-142–3p candidate targets were obtained through bioinformatics analysis. The relationship between miR-142–3p and SKG1 was verified. ResultsmiR-142–3p in hPDLSCs after osteogenic induction was down-regulated. Elevated miR-142–3p restricted hPDLSCs proliferation, and diminished ALP activity and mineralized nodule formation, as well as the expression of ALP, RUNX2, and OCN, while miR-142–3p inhibition led to inverse results. miR-142-3p inhibited SKG1 expression. SKG1 overexpression promoted hPDLSC proliferation and osteogenic differentiation, and reversed the inhibitory function of miR-142–3p on hPDLSCs. ConclusionThis study highlights that miR-142–3p represses osteogenic differentiation of hPDLSCs by reducing SGK1 expression.
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
More From: Journal of Stomatology oral and Maxillofacial Surgery
Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.