Inhibition of miR‑98‑5p promotes high glucose‑induced suppression of preosteoblast proliferation and differentiation via the activation of the PI3K/AKT/GSK3β signaling pathway by targeting BMP2
- Feng Zheng
- Fucai Zhang
- Furong Wang
Affiliations: Department of Orthopedics, Qinghai Provincial People's Hospital, Xining, Qinghai 810007, P.R. China, Department of Orthopedics, Qinghai Provincial People's Hospital, Xining, Qinghai 810007, P.R. China
- Published online on: July 29, 2022 https://doi.org/10.3892/mmr.2022.12808
Copyright: © Zheng
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Osteoporosis (OP) is a bone metabolic disease, in which low bone mass and the microarchitectural deterioration of bone tissue contribute to the fragility of bones and increase the risk of fracture. The aim of the present study was to determine the role of microRNA (miR)‑98‑5p in high glucose (HG)‑induced preosteoblasts. HG was used to induce preosteoblasts treated in a differentiation medium to establish an in vitro OP model. Next, miR‑98‑5p expression was determined using reverse transcription‑quantitative PCR. Following the transfection of an miR‑98‑5p inhibitor into HG‑treated osteoblasts, cell viability was assessed using a Cell Counting Kit‑8 assay, while alkaline phosphatase (ALP) activity, differentiation ability and the expression of differentiation‑regulated genes osteocalcin and osteopontin were measured using the corresponding ALP, Alizarin red staining, reverse transcription‑quantitative PCR and western blotting assays. The association between miR‑98‑5p and the PI3K/AKT/GSK3β signaling pathway was determined using western blotting. Next, the binding relationship between miR‑98‑5p and bone morphogenetic protein 2 (BMP2) was predicted and verified, and the role of BMP2 in the regulation of the PI3K/AKT/GSK3β signaling pathway was explored using western blotting. The results revealed that miR‑98‑5p expression was upregulated in HG‑induced osteoblasts, and the inhibition of miR‑98‑5p resulted in enhanced cell viability, alkaline phosphatase activity and differentiation in osteoblasts following HG induction. It was also discovered that miR‑98‑5p inhibition activated PI3K/AKT/GSK3β signaling, while knockdown of BMP2, which binds to miR‑98‑5p, enhanced the activation of this signaling pathway and the differentiation ability of osteoblasts. In conclusion, the findings of the present study suggested that the inhibition of miR‑98‑5p expression may activate PI3K/AKT/GSK3β signaling to promote HG‑induced suppression of preosteoblast viability and differentiation by targeting BMP2, which provides a novel insight into future potential molecular markers for OP treatment.