miR-141-3p Targeted SIRT1 to Inhibit Osteogenic Differentiation of Bone Marrow Mesenchymal Stem Cells

Abstract

Purpose. To explore the expression of miR-141-3p during the osteogenic differentiation of human bone marrow mesenchymal stem cells (BMSCs) and its regulatory effect. Methods. Differentiation of BMSCs was induced by dexamethasone. The mRNA expression of miR-141-3p, ALP, RUNX2, and OCN was measured using RT-qPCR. The protein expression was detected via western blot. The target of miR-141-3p was predicted through the TargetScan website and confirmed using luciferase reporter assay. Results. miR-141-3p expression declined during osteogenic differentiation. The relative ALP activities and the mRNA expression of ALP, RUNX2, and OCN were markedly reduced in the miR-141-3p mimic group while increased in the inhibitor group. Cell viability was suppressed in the miR-141-3p mimic group and promoted in the inhibitor group. SIRT1 was predicted to be a downstream gene of miR-141-3p, and this prediction was confirmed via the luciferase reporter assay. The results of the western blot assay demonstrated that SIRT1 expression was decreased in the miR-141-3p mimic group. SIRT1 reversed the inhibitory influence of miR-141-3p on the osteogenic differentiation ability of BMSCs. Conclusion. miR-141-3p targeted SIRT1 to inhibit osteogenic differentiation of BMSCs via the Wnt/β-catenin signaling pathway.

Tetrahedral Framework Nucleic Acids Promote Senile Osteoporotic Fracture Repair by Enhancing Osteogenesis and Angiogenesis of Callus

“…Although there is no study regarding how tFNA regulates SIRT1/FoxO1 expression currently, other related signaling pathways may be involved according to the available reports. For instance, SIRT1 is closely associated with Wnt/β-catenin signaling pathways, which could also be activated by tFNAs, , the synergy of SIRT1 and Wnt pathway has been extensively investigated in various cell lines and disease models. , Moreover, FoxO proteins compete for the binding sites of β-catenin with a T-cell transcription factor. The overexpression of FoxO proteins could inhibit the Wnt/β-catenin signaling pathway in the case of oxidative stress or senescence. , Thus, the Wnt/β-catenin pathway may be a bridge between SIRT1 and FoxO1, the detailed mechanism still requires further exploration.…”

“…For instance, SIRT1 is closely associated with Wnt/β-catenin signaling pathways, which could also be activated by tFNAs, 19,26 the synergy of SIRT1 and Wnt pathway has been extensively investigated in various cell lines and disease models. 48,49 Moreover, FoxO proteins compete for the binding sites of β-catenin with a T-cell transcription factor. The overexpression of FoxO proteins could inhibit the Wnt/βcatenin signaling pathway in the case of oxidative stress or senescence.…”

Retracted: miR‐141‐3p Targeted SIRT1 to Inhibit Osteogenic Differentiation of Bone Marrow Mesenchymal Stem Cells

“…This article has been retracted by Hindawi following an investigation undertaken by the publisher [ 1 ]. This investigation has uncovered evidence of one or more of the following indicators of systematic manipulation of the publication process: Discrepancies in scope Discrepancies in the description of the research reported Discrepancies between the availability of data and the research described Inappropriate citations Incoherent, meaningless and/or irrelevant content included in the article Manipulated or compromised peer review …”

“…This article has been retracted by Hindawi following an investigation undertaken by the publisher [1]. This investigation has uncovered evidence of one or more of the following indicators of systematic manipulation of the publication process:…”