ArticleStem cell research & therapy2022
Knockdown of FOXA1 enhances the osteogenic differentiation of human bone marrow mesenchymal stem cells partly via activation of the ERK1/2 signalling pathway.
Article in Stem cell research & therapy, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 23 citations in OpenAlex.
- MicroRNA signatures in inflammatory dental tissues: biomarkers and molecular mechanisms.Frontiers in molecular biosciences · 2026Review
- Curcumin Promotes Osteogenic Differentiation of Bone Marrow Mesenchymal Stem Cells from Anterior Cruciate Ligament Reconstruction via ERK1/2 Pathway.Current medicinal chemistry · 2026Article
- Silencing FOXA1 suppresses inflammation caused by LPS and promotes osteogenic differentiation of periodontal ligament stem cells through the TLR4/MyD88/NF-κB pathway.Biomolecules & biomedicine · 2025Article
- FoxA1 knockdown promotes BMSC osteogenesis in part by activating the ERK1/2 signaling pathway and preventing ovariectomy-induced bone loss.Scientific reports · 2025Article
- Foxa1 disruption enhances human cell integration in human-mouse interspecies chimeras.Cell and tissue research · 2025Article
- FOXA1 knockdown alleviates inflammation and enhances osteogenic differentiation of periodontal ligament stem cells via STAT3 pathway.Journal of orthopaedic surgery and research · 2024Article
- Review
- Article
- ATF2-driven osteogenic activity of enoxaparin sodium-loaded polymethylmethacrylate bone cement in femoral defect regeneration.Journal of orthopaedic surgery and research · 2023Article
- Resistin targets TAZ to promote osteogenic differentiation through PI3K/AKT/mTOR pathway.iScience · 2023Article
- Dental Pulp Stem Cells for Bone Tissue Engineering: A Literature Review.Stem cells international · 2023Review
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Authors and funding
9 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundThe available therapeutic options for large bone defects remain extremely limited, requiring new strategies to accelerate bone healing. Genetically modified bone mesenchymal stem cells (BMSCs) with enhanced osteogenic capacity are recognised as one of the most promising treatments for bone defects.
methodsWe performed differential expression analysis of miRNAs between human BMSCs (hBMSCs) and human dental pulp stem cells (hDPSCs) to identify osteogenic differentiation-related microRNAs (miRNAs). Furthermore, we identified shared osteogenic differentiation-related miRNAs and constructed an miRNA-transcription network. The Forkhead box protein A1 (FOXA1) knockdown strategy with a lentiviral vector was used to explore the role of FOXA1 in the osteogenic differentiation of MSCs. Cell Counting Kit-8 was used to determine the effect of the knockdown of FOXA1 on hBMSC proliferation; real-time quantitative reverse transcription PCR (qRT-PCR) and western blotting were used to investigate target genes and proteins; and alkaline phosphatase (ALP) staining and Alizarin Red staining (ARS) were used to assess ALP activity and mineral deposition, respectively. Finally, a mouse model of femoral defects was established in vivo, and histological evaluation and radiographic analysis were performed to verify the therapeutic effects of FOXA1 knockdown on bone healing.
resultsWe identified 22 shared and differentially expressed miRNAs between hDPSC and hBMSC, 19 of which were downregulated in osteogenically induced samples. The miRNA-transcription factor interaction network showed that FOXA1 is the most significant and novel osteogenic differentiation biomarker among more than 300 transcription factors that is directly targeted by 12 miRNAs. FOXA1 knockdown significantly promoted hBMSC osteo-specific genes and increased mineral deposits in vitro. In addition, p-ERK1/2 levels were upregulated by FOXA1 silencing. Moreover, the increased osteogenic differentiation of FOXA1 knockdown hBMSCs was partially rescued by the addition of ERK1/2 signalling inhibitors. In a mouse model of femoral defects, a sheet of FOXA1-silencing BMSCs improved bone healing, as detected by microcomputed tomography and histological evaluation.
conclusionThese findings collectively demonstrate that FOXA1 silencing promotes the osteogenic differentiation of BMSCs via the ERK1/2 signalling pathway, and silencing FOXA1 in vivo effectively promotes bone healing, suggesting that FOXA1 may be a novel target for bone healing.
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