ArticleBioengineered2022
Long non-coding RNA KCNQ1OT1 overexpression promotes osteogenic differentiation of staphylococcus aureus-infected human bone mesenchymal stem cells by sponging microRNA miR-29b-3p.
Article in Bioengineered, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 14 citations in OpenAlex.
- DAPK3-Ablation Regulates the AMPK/mTOR-GPX4 Signaling Pathway to Affect Biological Functions of Staphylococcus aureus-Treated Bone Marrow Mesenchymal Stem Cells and Potentially Ameliorate Osteomyelitis.Molecular biotechnology · 2026Article
- The role of non-coding RNAs in Staphylococcus aureus infections: mechanisms, biomarkers, and therapeutic implications.Antonie van Leeuwenhoek · 2026Review
- Bone marrow mesenchymal stem cell exosome-derived miR-223 regulated cellular pyroptosis of macrophage in osteomyelitis through regulating LACC1.Scientific reports · 2025Article
- Loss in Pluripotency Markers in Mesenchymal Stem Cells upon Infection withJournal of microbiology and biotechnology · 2024Article
- Effects of Staphylococcus aureus on stem cells and potential targeted treatment of inflammatory disorders.Stem cell research & therapy · 2024Review
- FRZB affectsExperimental and therapeutic medicine · 2023Article
- Review
- Recent advancements of miRNAs in the treatment of bone diseases and their delivery potential.Current research in pharmacology and drug discovery · 2023Review
- Effects of Ethanol on Expression of Coding and Noncoding RNAs in Murine Neuroblastoma Neuro2a Cells.International journal of molecular sciences · 2022Article
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Osteomyelitis (OM) is an orthopedic disease caused by bone infections in the bone cortex, bone marrow, periosteum, and surrounding soft tissues. Recent studies have implicated non-coding RNAs (ncRNAs) in the development of OM. However, little is known about the role of ncRNAs in the osteogenic differentiation during bone infection. In the present study, we investigated the role of KCNQ1OT1/miR-29b-3p axis in osteogenic differentiation in staphylococcus aureus (SpA)-infected human bone mesenchymal stem cells (hBMSCs). We first examined the expression of lncRNA KCNQ1OT1 and miR-29b-3p in the serum samples of OM patients and healthy controls. We also infected hBMSCs with different concentrations of SpA and studied the osteogenic differentiation after infection. Our results revealed that KCNQ1OT1 was downregulated while miR-29b-3p was upregulated in the serum samples of OM patients, as well as in SpA-infected hBMSCs. Overexpression of KCNQ1OT1 ameliorated the damage in hBMSCs caused by SpA infection. KCNQ1OT1 could support hBMSCs osteogenic differentiation by enhancing ALP activity, alizarin red S accumulation, expressions of osteogenic markers, and attenuating inflammatory responses after SpA infection. We further showed that miR-29b-3p was a downstream target of KCNQ1OT1, mediating the osteogenic differentiation of hBMSCs during SpA infection. Our data suggest that KCNQ1OT1 could ameliorate the SpA-induced suppression of osteogenic differentiation in hBMSCs by sponging miR-29b-3p. Modulating KCNQ1OT1 expression may serve as a strategy to ameliorate osteomyelitis.
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