ArticleJournal of orthopaedic surgery and research2023
Long non-coding RNA KCNQ10T1/miR-19a-3p/SMAD5 axis promotes osteogenic differentiation of mouse bone mesenchymal stem cells.
Article in Journal of orthopaedic surgery and research, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed, 2 citations in OpenAlex.
- Regulatory role of lncRNA DANCR in osteogenic differentiation of bone marrow mesenchymal stem cells through targeting the miR-19a-3p/PTEN/AKT/mTOR pathway.In vitro cellular & developmental biology. Animal · 2026Article
- Extracellular Vesicles Derived from Resveratrol-Treated BMSCs Promote the Repair of Bone Defects in Osteoporotic Rats.Stem cell reviews and reports · 2026Article
- LINC00662 regulates osteogenic differentiation of BMSCs and inhibits fracture healing via miR-330-3p/PTEN axis.BMC musculoskeletal disorders · 2025Article
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundBone fracture is a common orthopedic disease that needs over 3 months to recover. Promoting the osteogenic differentiation of bone mesenchymal stem cells (BMSCs) is beneficial for fracture healing. Therefore, this research aimed to study the roles of long non-coding RNA (lncRNA) KCNQ10T1 in osteogenic differentiation of BMSCs.
methodsBMSCs were treated with osteogenic medium and assessed by CCK-8 and flow cytometry assays. Alkaline phosphatase (ALP) staining, alizarin red staining (ARS), as well as concentration of osteoblast markers were measured to evaluate osteogenic differentiation of BMSCs. Western blot was employed to detect proteins; while, qRT-PCR was for mRNA levels. Additionally, targeted relationships between KCNQ10T1 and miR-19a-3p, as well as miR-19a-3p and SMAD5 were verified by dual luciferase reporter gene assay along with RNA pull-down method.
resultsUpregulation of KCNQ10T1 promoted the ALP staining and ARS intensity, increased the cell viability and decreased the apoptosis rate of BMSCs. Besides, KCNQ10T1 overexpression increased the ALP, OPG, OCN and OPN protein levels. KCNQ10T1 sponges miR-19a-3p, which targets Smad5. Upregulated miR-19a-3p reversed the overexpressed KCNQ10T1-induced effects, and depletion of SMAD5 reversed the miR-19a-3p inhibitor-induced effects on osteogenic medium-treated BMSCs.
conclusionsUpregulation of KCNQ10T1 promoted osteogenic differentiation of BMSCs through miR-19a-3p/SMAD5 axis in bone fracture.
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Registered trials
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