ArticleStem cell research & therapy2025
NEAT1 regulates BMSCs aging through disruption of FGF2 nuclear transport.
Article in Stem cell research & therapy, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed.
- Paraspeckle-Mediated Integration of Nuclear RNA Regulation in Skeletal Homeostasis and Pathological Disorder.Calcified tissue international · 2026Review
- Peptide nanoarchitectonics of biomimetic nanozyme synergistically inhibits smooth muscle cell proliferation and promotes endothelial repair to reduce poststenting complications.Journal of nanobiotechnology · 2026Article
- PDLSC-CM targets HAPLN1 in macrophages to reduce root resorption in delayed replanted teeth.Stem cell research & therapy · 2026Article
- The LAMB3-ITGA6 axis orchestrates epithelial repair in periodontitis via hemidesmosomal regulation and keratinization modulation.Frontiers in cell and developmental biology · 2026Article
- H3K18 lactylation-hexokinase 2 positive feedback loop promotes osteogenesis of ASPCs in facial infiltrating lipomatosis.Stem cell research & therapy · 2025Article
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15 authors.
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Abstract
backgroundThe aging of bone marrow mesenchymal stem cells (BMSCs) impairs bone tissue regeneration, contributing to skeletal disorders. LncRNA NEAT1 is considered as a proliferative inhibitory role during cellular senescence, but the relevant mechanisms remain insufficient. This study aims to elucidate how NEAT1 regulates mitotic proteins during BMSCs aging.
methodsBMSCs were isolated from alveolar bone of human volunteers aged 26-33 (young) and 66-78 (aged). NEAT1 expression and distribution changes during aging process were observed using fluorescence in situ hybridization (FISH) in young (3 months) and aged (18 months) mice or human BMSCs. Subsequent RNA pulldown and proteomic analyses, along with single-cell analysis, immunofluorescence, RNA immunoprecipitation (RIP), and co-immunoprecipitation (Co-IP), were conducted to investigate that NEAT1 impairs the nuclear transport of mitotic FGF2 and contributes to BMSCs aging.
resultsWe reveal that NEAT1 undergoes significant upregulated and shifts from nucleus to cytoplasm in bone marrow and BMSCs during aging process. In which, the expression correlates with nuclear DNA content during karyokinesis, suggesting a link to mitogenic factor. Within NEAT1 knockdown, hallmarks of cellular aging, including senescence-associated secretory phenotype (SASP), p16, and p21, were significantly downregulated. RNA pulldown and proteomic analyses further identify NEAT1 involved in osteoblast differentiation, mitotic cell cycle, and ribosome biogenesis, highlighting its role in maintaining BMSCs differentiation and proliferation. Notably, as an essential growth factor of BMSCs, Fibroblast Growth Factor 2 (FGF2) directly abundant binds to NEAT1 and the sites enriched with nuclear localization motifs. Importantly, NEAT1 decreased the interaction between FGF2 and Karyopherin Subunit Beta 1 (KPNB1), influencing the nuclear transport of mitogenic FGF2.
conclusionsOur findings position NEAT1 as a critical regulator of mitogenic protein networks that govern BMSC aging. Targeting NEAT1 might offer novel therapeutic strategies to rejuvenate aged BMSCs.
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