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Fig. 3 | Stem Cell Research & Therapy

Fig. 3

From: NEAT1 regulates BMSCs aging through disruption of FGF2 nuclear transport

Fig. 3

FGF2 and KPNB1 involves in BMSCs proliferation and bone regeneration. (A) Uniform Manifold Approximation and Projection (UMAP) plot illustrating distinct clusters of BMSCs, based on single-cell RNA sequencing data. Clusters are numbered and color-coded, reflecting heterogeneity within the BMSC population. (B) UMAP projection of BMSC cell cycle states, displaying cells in G1, S, and G2/M phases. The majority of cells reside in the G1 phase, with smaller subsets in the S and G2/M phases, indicating proliferative diversity within the population. (C) Partition-based graph abstraction (PAGA) was used to analyze and visualize cellular differentiation trajectories. (D-E) Expression density plots visualizing the distribution of FGF2, KPNB1, CCND1, and PCNA transcripts across BMSC populations.(F) RT-qPCR analysis of FGF2 and KPNB1 expression levels in young and aged BMSCs. Expression levels of FGF2 are upregulated in young BMSCs (*P< 0.05). Data represent mean ± s.d. (G) Immunofluorescence staining of FGF2 (green) and KPNB1 (red) in cultured BMSCs. Nuclei are counterstained with DAPI (blue). Merged images reveal colocalization of FGF2 and KPNB1 within the nuclear compartment. Scale bar, 10 μm. (H) Histological analysis of regenerated alveolar bone from mice. Hematoxylin and eosin (H&E) staining highlights bone regeneration morphology, whereas immunofluorescence staining demonstrates the presence of FGF2 (green) and KPNB1 (red) within the newly formed bone matrix. Nuclei are counterstained with DAPI (blue), and merged images show the spatial localization of FGF2 and KPNB1. Scale bar, 50 μm

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