Fig. 4

The expression of STAT3 and FGF7 in SSCs increased during OA progression. A Schematic of the protein interaction diagram related to Lepr. B mRNA levels of STAT3 in SSCs at different time points after ALCT. C, D QPCR analysis of the expression levels of STAT3 in OA mouse (C) and human (D) samples. The N side represents the less severely diseased side of the s source joint, whereas the O side represents the more severely diseased side of the joint. E CellChat analysis was performed to investigate the cell‒cell communication patterns between clusters in articular cartilage. The overall outgoing and incoming signal strengths of each cluster were visualized in a scatter plot. F The relative strength of all enriched signals (outgoing and incoming) across various clusters was visualized in a heatmap. G Violin plot showing the expression of canonical markers in the FGF signal. H FGF signaling pathway-associated ligand‒receptor. I Circle plots showing the dynamic alterations in the interaction networks between Fgf7 and Fgfr1 as well as between Fgf7 and Fgfr2. J, L Representative images of FGF7 IHC in articular cartilage and subchondral bone in OA mouse (J) (n = 3) and human (L) (n = 2) samples. Scale bar, 100 μm. K, M Quantitative analysis of the FGF7 area in articular cartilage and subchondral bone in OA mouse (K) and human (M) samples. N, O QPCR analysis of the expression levels of FGF7 in OA mouse (N) and human (O) samples. Quantitative analyses were conducted using the IHC Profiler plug-in for ImageJ. All data are presented as the mean ± S.D. *P < 0.05; **P < 0.01; ***P < 0.001; ns, not significant