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. 2017 May 16;8:15040. doi: 10.1038/ncomms15040

Figure 2. Contribution of Gdf5 lineage to synovial hyperplasia after cartilage injury.

Figure 2

(a) Schematic experimental design for data in b–f. (b) IF staining for Tom (red) and CldU (green) in control and injured knee synovium. Nuclei were counterstained with DAPI (blue). (c) Tom+ cells, as percentage of total cells in synovium as shown in b, increased after injury (***P<0.0001; n=4; Student's t-test). (d) Tom+ (red) cells in injured knee synovium negative for the haematopoietic marker CD16/CD32 (green; n=3; image on left) and endothelial marker CD31 (green; n=4; image on right). Nuclei were counterstained with DAPI (blue). (e) CldU-labelling showing higher rate of proliferation in Tom+ compared to Tom− cells after injury (***P<0.0001; n=4; two-way ANOVA with Bonferroni post-test). (f) IF staining for IdU (red), CldU (green) and Tom (blue) in injured knee synovium (n=3). Nuclei were counterstained with DAPI (grey). Left: IdU and CldU overlaid; right: all channels overlaid. Arrows indicate triple-labelled cells. (g) Tom+ (red) cells in control and injured knee synovium of adult LepR-Cre;Tom mice (n=4) with CD31 in green. Nuclei were counterstained with DAPI (blue). (h) Tom+ cells in synovium as percentage of total cells. Dashed lines, synovial boundary; S, synovium; P, patella; F, femur; C, capsule. Scale bars, 20 μm. Data in b,c,e are representative of two experiments.