Figure 4. Senescent melanocytes transmit paracrine telomere dysfunction to neighbouring cells via mechanisms involving IP‐10‐CXCR3‐ROS signalling.

1. Dermal fibroblasts were cultured with either young or senescent melanocyte conditioned medium. CXCR3 inhibition was achieved either by siRNA knockdown of CXCR3 or by treating fibroblasts with the CXCR3 inhibitor, AMG487.
2. Graph showing the mean number of TAF in fibroblasts cultured with young or senescent melanocyte CM with or without AMG487. Data are shown as mean ± SEM of n = 3 independent experiments.
3. Knockdown efficiency of two different siRNAs against CXCR3. Data are shown as mean ± SD of n = 2 independent experiments.
4. Mean number of TAF in fibroblasts cultured with young or senescent melanocyte CM after CXCR3 knockdown. Data are shown as mean ± SEM of n = 3 independent experiments.
5. Mean number of TAF in fibroblasts cultured with IP‐10 with or without AMG487. Data are shown as mean ± SEM of n = 3 independent experiments.
6. Graph showing MitoSOX fluorescence intensity of fibroblasts treated with IP‐10 with or without MitoQ at the time points indicated. Values are a percentage fold change normalised to controls. Graph is representative of one out of n = 3 independent experiments.
7. Dermal fibroblasts were cultured with either young or senescent melanocyte conditioned medium with or without MitoQ.
8. Mean number of TAF in fibroblasts cultured with young or senescent melanocyte CM with or without MitoQ. Data are shown as mean ± SEM of n = 3 independent experiments.
9. Mean number of TAF in fibroblasts treated with IP‐10 with or without MitoQ. Data are shown as mean ± SEM of n = 3 independent experiments.

Data information: *P < 0.05, **P < 0.01, ***P < 0.001. Statistical tests: one‐way ANOVA (B, E, H–I), two‐way ANOVA (D).