An a priori list of splicing factor candidate genes were chosen on the basis that they were associated with human aging in populations and had been characterised in primary human fibroblasts and endothelial cells in our previous work [17 (link),18 (link)]. The list of genes included the positive regulatory splicing factors SRSF1, SRSF2, SRSF3, SRSF6, SRSF7, PNSIR and TRA2B, the negative regulatory splicing inhibitors HNRNPA0, HNPNPA1, HNPNPA2B1, HNPNPD, HNPNPH3, HNPNPK, HNPNPM, HNPNPUL2 and the core spliceosomal factors AKAP17A, LSM2, LSM14, IMP3 and SF3B1. Gene expression was measured as described above, using a custom TaqMan Low Density Array (TLDA) format from Life Technologies (Foster City, U.S.A.) as previously described [17 (link)]. Transcript expression was assessed by the Comparative Ct approach, relative to the IDH3B, GUSB and PPIA endogenous control genes and normalised to their expression in RNA from early passage cells.