Transcriptional profiling of growing and senescent WT and IL-1R-depleted IMR90 cells

Senescent cells no longer divide, but remain metabolically active and secrete an array of cytokines, growth factors, and proteases termed the senescence-associated secretory phenotype (SASP). Previous studies have indicated that the SASP factor IL-1a may be an upstream regular of the SASP. We show here that knockdown of the IL-1a receptor IL-1R results in a sizable reduction of SASP expression late in senescence induction. Our results suggest that targeting the IL-1 signaling pathway is a reliable method to dissociate the SASP from cell-cycle exit. Overall design: Cells were induced to senesce via activation of oncogene Ras. Samples were collected at day 0 (growing phase), day 4 (beginning of SASP induction) and day 10 (senescent phase) of Ras induction. Samples were collected from control cells expressing a scramble shRNA and samples expressing 1 of 2 independent shRNAs against IL-1R. Two replicates were collected per condition per timepoint for a total of 12 samples.