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. 2024 Jul 17;632(8023):157–165. doi: 10.1038/s41586-024-07701-9

Extended Data Fig. 3. IL11 causes ERK and mTORC1-dependent senescence and senescence-associated secretory phenotypes.

Extended Data Fig. 3

a-d, f,g Data for IL11 (24 h)-stimulated primary human cells in the presence of either DMSO, U0126, or rapamycin (n = 6/group). a-b WB showing the activation status of ERK1/2, mTOR, p16, p21, Cyclin D1, and PCNA protein expression by WB from IL11-stimulated a primary human cardiac fibroblasts (HCFs) and b hepatocytes. Levels of secreted c IL6 and d IL8 by ELISA from HCF supernatant. e Relative levels of IL6, IL8, LIF, VEGFA, HGF, CCL2, CXCL1, CXCL5, CXCL6, and CCL20 in the supernatant of IL11-stimulated primary human hepatocytes (6 and 24 h) as measured by Olink proximity extension assay (n = 4/group). Concentrations of f IL6 and g IL8 in the hepatocyte supernatant (as measured by ELISA). a-d, f-g IL11 (5 ng/ml for HCF, 10 ng/ml for hepatocytes), U0126 (10 µM), rapamycin (10 nM). c-g Data are shown as mean ± SD. c, d, f, g One-way ANOVA with Tukey’s correction; e one-way ANOVA with Dunnett’s correction. For gel source data, see Supplementary Fig. 1.

Source Data