Fig. 2
The SASP is inhibited by rapamycin in endothelial cells (ECs) subjected to SIPS. a Real-time PCR analysis of SASP factors using cDNA derived from human coronary artery endothelial cells (HCAECs) at 72 h in Fig. 1a. The results are shown after normalization to values obtained from control HCAECs (value = 1). Results are presented as means ± SD from three independent experiments. ap < 0.05 vs. the Ctr and bp < 0.05 vs. the H2O2-treated HCAECs. b Immunoblotting for the levels of mTOR, RICTOR, RAPTOR, and MAPKAPK2 was performed using cell lysates and mTOR immunoprecipitates from HCAECs at 72 h in Fig. 1a. β-ACTIN was used as a loading control. The histogram shows mean densitometric readings for the proteins normalized to β-ACTIN or mTOR from three independent experiments. ap < 0.01 vs. the Ctr and bp < 0.01 vs. the H2O2-treated HCAECs. Control (Ctr): untreated cells. SIPS, stress-induced premature senescence. SASP, senescence-associated secretory phenotype