Fig. 1: Apoptosis-prone CAV1-deficient EC expresses higher levels of HSP27 while the survival protein AKT/PKB is downregulated. | Cell Death & Disease

Fig. 1: Apoptosis-prone CAV1-deficient EC expresses higher levels of HSP27 while the survival protein AKT/PKB is downregulated.

From: Caveolin-1 regulates the ASMase/ceramide-mediated radiation response of endothelial cells in the context of tumor–stroma interactions

Fig. 1: Apoptosis-prone CAV1-deficient EC expresses higher levels of HSP27 while the survival protein AKT/PKB is downregulated.The alternative text for this image may have been generated using AI.

CAV1-proficient [CAV1(+)] and CAV1-deficient [CAV1(−)] ECs were subjected to radiation treatment (0 Gy control or 10 Gy) with or without p38 inhibitor treatment (SB203580, 10 µM). a Cell cycle phases and apoptotic cells (sub-G1) were analyzed by flow cytometry 48 h after irradiation. Graphs consist of data from 3 to 4 individual experiments (with SEM). *p < 0.05 (for G1/G0 and G2/M: 0 Gy vs. 10 Gy CAV(+) SB203580) and ****p < 0.001 (for G1/G0 and G2/M: 0 Gy vs. 10 Gy CAV1(−) NGM and SB203580) by two-way ANOVA with post hoc Tukey multiple-comparison test (not depicted). b ECs were plated for colony formation assay, pretreated for 2 h with SB203580, irradiated with indicated doses, and subsequently further incubated for an additional 10 days. Data show the surviving fractions (SF) from three independent experiments (means ± SD). Dashed lines depict the survival fraction upon p38 inhibition. ****p < 0.001 by two-way ANOVA with post hoc Tukey multiple-comparison test. c Whole-cell lysates were used for Western blot analysis of the p38/MAPK and AKT/PKB pathways by detecting the indicated proteins in control and 10 Gy irradiated cells 48 h after treatment. In addition, CAV1 expression levels were measured at the same time points. β-ACTIN was used as a loading control. Representative blots of 3–4 individual experiments are shown.

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