ASK1 Mediates Apoptosis and Autophagy during oxLDL-CD36 Signaling in Senescent Endothelial Cells

Figure 2

Augmented intracellular ROS derived by oxLDL induces apoptotic cell death rather than autophagy via the MAP kinase pathway in senescent HAECs (P30). (a) The inhibition of ASK1 or blocking of CD36 did not change the total ROS amounts that were increased by oxLDL. (b) CD36 and Trx expression were detected by each antibody in each treated group via immunocytochemistry. (c) Western blot analysis showed the protein level of CD36, Trx, pASK1, pJNK, p-p38, and CHOP. Trx, the redox sensor molecule, was downregulated by blocking CD36 and raised again by adding the ASK1 peptide. (d) Apoptotic cell death was assayed by analyzing cleaved caspase-3 activity via ELISA. Cell death was reduced by inhibiting ASK1 or blocking CD36, but supplemented ASK1 on CD36-masked HAECs caused its reversal. (e) Autophagy assay showed that oxLDL led to autophagy. Autophagy increased by blocking CD36, not by inhibiting ASK1. Normal: senescent HAECs without oxLDL; FA6-152: masking antibody for CD36; NQDI-1: ASK1 inhibitor. Results are expressed by the mean and standard deviation. Significance is presented as follows: ns: not significant. and .

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