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. 2023 Aug 17;13(12):4765–4784. doi: 10.1016/j.apsb.2023.08.015

Figure 2.

Figure 2

Mitochondrial dsDNA leaking mediated the non-canonical STING–PERK pathway activation in the oxidized LDL-induced endothelial injury. (A–D) The cytoplasmic double-stranded DNA (dsDNA) concentration (A), qPCR analysis of cytoplasmic mitochondrial DNA (mtDNA, MT-ND1 and MT-ND2), nuclear LINE1 elements (L1ORF1 and L1ORF2), ribosomal gene (RNA 18S) (B), cyclic GMP-AMP (cGAMP) concentration (C) and immunofluorescence staining of mitochondria by TOMM20 (mitochondria, red) and dsDNA (green) (D) in HCAECs treated with or without ox-LDL (Scale bar = 10 μm). (E–J) Western blot analysis of the non-canonical STING-PERK pathway (E), co-immunoprecipitation analysis of STING-PERK binding (F), cGAMP concentration (G), immunofluorescence staining of STING (H), THP-1 monocytes adhesion (I), and adhesions molecules and chemokines mRNA expression (J) in mtDNA (3 μg/mL)-transfected HCAECs combined with DNase I (1 μg/mL) or C-176. (K–O) Western blot analysis of the non-canonical STING–PERK pathway (K), co-immunoprecipitation analysis of STING-PERK binding (L), cyclic GMP–AMP synthase (cGAS) bound mtDNA by cytosolic DNA immunoprecipitation (M), cGAMP concentration (N) and adhesions molecules and chemokines mRNA expression (O) in ox-LDL-treated HCAECs combined with ethidium bromide (EtBr). Data are expressed as mean ± SEM, n = 3; ∗∗P < 0.01, ∗∗∗P < 0.001; ND, not detected; ns, no significance.