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. 2022 Dec 30;26(1):105909. doi: 10.1016/j.isci.2022.105909

Figure 5.

Figure 5

Inhibiting PKR decreases GSDMD-mediated endothelial cell hyperactivation

(A) Representative micrographs and positive rate analysis of senescence-associated β-galactosidase (SA-β-gal) staining in siCon and PKR knockdown (siPKR) HUVECs stimulated with H2O2 (n = 3).

(B) Representative immunoblots and densitometric analysis of GSDMD, N-GSDMD, PKR and p-PKR level in siCon and PKR knockdown (siPKR) HUVECs stimulated with H2O2 (n = 3).

(C) LDH assay in the supernatants of siCon and PKR knockdown (siPKR) HUVECs stimulated with H2O2 (n = 3).

(D) Representative scanning electronic micrographs of siCon and PKR knockdown (siPKR) HUVECs stimulated with H2O2.

(E) Representative immunoblots and densitometric analysis of arterial β-actin, GSDMD, N-GSDMD, PKR and p-PKR level in young and old WT or PKR knockout mice (n = 4).

(F) Tunnel staining of aorta in aging WT or PKR knockout mice (n = 4). Scale Bar = 50 μm. ∗p< 0.05; ∗∗p< 0.01; ∗∗∗p< 0.001; ###p< 0.001 (two-way ANOVA test). Data are represented as mean ± SEM.