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. 2020 Feb 6;32:101453. doi: 10.1016/j.redox.2020.101453

Fig. 9.

Fig. 9

Ablation of p62 offsets Tsg101-elicited protective effects on cardiac I/R injury. (A) A diagram depicting the generation of the cross mouse model (Tsg101-TG/p62-KO, FVB/B6 background) in which Tsg101 was overexpressed and p62 was ablated in the mouse hearts. (B) Representative Western-blots and (C) quantification analysis showing the expression levels of Tsg101, Keap1, p62, Nrf2 and LC3A/B in the indicated mouse hearts upon pre-I/R and post-I/R. *, p < 0.05; n = 4 for each group. Cardiac functional recovery assessed by (D) LV dp/dt (max) and (E) LV dp/dt (min) in WT, TG, p62-KO and TG/KO hearts during I/R. n = 5 for each group, *, p < 0.05 vs. WTs. (H) Total LDH levels in the coronary effluent collected during the first 10 min of reperfusion. *, p < 0.05 vs. WTs. (G) Caspase-3 activity determined in WT, TG, p62-KO and TG/KO hearts subjected to ex vivo I/R (45min/1 h). *, p < 0.05 vs. WTs. (H) Representative images and (I) quantification analysis of DHE staining in heart sections from WT, TG, p62-KO and TG/KO hearts subjected to ex vivo I/R (45min/5min). *, p < 0.05 vs. WTs. (J) Representative infarction images of mouse hearts upon in vivo I/R (1h/24 h) and (K) quantitative results of infarction size and (L) the ratio of risk region to left ventricular (LV) area. *, p < 0.05 vs. WTs. n.s. stands for no significance.