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. 2022 Jun 11;11(12):1894. doi: 10.3390/cells11121894

Figure 1.

Figure 1

Renal I/R increases RIP3 expression and reduces Mitofilin levels. (A) Immunoblot and graph showing increases in RIP3 levels after 60 min of mono-lateral kidney ischemia followed by 12 h of reperfusion compared to sham animals (non-ischemic). Values are expressed as means ± SEM; * p < 0.05 versus sham group (n = 4/group). (B) Confocal images and graph showing increases in RIP3 levels in the kidney sections after 60 min ischemia followed by 12 min reperfusion compared to sham animals (non-ischemic). Values are expressed as means ± SEM; * p < 0.05 versus sham group (n = 4/group). (C) Immunoblot and graph showing increases in RIP3 levels in isolated mitochondria from kidney lysate in sham animals (non-ischemic) after 60 min of ischemia followed by several durations of reperfusion (12, 24, and 48 h) compared to sham animals (non-ischemic). This result indicates that RIP3 translocates in mitochondria after AKI. Values are expressed as means ± SEM; * p < 0.05 versus sham group (n = 4/group). (D) Immunoblot and graph showing reductions in Mitofilin levels in the isolated mitochondria from kidney lysate in sham animals (non-ischemic) and after 60 min of ischemia followed by several durations of reperfusion (12, 24, and 48 h) compared to sham animals (non-ischemic). Values are expressed as means ± SEM; * p < 0.05 versus sham group (n = 4/group).