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. 2020 Apr 14;31(5):1050–1065. doi: 10.1681/ASN.2019101060

Figure 5.

Figure 5.

PKCδ deficiency suppresses Drp1 activation and mitochondrial fragmentation in cold storage–transplanted kidneys. The left kidney was collected from PKCδ-KO or WT mice for 10 hours of cold storage, followed by transplantation into WT mice. The right kidney of donor mice without cold-storage transplantation was used as sham control. (A and B) At 30 minutes after transplantation, the kidneys were perfusion fixed for electron microscopy. (A) Representative electron micrographs of mitochondrial morphology in proximal tubule cells. (B) Percentage of proximal tubule cells with mostly fragmented mitochondria (<1% filamentous mitochondria). (C–F) Kidneys were collected from sham, 10 hours of cold storage, 10 hours of cold storage with transplantation/reperfusion for 0.5 hours, 24 hours, or 6 days (labeled as condition 1–5). (C and D) Whole tissues or (E and F) mitochondrial fractions were analyzed by immunoblotting and densitometry for indicated proteins. Quantitative data are expressed as mean±SD (n=3–4). *P<0.05 versus the respective sham control, #P<0.05 versus cold storage–transplanted WT kidneys. Rep, reperfusion.