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. 2019 Mar 11;30(12):1521–1538. doi: 10.1089/ars.2017.7375

FIG. 4.

FIG. 4.

Cx32 deficiency inhibited the activation of NF-κB/p53/PUMA-mediated mitochondrial apoptotic signaling pathways and mitochondrial injury after renal IR. (A) Dynamic changes of expression of mitochondrial-apoptosis-related protein by Western blot analysis at the time point of 6, 12, 24, and 48 h after reperfusion, including p-p65, p53, PUMA, cytochrome-C, Apaf-1, caspase-3 expression. (B–C) Cx32 gene deficiency attenuated the activation of NF-κB/p53/PUMA-mediated mitochondrial apoptotic signaling pathways at 24 h after reperfusion, manifested as the decrease of p-p65, p53, PUMA, cytochrome-C, Apaf-1, caspase-3 expression. [(B), Western blot analysis; (C), IF staining, target protein stained in green and cell nuclei stained in blue with DAPI, scale bar 50 μm; TEM images, scale bar 10 μm. Red arrow: mitochondrial edema and loss of inner membrane cristae]. Apaf-1, apoptotic protease activating factor-1; cyto-C, cytochrome C; IF, immunofluorescence; p-p65, phosphorylated p65 nuclear factor-κB; PUMA, p53 upregulated modulator of apoptosis. Color images are available online.