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. 2021 Nov 23;9(3):2103248. doi: 10.1002/advs.202103248

Figure 4.

Figure 4

AKI‐induced by SARS‐CoV‐2 N protein is associated with activation of Smad3‐p21‐dependent G1 cell cycle arrest pathway under ischemic stress conditions. A) Western blotting for activation of Smad3 (p‐Smad3) and expression of p21 and cyclin E. B) Real‐time PCR for levels of SARS‐CoV‐2 N, p21, and cyclin E mRNA expression. C and D) Immunohistochemistry for detecting SARS‐CoV‐2 N protein expression, activation of Smad3 (p‐Smad3 nuclear translocation), cell apoptosis by TUNEL‐labeling, and TEC proliferation by PCNA‐labeling and S‐phase cell cycle by BrdU‐labeling. Note that overexpression of SARS‐CoV‐2 N protein can promote ischemic stress‐induced activation of Smad3 signaling to cause cell death via p21‐dependent G1 cell cycle arrest mechanism. Each dot represents one mouse and data are expressed as the mean ± SEM for groups of six mice. *p < 0.05, ***p < 0.001 versus sham group; #p < 0.05, ##p < 0.01, ###p < 0.001 versus AKI with empty vector control (IRI+VC) group. g, glomerulus; scale bars = 50 µm.