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. 2023 Nov 8;8(21):e170521. doi: 10.1172/jci.insight.170521

Figure 2. Knockdown of CNN2 mitigates ischemic AKI.

Figure 2

(A) Experiment design. ShCNN2 plasmid was administrated in mice 7 days (d) and 1 d before IRI, respectively. The mice were sacrificed at 1 d after IRI. (B) Quantitative real-time PCR analysis showed the changes of CNN2 mRNA levels in kidneys of ShNC and ShCNN2 mice after IRI. *P < 0.05 (n = 6). (C and D) Western blot assay demonstrated CNN2 protein expression in kidneys of ShNC and ShCNN2 mice after IRI (C), and quantified data were presented (D). Numbers indicate individual animals within each group. *P < 0.05 (n = 5). (E) Immunohistochemical staining showed CNN2 expression and distribution in kidneys of ShNC and ShCNN2 mice after IRI. Scale bar, 25 μm. Arrows indicate positive staining. (F) Costaining for CNN2 (red) and PDGFR-β (green) in the kidneys demonstrated CNN2 induction was largely abolished in fibroblasts/pericytes. Scale bar, 50 μm. Arrows indicate positive staining. (G) Serum creatinine (Scr) and blood urea nitrogen (BUN) levels in ShNC and ShCNN2 mice at 1 d after IRI or 3 d after cisplatin injection. *P < 0.05 (n = 7–9). (H–J) Representative Western blots (H and I) and quantified data (J) of NGAL protein expression in ShNC and ShCNN2 kidneys at 1 day after IRI or 3 days after cisplatin injection. Numbers indicate individual animals within each group. *P < 0.05 (n = 6). (K) The changes of kidney histology as shown by periodic acid–Schiff (PAS) staining in ShNC and ShCNN2 mice at 1 d after IRI or 3 d after cisplatin injection. Scale bar, 50 μm. Blue asterisks indicate injured tubules. Graphs are presented as means ± SEM. Differences between groups were analyzed using unpaired t tests.