Fig. 3: Downregulation of KLF10 was correlated with cell proliferation and the outcome of cisplatin-induced AKI in vivo. | Cell Death Discovery

Fig. 3: Downregulation of KLF10 was correlated with cell proliferation and the outcome of cisplatin-induced AKI in vivo.

From: Downregulation of KLF10 contributes to the regeneration of survived renal tubular cells in cisplatin-induced acute kidney injury via ZBTB7A-KLF10-PTEN axis

Fig. 3

A Flowchart detailing cisplatin treatment regime in C57BL/6 J mice. n = 6 per group. B Representative H&E staining image of kidney sections from the model. C Representative immunofluorescence staining image of Ki67 in the model and counts of positive cells per 40x field (objective lens). D Renal dysfunction was determined in cisplatin (20 mg/kg, ip) treated mouse model. Serum creatinine (SCr) was measured in sera. Degree of renal injury was determined in the model through relative mRNA levels of KIM1, NGAL and IGFBP7 in mouse kidney tissues. Degree of renal cellular proliferation was determined in the model through relative mRNA levels of PCNA, FOXM1 and Ki67 in mice kidney tissues. E Representative immunoblot analysis of KLF10, KIM1 and PCNA in the model. ACTIN served as the standard. F Regression analysis was undertaken to determine correlation between relative protein level of KLF10 in mice kidney tissues and SCr. Relative protein level of KLF10 was examined and normalized by Fiji. G–I Representative immunofluorescence staining image and rate of positive nuclear of KLF10 in the model. *p < 0.05, **p < 0.01, ***p < 0.001, ns no significantly difference vs control group at the same experimental conditions.

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