Figure 7: phf14 deletion in adult mice exacerbated renal fibrosis following folic acid-induced renal injury.

(A) Morphological analyses of lung, liver, and kidney tissues from PHF14-knockout mice compared with those from phf14 flox/flox Cre− mice on the 28th day after tamoxifen administration for 5 days. (B) Western blot results showing increased collagen I and α-SMA expression levels in the PHF14-knockout mice at the indicated time points (day 14 and day 28) after folic acid injection, compared with phf14 flox/flox Cre− mice. Anti-GAPDH was used to verify equivalent loading. (C–E) Semiquantitative analysis of collagen I, α-SMA, and PDGFR-α protein abundance in the kidneys. *P < 0.05, compared with sham controls (n = 5). (F) Representative Masson and immunohistochemical staining assay images demonstrating the severity of renal fibrosis in the PHF14-knockout mice on day 14 and day 28 after folic acid administration, compared with the sham control. (G) Quantitative analysis of fibrotic area/α-SMA-positive area/collagen I-positive area based on Masson staining and immunohistochemical staining. *P < 0.05, compared with the corresponding time point in the controls (n = 5). KO, knockout; Col 1, collagen I; PDGFR-α, platelet-derived growth factor receptor-α; α-SMA, α-smooth muscle actin; GAPDH, glyceraldehyde 3-phosphate dehydrogenase.