Figure 4: PHF14 knockdown enhances collagen I and α-SMA synthesis induced by TGF-β in NRK-49F cells. | Scientific Reports

Figure 4: PHF14 knockdown enhances collagen I and α-SMA synthesis induced by TGF-β in NRK-49F cells.

From: PHF14: an innate inhibitor against the progression of renal fibrosis following folic acid-induced kidney injury

Figure 4

NRK-49F cells were pretreated with scrambled or PHF14 siRNA for 36 h. (A) Quantitative PCR (Q-PCR) demonstrating the decreased transcriptional activity of PHF14 mRNA (upper panel) and western blot analysis showing the siRNA-mediated knockdown of PHF14 (lower panel). (B) Western blot results demonstrating the changes of collagen I and α-SMA synthesis in the PHF14-knockdown group under conditions of TGF-β stimulation. Anti-GAPDH was used to verify equivalent loading. (C,D) Semiquantitative analysis of collagen I and α-SMA protein abundance in the TGF-β-treated NRK-49F cells. (E) Immunofluorescence staining revealing collagen I and α-SMA protein expression regulation in TGF-β-treated NRK-49F cells. Nuclei were visualized with DAPI (high-power field; 400 × magnification). *P < 0.05, compared with NRK-49F cells treated with vehicle; #P < 0.05, compared with NRK-49F cells pretreated with scrambled control siRNA and cultured in the media with TGF-β (n = 3). GAPDH, glyceraldehyde 3-phosphate dehydrogenase; TGF-β, transforming growth factor-β; α-SMA, α-smooth muscle actin; Col 1, collagen I; DAPI, 4′,6-diamidino-2-phenylindole.

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