Fig. 5.

ACSL1 is essential for lncRNA H19-mediated suppression of lipid deposition. (A) Quantitative real-time polymerase chain reaction and (B, C) Western blotting detection of ACSL1 in kidneys from sham and UUO mice infected with adenoviruses expressing lncRNA H19 or control adenoviruses (n = 3). (D) Quantitative real-time polymerase chain reaction and (E, F) Western blotting detection of ACSL1 in HK-2 cells infected with adenoviruses expressing lncRNA H19 or control adenoviruses following TGF-β1 stimulation (n = 3). (G, H) Cells were co-transfected with ACSL1 siRNA or negative control siRNA and adenoviruses expressing lncRNA H19 or control adenoviruses before stimulated with TGF-β1 and the level of ACSL1 was examined by Western blotting (n = 3). (I, J) Oil Red O staining of lipid deposition in cells with various treatments were shown (n = 3). Data were presented as mean ± standard deviation, *p < 0.05, **p < 0.01 and ***p < 0.001. UUO, unilateral ureteral obstruction; ACSL1, long-chain acyl-CoA synthetase 1; GAPDH, glyceraldehyde-3-phosphate dehydrogenase; TGF-β1, transforming growth factor-β1; si-NC, negative control siRNA; si-ACSL1, long-chain acyl-CoA synthetase 1 siRNA.