Role of nitric oxide in the inhibition of TGF-βRII expression by AT₂R activation in HK-2 cells.

<p>(A) The cells were incubated with the indicated reagents (CGP42112A, 10⁻⁷ M; L-NAME, 10⁻⁴ M) for 24 h. Results are expressed as the ratio of TGF-βRII to GAPDH densities (n = 4, *<i>P</i><0.05 vs. others, one-way factorial ANOVA followed by Holm-Sidak post-hoc test). (B) The cells were treated with different concentrations of the NO donor, S-nitroso-N-acetyl-DL-penicillamine (SNAP, 50–300 μM) for 24 h. Results are expressed as the ratio of TGF-βRII to GAPDH densities (n = 3, *<i>P</i><0.05 vs. control, one-way factorial ANOVA followed by Holm-Sidak post-hoc test). (C). HK-2 cells were incubated with the indicated reagents (CGP42112A, 10⁻⁷ M; cycloheximide [CHX], 10 μg/mL; L-NAME, 10⁻⁴ M) for 3 h. Results are expressed as the ratio of TGF-βRII to GAPDH densities (n = 3, *<i>P</i><0.05 vs. control, ^#<i>P</i><0.05 vs. cycloheximide alone, one-way factorial ANOVA followed by Holm-Sidak post-hoc test). (D and E) Expression of α-SMA (D) and E-cadherin (E) in HK-2 cells treated with the indicated reagents (CGP42112A, 10⁻⁷ M; TGF-β1, 5 ng/mL; L-NAME, 10⁻⁴ M) for 24 h. Results are expressed as the ratio of TGF-βRII to GAPDH densities (n = 3, *<i>P</i><0.05 vs. control, one-way factorial ANOVA followed by Holm-Sidak post-hoc test).