Fig 1: Vitamin D targets the pulmonary renin–angiotensin system to suppress BLM-induced lung fibrosis. (A) Relative mRNA levels of RAS components in paricalcitol-treated BLM-induced mice. *P < 0.05, **P < 0.01, versus CON group; #P < 0.05, ##P < 0.01, versus BLM group; by two-way ANOVA. n = 3–4 each group. (B,C) Western blot (B) and densitometric quantitation (C) of renin, angiotensin type 1 receptor (AT1R), and angiotensinogen (AGT) in paricalcitol-treated BLM-induced mice. ***P < 0.001, versus CON group; #P < 0.05, ##P < 0.01, versus BLM group; by two-way ANOVA and Kruskal–Wallis one-way ANOVA (for AT1R levels). n = 5–7. (D) Relative mRNA expressions of RAS components in BLM-induced VDS and VDD mice. *P < 0.05, **P < 0.01, versus VDS group; #P < 0.05, versus VDS + BLM group; by two-way ANOVA. n = 3–4 each group. (E,F) Western blot (E) and densitometric quantitation (F) of renin, AT1R and AGT in BLM-treated VDS and VDD mice. *P < 0.05, **P < 0.01, ***P < 0.001, versus VDS group; &&&P < 0.001, versus VDD group; #P < 0.05, ##P < 0.01, ###P < 0.001, versus VDS + BLM group; by two-way ANOVA. n = 6–8 each group. (G) Quantitation of Ang II levels in lung lysates. *P < 0.05, versus VDS group; &&&P < 0.001, versus VDD group; ##P < 0.01, versus VDS + BLM group; by two-way ANOVA. n = 5–7 each group.