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. 2022 Jun 28;206(5):596–607. doi: 10.1164/rccm.202106-1503OC

Figure 2.

Figure 2.

Deleting TBXA2R (thromboxane–prostanoid receptor) protects against experimental lung fibrosis. (A) Representative Masson’s trichrome–stained lung sections from wild-type (WT) and TBXA2RiKO (Rosa26-CreER+TBXA2Rf/f) mice at 21 days after intratracheal bleomycin (Bleo). (B) Morphometric evaluation of lung fibrosis on lung sections. n = 3 for control WT and TBXA2RiKO mice, and n = 5 for the Bleo treatment groups. (C) Hydroxyproline content in the right upper lobe. n = 3 for control WT mice, n = 2 for control TBXA2RiKO mice, n = 11 for the Bleo-treated WT mice, and n = 8 for the Bleo-treated TBXA2RiKO mice. Statistical comparison was performed using the Wilcoxon rank sum test (also P < 0.05 by two-way ANOVA with Tukey’s honestly significant difference test). (D) Representative Masson’s trichrome–stained lung sections from WT mice at 21 days after treatment with intratracheal Bleo or vehicle (Veh), with or without thromboxane synthesis inhibitor (Oza) beginning on Day 7. (E) Morphometric evaluation of lung fibrosis on lung sections. n = 6 for each group. (F) Hydroxyproline content in right upper lobe. n = 6 for each group. Error bars in all panels denote SEM. N.S. = not significant by Wilcoxon rank sum test; Oza = ozagrel; Rt = right.