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. 2019 May 2;4(9):e98101. doi: 10.1172/jci.insight.98101

Figure 9. CBAs inhibit the UPR and airway inflammation via direct binding of the UPR transducer ATF6α.

Figure 9

(A) Outline of the IP and subsequent bile acid assay protocol. (B) Bile acid assay performed on ATF6α, PERK, and IRE1α IP from HBE cells stimulated with or without TUDCA. One-way ANOVA, Tukey’s post hoc test. *P < 0.05; n = 3 samples per group from 1 experiment. (C and D) Bile acid assay performed on ATF6α and IRE1α IP from lung lysates of untreated and CBA/UBA–treated mice challenged with HDM. One-way ANOVA, Tukey’s post hoc test. #P < 0.05 vs. both PBS and HDM control groups; n = 4 mice per group from 2 experiments. (E) Representative Western blots from IPs of ATF6α and IRE1α from mouse lung lysates. (F) IP and subsequent bile acid assay from cell lysates of untreated and TUDCA/AβM–treated cells challenged with Tm. One-way ANOVA, Tukey’s post hoc test. *P < 0.05; n = 3 samples per group from 1 experiment. (G) Western blots for UPR markers from cell lysates of untreated and TUDCA/AβM–treated cells challenged with Tm. IP, immunoprecipitation; UBA, unconjugated bile acid; CBA, conjugated bile acid; Ab, antibody; 3α-HSD, 3α-hydroxysteroid dehydrogenase; Red, reduced; Ox, Oxidized; ns, not significant. Error bars represent ± SEM.