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. 2023 Dec 20;70(4):247–258. doi: 10.1165/rcmb.2023-0109OC

Figure 5.


Figure 5.

Activation of IRE1α by inhibition of BCL-2 results in MRC2 expression in vitro. (A) Schematic of in vitro model developed to test BCL-2 inhibition, IRE1α activation, and expression of the Mrc2 gene. (B) Bar graph representation of the ratio of spliced amplicons to (spliced plus unspliced amplicons measured in bleomycin-injured MRC5 fibroblasts treated with navitoclax (50 nM) and/or Kira8 (1 μM). N = 3 biological replicates. (C) Level of expression of Mrc2 mRNA in bleomycin-treated MRC5 fibroblasts treated with navitoclax (50 nM) and/or Kira8 (1 μM). n = at least 3 technical triplicates in 3 biological replicates. (D) Bar graph representation of the level of expression of the transcript of UPR-associated genes measured in bleomycin-injured MRC5 fibroblasts treated with venetoclax (1 μM). n = 3 biological replicates. (E) Schematic summary of the sequestering role of BCL-2 of BAX, resulting in the activation of IRE1α activation and lack of collagen resolution was prepared using Biorender. Data represent mean ± SD. *P < 0.05, **P < 0.01, and ***P < 0.001, as determined by one-way ANOVA followed by Tukey multiple comparison test (B), Holm-Šídák’s multiple comparison test (C), or unpaired two-tailed t test (D). ER = endoplasmic reticulum; RIDD = regulated IRE1α-dependent decay.