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. 2020 Nov 30;15(11):e0242695. doi: 10.1371/journal.pone.0242695

Fig 6. Pro-fibrotic and pro-inflammatory signaling is increased in severe asthmatic fibroblasts.

Fig 6

The fibroblasts were cultured in DMEM complete medium for 2 hours post serum-starvation. Under basal conditions, mRNA expression of (A) ECM components COL1A1, COL3A1, COL5A1 and FN1, (B) cytokines IL-6 and IL-11, and (C) chemokines IL-8 and GROα, in control and S-As fibroblasts was analysed by qRT-PCR and expressed as fold expression change relative to control fibroblasts post normalization to housekeeping gene 18s rRNA. (D) The fibroblasts were treated with autophagy inhibitor, 3-MA (1mM), for 48 hours, and the mRNA expression of ECM components COL1A1, COL3A1, COL5A1 and FN1, in control and S-As fibroblasts was analysed by qRT-PCR and expressed as fold expression change relative to control fibroblasts post normalization to housekeeping gene 18s rRNA. Data are represented as mean ± SEM from at least 2 independent experiments. *p < 0.05, **p < 0.01, ***p < 0.001, ****p < 0.0001, determined by unpaired two-tailed Student t-test (Control vs Severe Asthma) or unpaired t-test with multiple comparisons using the Holm-Sidak method (Complete Medium vs 3-MA).