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. 2016 May 25;8(7):729–744. doi: 10.15252/emmm.201505925

Figure 6. Inhibition of IRE1α reverts the fibrotic phenotype of myofibroblasts isolated from scleroderma patients.

Figure 6

  1. CTGF mRNA expression levels in skin (dSSc) and lung (LSSc) fibroblasts isolated from scleroderma patients and treated with the IRE1α inhibitor 4μ8C. *= 0.018 for dSSc (n = 6) and = 0.003 for LSSc (n = 3).
  2. Collagen 1α2 mRNA expression levels in the same samples as in (A). *= 0.0030 for dSSc and = 0.0036 for LSSc.
  3. Quantification of collagen protein levels in the same samples as in (A). *= 0.010.
  4. Immunohistochemical staining to detect BiP protein in fibroblasts isolated from scleroderma patients treated or not with 4μ8C. Scale bars = 20 μm.
  5. mRNA levels of αSMA in primary lung fibroblasts isolated from patients with either cystic fibrosis (CF), chronic obstructive pulmonary disease (COPD), or asthma. *= 0.00001 for asthma versus healthy controls, and = 0.00003 for ctrl versus 4μ8C in asthma patients.
  6. Quantification of mRNA levels for BiP in same samples as in (E). *= 0.0023 between asthma and healthy controls and = 0.0031 between 4μ8C‐treated and control treatment in fibroblasts from asthma patients.
Data information: Statistical significance was evaluated using Student's t‐test. Significant differences are indicated with * and exact P‐values given. Error bars indicate s.e.m. n = 3 in (E, F).