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. 2019 May 14;2019:6408352. doi: 10.1155/2019/6408352

Figure 6.

Figure 6

TRPA1 mediates CMF transdifferentiation via the Ca2+-calcineurin- (CaN-) NFAT pathway. (a) Quantification of CaN activity in cultured neonatal WT mouse primary CFs treated with TGF-β or transfected with negative control (NC) adenoviral vector (not shown), Ad-TRPA1 (Ad), negative control (NC) siRNA (not shown), or si-TRPA1 (si) and treated 48 hr later with TGF-β. n ≥ 3 per group. (b and c) Immunofluorescence staining (b) and quantification (c) of α-SMA-positive (red) stress fibers and DAPI (blue) in CFs treated with TGF-β or transfected with Ad-TRPA1 and stimulated 48 hr later with TGF-β, with and without FK506 treatment (scale bars = 25 μm). n ≥ 3 per group. (d) α-SMA-luciferase promoter activity in CFs treated as described above. (e and f) Images (e) and quantification (f) of the contraction of floating collagen gel matrices seeded with CFs treated as described above. n ≥ 3 per group. (g and h) Western blot analysis and quantification of NFATc3 protein expression in the cytosolic and nuclear fractions of CFs treated as described above. Molecular weights in kDa are shown to the right of the blots. n ≥ 3 per group. The error bars represent the means ± s.e.m.∗ P < 0.05 and ∗∗ P < 0.01. The data are representative of the results of three or more independent experiments.