Transient Receptor Potential Channel Canonical Type 3 Deficiency Antagonizes Myofibroblast Transdifferentiation In Vivo

Figure 4

Trpc3^-/- attenuated myofibroblast transdifferentiation through inhibition of NOX4/pSmad in vivo. Wound granulation tissues were harvested 6 days after wounding, and immunochemistry with a primary antibody against αSMA was performed. (a) Representative immunohistochemical images showing αSMA expression in wound granulation tissues from Trpc3^+/+ mice and Trpc3^-/- mice. Vascular smooth muscle cells were stained with an anti-αSMA antibody in granulation tissues from Trpc3^+/+ mice as an internal positive control. The scale bar represents 100 μm. (b, c) Western blot analysis of TGFβ1, αSMA, fibronectin (Fibro), and Col1a1 levels in wound granulation tissues from Trpc3^+/+ and Trpc3^-/- mice. . vs. Trpc3^+/+ mice. (d) TRPC3 immunoreactivity was detected with an anti-TRPC3 antibody (96 kDa) in homogenates of primary fibroblasts from Trpc3^+/+ mice but not in those from Trpc3^-/- mice. (e) Quantification of thapsigargin (TG, 1 μmol/L)-induced SOCE and additional Ca²⁺ (1 mmol/L) in dermal fibroblasts from Trpc3^+/+ and Trpc3^-/-mice. (f, g) Western blot analysis of NOX4, pSmad2/3, and Smad2/3 in wound granulation tissues from Trpc3^+/+ and Trpc3^-/- mice. . vs. Trpc3^+/+ mice.

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