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

Figure 1

Effects of TRPC3 on myofibroblast transdifferentiation of human fibroblasts. Human fibroblasts were treated with TGFβ1 alone (10 ng/mL) or with TGFβ1 and Pyr3 (10 μmol/L) for 12 h (upper panel) or 24 h (lower panel). (a) Immunofluorescence staining and (b) myofibroblasts (αSMA⁺, green) and nucleic acid staining (blue). This experiment was repeated three times, and the percentage of αSMA⁺ myofibroblasts was quantified over the three experiments. The bars are 100 μm. , ^# vs. control (cont); independent experiments. (c) Immunohistochemical staining of TRPC3 and TGFβ1 expression in hypertrophic scar (HTS) tissues and normal skin tissues. Vascular smooth muscle cells were stained with anti-TRPC3 and anti-TGFβ1 antibodies in HTS tissue sections as internal positive controls. The scale bar represents 100 μm in the 10x images. (d, e) TRPC3 and TGFβ1 mRNA levels as assessed by RT-PCR in human HTS tissues and normal skin tissues. , vs. normal skin tissues by Student’s -test. (f, g) Western blot analysis of TRPC3 and αSMA in human fibroblasts under treatment with TGFβ1 alone (TGFβ1, 10 ng/mL) or with TGFβ1 and Pyr3 (10 μmol/L) for 24 h or under control conditions without TGFβ1 treatment. , ^# vs. control (cont).

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