Figure 7. TRPV4 activity potentiates TGF-β1 actions in a SMAD2/3-independent manner.
(A) TRPV4-mediated Ca2+ influx in HLFs (measured as in Figure 2C) is not blocked by supraphysiologic concentrations of the TGF-βRI kinase inhibitor, SD208. Results are expressed as mean ± SEM. (B) Immunoblots of fibroblast cell lysates, treated as indicated, show no inhibition of TGF-β1–induced phosphorylation of SMAD2/3 or of expression of total TRPV4 proteins by the TRPV4 antagonist, AB1. Total SMAD2/3 was used as loading control. The experiments were repeated 2 times.