SMAD2 and ulcer disease: We showed that recombinant TGF-β1 reduced TGF-βRI, TGF-βRII, TGF-βRIII, and SMAD2 expression in human fibroblasts, suggesting that continuous higher TGF-β1 levels in the skin around the ulcer than in normal skin contribute to TGF-β signaling down-regulation in human ischemic ulcers and magnet-implanted mice.