Taken together, our experimental results show that Smad3 and TGF-β1 play a protective role against ischemic stroke, as demonstrated by the reduced infarct size.
The overall estimates did not show any significant association between TGF-β1T869C polymorphism and risk of IS under all genetic models (C vs. T: OR = 1.08,95%CI = 0.88-1.32; CC vs. TT:OR = 1.17,95%CI = 0.79-1.72; CT vs. TT: OR = 0.91, 95%CI = 0.68-1.22; CC+CT vs. TT: OR = 0.99, 95%CI = 0.73-1.35; CC vs. CT+TT: OR = 1.23, 95%CI = 0.95-1.59).
We recently reported that transforming growth factor-beta1 (TGF-beta1) might be involved in angiogenesis after ischemic stroke in humans; here we present data of an extensive study on platelet-derived growth factor (PDGF) and its receptors.