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NPN 80078286 Licensed by Health Canada

AR, AS, IS, JPS, and HH provided resources and reagents

S.PeralesM

In line with our expectations, the cotreatment of CuSO 4 with a GHK tripeptide at every concentration tested minimized the effect of CuSO 4 , which was shown by a similar value in both sd1 and sd2 (Figure 5A)

Because typical early atherosclerotic lesion formation observed in hyperhomocysteinemic animals can be prevented by an antiplatelet therapy with dipyridamole, the authors concluded that platelet-mediated proliferation of smooth muscle cells is a potential cellular mechanism involved in the atherogenicity of hyperhomocysteinemia