Antagonism of proangiogenic responses by CD36. In response to ligand engagement, a proangiogenic receptor (such as the VEGF or bFGF receptor) induces proliferation, migration, and tube formation of microvascular endothelial cells. In the presence of TSP-1, which interacts with a specific motif (CLESH) on its receptor, CD36, this response is inhibited. Inhibition is mediated through interaction with fyn, the activation of p38 MAP kinase, and, ultimately, caspase DNA cleavage, resulting in endothelial cell apoptosis.