Moreover, we demonstrate that the antiangiogenic properties of miR-503 are conferred by the production and transfer of endothelial MPs carrying miR-503 into recipient pericytes, where miR-503 further suppresses the endothelial–pericyte crosstalk by targeting EFNB2 and VEGFA. The passage of miR-503 from ECs to pericytes, where miR-503 is expressed in lower amount compared with ECs and is not transcribed or processed under diabetes and ischaemia, yet it is in part regulated by β3-integrin antagonists. The gene discussed is VEGFA; the disease is diabetes mellitus.