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Background  Kawasaki disease ( KD ) is now the most common cause of acquired cardiac disease in children due to permanent coronary artery damage with unknown etiology. The study sought to determine the role of blood micro RNA  miR‐223 in  KD  and  KD ‐induced injuries in vascular endothelial cells ( EC s) as well as the mechanisms involved.    Methods and Results  Micro RNA  profiles in serum from patients with  KD  and from healthy controls were assessed by microarray analysis. We noted that multiple serum micro RNA s were aberrantly expressed in  KD , among them miR‐223, which was the most upregulated abundant serum micro RNA . We found that bone marrow–derived blood cells (leukocytes and platelets) were able to secrete miR‐223 into serum. Vascular  EC s had no endogenous miR‐223; however, the blood cell–secreted serum miR‐223 could enter into the vascular  EC s in the vascular walls. The exogenous miR‐223 had strong biological effects on  EC  functions via its target genes such as  IGF 1R. Interestingly,  KD ‐induced  EC  injuries were related to increased miR‐223 because they were inhibited by miR‐223 knockdown. Finally, these observations were verified using miR‐223 knockout mice and the chimeric mice generated by transplantation of bone marrow from miR‐223 knockout mice into wild‐type mice.    Conclusions  In  KD  patients, the levels of blood cell–derived miR‐223 in  EC s are significantly increased. The increased miR‐223 in  EC s could work as a novel endocrine genetic signal and participate in vascular injury of  KD . MiR‐223 may provide a novel mechanism and a new therapeutic target for vascular complication of  KD .

journal of the american heart association

Bone Marrow–Derived Micro RNA ‐223 Works as an Endocrine Genetic Signal in Vascular Endothelial Cells and Participates in Vascular Injury From Kawasaki Disease