Endothelial HuR deletion reduces the expression of proatherogenic molecules and attenuates atherosclerosis.

Atherosclerosis is a chronic inflammatory disease of arterial wall, and the proatherogenic molecules derived from endothelium and leukocyte recruitment are major contributors to its pathogenesis. The RNA-binding protein HuR plays several physiological roles in endothelial cells, but its relevance to atherosclerosis is not yet determined. Here, by utilizing the ApoE-/- mice depleted of endothelia HuR (ApoE-/-; HuRfl/fl; Cdh5-Cre), we observed that these mice exhibited attenuated atherosclerosis compared with wild-type littermates (ApoE-/-; HuRfl/fl). Mechanistically, this phenomenon may not be associated with systemic effects on lipid metabolism, however, we found that the expression levels of proatherogenic molecules, degree of local inflammation and extent of leukocyte recruitment to aortic endothelium were all decreased when endothelia HuR was absent. Collectively, our study uncovers the role of endothelia HuR deletion in attenuating atherosclerosis, and suggests that this effect is at least in part attributed to the decreased expression of proatherogenic molecules and suppressed local inflammation. Hence, our study might offer a potential strategy for atherosclerosis treatment via manipulating endothelia HuR.