Stacked human aortic endothelial cells induce atherosclerotic fatty streaks and release proinflammatory cytokines and chemokines.

Fatty streaks, one of the earliest signs of atherosclerosis, comprise lipid-laden foam cells, which are traditionally thought to be derived from circulating monocytes that have infiltrated through the leaky endothelium and from vascular smooth muscle cells that have migrated into the intima from the media. Here we demonstrate that fatty streaks can also be induced by stacked human aortic endothelial cells (HAECs). Scanning electron microscopy revealed that these stacked HAECs form a new cellular phenotype presenting a streak/coral-like structure: "coralthelial cells". These coralthelial cells exhibit considerable lipid accumulation and increased expression of Golgi and coat protein II markers in their nuclei. Moreover, proinflammatory mediators, including interleukin-6, monocyte chemoattractant protein-1, and C-X-C motif chemokine ligand 8, are upregulated in the coralthelial cell, potentially due to the nuclear translocation of the Golgi apparatus and an elevated expression of the ribosomal protein RPL23 in the nucleolus. To our knowledge, we demonstrate for the first time that fatty streak-like structures found in atherosclerotic plaques can also be generated from the stacked HAECs.