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Disturbed flow increases caveolae‐mediated oxLDL uptake in endothelial cells

Oxidized low density lipoprotein (oxLDL) is a major risk factor in the development of atherosclerotic plaques, which form at vessel bifurcations and under recirculating (disturbed) flow patterns. It is also known that oxLDL‐induced endothelial injury is the first step in plaque formation. In this study, we tested the impact of different hemodynamic conditions on endothelial cell (EC) uptake of oxLDL. ECs were exposed to shear stress (SS): laminar and oscillatory SS were generated using a parallel plate flow chamber and recirculating SS was created by designing and microfabricating a flow channel with a single step occlusion. We show that ECs exposed to recirculating flow had greater oxLDL uptake compared to ECs in laminar regions. Surprisingly, oscillatory flow inhibited rather than facilitated oxLDL uptake into ECs as compared to laminar flow. Furthermore, we show that EC uptake of oxLDL was significantly reduced by knocking out caveolin‐1, the major protein of caveolae. This indicates that caveolae play a major role in oxLDL uptake into ECs and is consistent with studies showing that Cav‐1‐KO mice do not develop atherosclerosis. Finally, since our previous studies show that exposing ECs to oxLDL increases EC stiffness in vitro, we compared EC stiffness of intact vessels in WT and ApoE KO mice. Surprisingly, ECs in ApoE KO mice are softer than in WT mice. Further studies are required to investigate this phenomenon.