Abstract
Background: Primary cilia are mechanosensory organelles that transduce fluid shear stress into intracellular signals. In endothelial cells, their role in atheroprone flow regions remains poorly understood. This study investigates how primary cilia mediate mechanotransduction under disturbed flow conditions that promote atherosclerosis.Methods: Human umbilical vein endothelial cells (HUVECs) were cultured under atheroprone (low and oscillatory shear stress, 0.5±4 dyn/cm²) and atheroprotective (steady laminar shear stress, 12 dyn/cm²) flow conditions using a parallel-plate flow chamber. Cilia presence and length were quantified by immunofluorescence. Intracellular calcium flux was measured using Fluo-4 AM. Gene expression of endothelial-to-mesenchymal transition (EndoMT) markers (CDH5, SNAI1, TWIST1) and inflammatory genes (VCAM1, ICAM1) was analyzed by qPCR. Fluid-structure interaction simulations modeled cilia bending.Results: Atheroprone flow significantly reduced cilia incidence (38.2% vs. 72.5% in static) and shortened cilia length (1.8±0.4 μm vs. 3.1±0.6 μm; pConclusions: Primary cilia dysfunction under atheroprone flow contributes to endothelial activation and EndoMT, highlighting cilia as potential therapeutic targets for atherosclerosis.