Key result
Simulated microgravity drives endothelial cytoskeletal disorganization and alters angiogenic factor secretion.
Why the study?
Microgravity alters vascular homeostasis by disrupting mechanical cues critical to endothelial function.
A novel dual-stimulus bioreactor integrating simulated microgravity and physiological shear stress reveals acute endothelial dysfunction, offering a new model for spaceflight-relevant vascular research.
May prompt endothelial monitoring in astronauts; leaves open translation to human spaceflight physiology.
Microgravity alters vascular homeostasis by disrupting mechanical cues critical to endothelial function. Here, we report a benchtop bioreactor that integrates simulated microgravity with physiological laminar shear stress ( ~ 3 dyn/cm²) to examine acute endothelial responses (16 h exposure). Using human umbilical vein endothelial cells (HUVECs), we observed cytoskeletal disorganization, loss of vascular endothelial cadherin junctions, and altered secretion of angiogenic factors, including Angiopoietin 2 (Angpt-2), Vascular Endothelial Growth Factor (VEGF), and Platelet-Derived Growth Factor (PDGF). This dual-stimulus platform bridges static microgravity and flow-driven endothelial models, enabling mechanistic studies of vascular dysfunction in spaceflight-relevant conditions and offering a framework for standardized microgravity-flow experimentation.
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Pipis et al. (2026) studied Vascular dysfunction in spaceflight-relevant conditions. Simulated microgravity with physiological laminar shear stress was evaluated on Acute endothelial responses (cytoskeletal disorganization, loss of vascular endothelial cadherin junctions, and altered secretion of angiogenic factors). Exposure of human umbilical vein endothelial cells to simulated microgravity with physiological shear stress for 16 hours resulted in cytoskeletal disorganization and altered angiogenic factor secretion.
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