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<p>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 <i>static</i> 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.</p>

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Simulated microgravity with physiological shear reveals endothelial disruption in a dual-stimulus bioreactor

  • 期刊论文

  • 出版模式：

    开放获取

  • 发表日期：

    2026年7月11日

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  • Nikolaos Pipis,
  • Rachel Garner,
  • Christopher Ludtka,
  • Josephine B. Allen

摘要

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.