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Area of Science:

  • Toxicology
  • Nanotechnology
  • Vascular Biology

Background:

  • Inhaled atmospheric nanoparticles (ANPs) can enter the bloodstream, but their precise impact on human blood vessels remains unclear.
  • Understanding the pathogenesis of ANP-induced vascular effects is crucial for public health.

Purpose of the Study:

  • To elucidate the pathogenesis of atmospheric nanoparticle (ANP) migration into human blood vessels.
  • To investigate the vascular responses to ANP exposure using a novel 3D microvessel model.

Main Methods:

  • Construction of a perfusable 3D human microvessel network in a microfluidic device.
  • Assessment of vascular inflammation, permeability, and endothelial cell responses following ANP exposure.
  • In vivo validation of ANP-induced vascular toxicity in a mouse model.

Main Results:

  • ANP exposure led to protein corona formation, vascular inflammation, and increased permeability.
  • Observed abnormal expression of nuclear factor-κB (NF-κB), intracellular calcium ([Ca2+]i), intercellular cell adhesion molecule 1 (ICAM-1), and vascular endothelial growth factor (VEGF).
  • ANP-induced imbalance in nitric oxide (NO) and endothelin-1 (ET-1) caused endothelial cell contraction and loss of tight junctions (ZO-1).

Conclusions:

  • The study provides a mechanistic explanation for how ANPs affect human vascular function, linking exposure to inflammation and toxicity.
  • The developed 3D "vessel-on-chip" model effectively mimics human vascular responses to ANPs, serving as a valuable tool for toxicity evaluation.