PM2.5 induces endothelial dysfunction via activating NLRP3 inflammasome.

Area of Science:

• Cardiovascular Research
• Environmental Health Science
• Cellular Biology

Background:

• Atherosclerosis development is linked to particulate matter (PM2.5) exposure.
• Endothelial cell dysfunction represents the initial stage of atherosclerosis.
• Mechanisms underlying PM2.5-induced endothelial damage remain unclear.

Purpose of the Study:

• To investigate the effects of PM2.5 on endothelial cells.
• To elucidate the role of NLRP3 inflammasome in PM2.5-induced endothelial dysfunction.

Main Methods:

• C57BL/6 male mice were exposed to PM2.5 via intranasal instillation for 2 weeks.
• Human umbilical vein endothelial cells (HUVECs) were treated with PM2.5 in vitro.
• Immunohistochemistry, cell viability assays, and ROS level measurements were performed.

Main Results:

• PM2.5 exposure increased proinflammatory cytokines and adhesion markers in mouse aortas.
• In vitro, PM2.5 reduced HUVEC viability and migration, downregulated eNOS, and increased ROS.
• PM2.5 activated the NLRP3 inflammasome in HUVECs; NLRP3 knockdown reversed PM2.5-induced effects.

Conclusions:

• PM2.5 exposure causes endothelial dysfunction.
• NLRP3 inflammasome activation is a key mechanism mediating PM2.5-induced endothelial damage.