Diesel Exhaust Particles Impair Endothelial Progenitor Cells, Compromise Endothelial Integrity, Reduce Neoangiogenesis, and Increase Atherogenesis in Mice - Archive ouverte HAL Access content directly
Journal Articles Cardiovascular Toxicology Year : 2013

Diesel Exhaust Particles Impair Endothelial Progenitor Cells, Compromise Endothelial Integrity, Reduce Neoangiogenesis, and Increase Atherogenesis in Mice

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Janine Pöss
  • Function : Author
Dominik Lorenz
  • Function : Author
Christian Werner
  • Function : Author
Valerie Pavlikova
  • Function : Author
Christoph Gensch
  • Function : Author
Thimoteus Speer
  • Function : Author
Francesca Alessandrini
  • Function : Author
Martin Mempel
  • Function : Author
Matthias Endres
  • Function : Author
Michael Böhm
Ulrich Laufs
  • Function : Author

Abstract

The mechanisms of the harmful cardiovascular effects of small particulate matter are incompletely understood. Endothelial progenitor cells (EPCs) predict outcome of patients with vascular disease. The aim of our study was to examine the effects of diesel exhaust particles (DEP) on EPC and on the associated vascular damage in mice. C57Bl/6 mice were exposed to DEP. 2 μg DEP/day was applicated intranasally for 3 weeks. Exposure to DEP reduced DiLDL/lectin positive EPC to 58.4 ± 5.6% (p < 0.005). Migratory capacity was reduced to 65.8 ± 3.9% (p < 0.0001). In ApoE(-/-) mice, DEP application reduced the number of EPC to 75.6 ± 6.4% (p < 0.005) and EPC migration to 58.5 ± 6.8% (p < 0.005). Neoangiogenesis was reduced to 39.5 ± 14.6% (p < 0.005). Atherogenesis was profoundly increased by DEP treatment (157.7 ± 18.1% vs. controls, p < 0.05). In cultured human EPC, DEP (0.1-100 μg/mL) reduced migratory capacity to 25 ± 2.6% (p < 0.001). The number of colony-forming units was reduced to 8.8 ± 0.9% (p < 0.001) and production of reactive oxygen species was elevated by DEP treatment (p < 0.001). Furthermore, DEP treatment increased apoptosis of EPC (to 266 ± 62% of control, p < 0.05). In a blood-brain barrier model, DEP treatment impaired endothelial cell integrity during oxygen-glucose deprivation (p < 0.001). Diesel exhaust particles impair endothelial progenitor cell number and function in vivo and in vitro. The reduction in EPC was associated with impaired neoangiogenesis and a marked increase in atherosclerotic lesion formation.
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hal-02515413 , version 1 (23-03-2020)

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Janine Pöss, Dominik Lorenz, Christian Werner, Valerie Pavlikova, Christoph Gensch, et al.. Diesel Exhaust Particles Impair Endothelial Progenitor Cells, Compromise Endothelial Integrity, Reduce Neoangiogenesis, and Increase Atherogenesis in Mice. Cardiovascular Toxicology, 2013, 13 (3), pp.290-300. ⟨10.1007/s12012-013-9208-0⟩. ⟨hal-02515413⟩

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