CD36 mediates endothelial dysfunction downstream of circulating factors induced by O3 exposure
Open accessAbstract
Inhaled pollutants induce the release of vasoactive factors into the systemic circulation, but little information is available regarding the nature of these factors or their receptors. The pattern recognition receptor CD36 interacts with many damage-related circulating molecules, leading to activation of endothelial cells and promoting vascular inflammation; therefore, we hypothesized that CD36 plays a pivotal role in mediating cross talk between inhaled ozone (O3)-induced circulating factors and systemic vascular dysfunction. O3 exposure (1 ppm × 4h) induced lung inflammation in wild-type (WT) mice, which was absent in the CD36 deficient (CD36(-/-)) mice. Acetylcholine (ACh)-evoked vasorelaxation was impaired in isolated aortas from O3-exposed WT mice but not in vessels from CD36(-/-) mice. To delineate whether vascular impairments were caused by lung inflammation or CD36-mediated generation of circulating factors, naïve aortas were treated with diluted serum from control or O3-exposed WT mice, which recapitulated the impairments of vasorelaxation observed after inhalation exposures. Aortas from CD36(-/-) mice were insensitive to the effects of O3-induced circulating factors, with robust vasorelaxation responses in the presence of serum from O3-exposed WT mice. Lung inflammation was not a requirement for production of circulating vasoactive factors, as serum from O3-exposed CD36(-/-) mice could inhibit vasorelaxation in naïve WT aortas. These results suggest that O3 inhalation induces the release of circulating bioactive factors capable of impairing vasorelaxation to ACh via a CD36-dependent signaling mechanism. Although lung inflammatory and systemic vascular effects were both dependent on CD36, the presence of circulating factors appears to be independent of CD36 and inflammatory responses.
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Animal studies with high ozone exposures have generated more consistent findings on cardiovascular effects of ozone through altering vascular tone, mRNA for genes encoding thrombogenic factors, and atherogenesis.
“In contrast, animal studies with high ozone exposures have generated more consistent findings on cardiovascular effects of ozone through altering vascular tone (60–62), mRNA for genes encoding thrombogenic factors (63), and atherogenesis (60).”
From Ozone pollution: A Major health hazard worldwide (2019) · cites this paper as [62]
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CD163 protects against pulmonary injury and inflammation induced by acute O 3 exposurePreprint
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- Authors
- Robertson, S., Colombo, E. S., Lucas, S. N., Hall, P. R., Febbraio, M., Paffett, M. L., & Campen, M. J.
- Affiliations
- University of New Mexico (US)
- University of Alberta (CA)
- Venue
- Toxicological Sciences
- Publisher
- Oxford University Press (OUP)
- Published
- 2013-05-06
- Volume
- 134
- Issue
- 2
- Pages
- 304-311
- ISSN
- 1096-0929 (ISSN-L)
- 1096-6080
- PMC
- PMC3707435
- OpenAlex
- W2119981163
- Cited by
- 82
- References
- 43
- Citations by year
- 2026: 4 · 2025: 4 · 2024: 5 · 2023: 2 · 2022: 3 · 2021: 15 · 2020: 6 · 2019: 5 · 2018: 7 · 2017: 7 · 2016: 7 · 2015: 7 · 2014: 6 · 2013: 4
- FWCI
- 5.56
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Toxicological Sciences (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- HighWire Press Open Archive (submittedVersion)
- Funders
- National Institutes of Health (UL1TR000041, UL1TR001449)
- National Institute of Allergy and Infectious Diseases (AI090917)
- National Institute of Environmental Health Sciences (R01ES014639, ES 014639)
- National Center for Advancing Translational Sciences
- Topics
- Health Sciences › Medicine › Physiology › Nitric Oxide and Endothelin Effects
- Life Sciences › Immunology and Microbiology › Immunology › Atherosclerosis and Cardiovascular Diseases
- Physical Sciences › Environmental Science › Health, Toxicology and Mutagenesis › Air Quality and Health Impacts
- Keywords
- CD36, ozone exposure, endothelial dysfunction, vascular dysfunction, pattern recognition receptors, lung inflammation, aorta, air pollution, vascular inflammation
- MeSH terms
- Animals, Bronchoalveolar Lavage Fluid, Endothelium, Vascular, Female, Mice, Inbred C57BL, Ozone, CD36 Antigens, Inhalation Exposure, Mice
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