ArticleEnvironmental health perspectives2012
Exposure to ambient air fine particulate matter prevents VEGF-induced mobilization of endothelial progenitor cells from the bone marrow.
Article in Environmental health perspectives, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 papers, 1 of them a synthesis that pooled it.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
56 citing papers in PubMed, 1 synthesis or guideline pooled it, 98 citations in OpenAlex.
- Effects of fine particulate matter on bone marrow-conserved hematopoietic and mesenchymal stem cells: a systematic review.Experimental & molecular medicine · 2024Pooled it
- Effects of ambient coarse, fine, and ultrafine particles and their biological constituents on systemic biomarkers: a controlled human exposure study.Environmental health perspectives · 2015Trial
- The effect of acute exposure to coarse particulate matter air pollution in a rural location on circulating endothelial progenitor cells: results from a randomized controlled study.Inhalation toxicology · 2013Trial
- Breathing in harm: current insights into the effects of air pollution on cardiorespiratory health.Medical gas research · 2027Review
- Senolytics Reverse PMCardiovascular toxicology · 2026Article
- Exposure timing is a determinant of fine particulate matter (PM2.5) pulmonary, vascular, and metabolic toxicity in male mice.Toxicological sciences : an official journal of the Society of Toxicology · 2026Article
- Ovarian hormone deficiency enhances wood smoke-induced immune dysfunction via transcriptomic and metabolic alterations.Toxicological sciences : an official journal of the Society of Toxicology · 2026Article
- Ovarian hormone deficiency enhances wood smoke-induced immune dysfunction via transcriptomic and metabolic alterations.bioRxiv : the preprint server for biology · 2026Article
- Inhalation of concentrated ambient PM2.5 promotes inactivation of telomerase reverse transcriptase, telomere shortening, and senescence of multiple cell types in mice.Toxicological sciences : an official journal of the Society of Toxicology · 2025Article
- Endothelial progenitor cells and chronic obstructive pulmonary disease: From basic research to clinical application.Zhong nan da xue xue bao. Yi xue ban = Journal of Central South University. Medical sciences · 2024Review
- Impact of the environmental pollution on cardiovascular diseases: From epidemiological to molecular evidence.Heliyon · 2024Review
- Inhaled Pollutants of the Gero-Exposome and Later-Life Health.The journals of gerontology. Series A, Biological sciences and medical sciences · 2024Review
- Exposure to Fine Particulate Matter Air Pollution Disrupts Erythrocyte Turnover.Circulation research · 2024Article
- Non-Conventional Risk Factors: "Fact" or "Fake" in Cardiovascular Disease Prevention?Biomedicines · 2023Review
- Contaminant Metals as Cardiovascular Risk Factors: A Scientific Statement From the American Heart Association.Journal of the American Heart Association · 2023Article
- Fine particulate matter (PMThe Science of the total environment · 2023Article
- Cigarette smoking and air pollution exposure and their effects on cardiovascular diseases.Frontiers in public health · 2023Review
- Environmental exposure to volatile organic compounds is associated with endothelial injury.Toxicology and applied pharmacology · 2022Article
- Tempol Preserves Endothelial Progenitor Cells in Male Mice with Ambient Fine Particulate Matter Exposure.Biomedicines · 2022Article
- Cardiovascular Effects of Particulate Air Pollution.Annual review of medicine · 2022Review
Corrections and comments
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
Abstract
backgroundExposure to ambient fine particulate matter air pollution (PM(2.5); < 2.5 µm in aerodynamic diameter) induces endothelial dysfunction and increases the risk for cardiovascular disease. Endothelial progenitor cells (EPCs) contribute to postnatal endothelial repair and regeneration. In humans and mice, EPC levels are decreased upon exposure to elevated levels of PM(2.5).
objectiveWe examined the mechanism by which PM(2.5) exposure suppresses circulating levels of EPCs.
methodsMice were exposed to HEPA-filtered air or concentrated ambient fine particulate matter (CAP, 30-100 µg/m³) from downtown Louisville (Kentucky) air, and progenitor cells from peripheral blood or bone marrow were analyzed by flow cytometry or by culture ex vivo.
resultsExposure of the mice to CAP (6 hr/day) for 4-30 days progressively decreased circulating levels of EPCs positive for both Flk-1 and Sca-1 (Flk-1(+)/Sca-1(+)) without affecting stem cells positive for Sca-1 alone (Sca-1(+)). After 9 days of exposure, a 7-day exposure-free period led to complete recovery of the circulating levels of Flk-1(+)/Sca-1(+) cells. CAP exposure decreased circulating levels of EPCs independent of apoptosis while simultaneously increasing Flk-1(+)/Sca-1(+) cells in the bone marrow. We observed no change in tissue deposition of these cells. CAP exposure suppressed vascular endothelial growth factor (VEGF)-induced Akt and endothelial nitric oxide synthase (eNOS) phosphorylation in the aorta, and it prevented VEGF/AMD3100-induced mobilization of Flk-1(+)/Sca-1(+) cells into the peripheral blood. Treatment with stem cell factor/AMD3100 led to a greater increase in circulating Flk-1(+)/Sca-1(+) cells in CAP-exposed mice than in mice breathing filtered air.
conclusionExposure to PM(2.5) increases EPC levels in the bone marrow by preventing their mobilization to the peripheral blood via inhibition of signaling events triggered by VEGF-receptor stimulation that are upstream of c-kit activation. Suppression of EPC mobilization by PM(2.5) could induce deficits in vascular repair or regeneration.
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Registered trials
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