ArticleParticle and fibre toxicology2021
Airborne particulate matters induce thrombopoiesis from megakaryocytes through regulating mitochondrial oxidative phosphorylation.
Article in Particle and fibre toxicology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 19 citations in OpenAlex.
- GEVResearch (Washington, D.C.) · 2025Article
- Regulating mitochondrial oxidative phosphorylation and MAPK signaling: wedelolactone as a novel therapeutic for radiation-induced thrombocytopenia.Frontiers in pharmacology · 2025Article
- Spatiotemporal trends of ischemic stroke burden attributable to PM2.5 from 1990 to 2021.Frontiers in public health · 2025Article
- Research progress of megakaryocytes and platelets in lung injury.Annals of medicine · 2024Review
- Lung megakaryocytes engulf inhaled airborne particles to promote intrapulmonary inflammation and extrapulmonary distribution.Nature communications · 2024Article
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundAlthough airborne fine particulate matter (PM) pollution has been demonstrated as an independent risk factor for pulmonary and cardiovascular diseases, their currently-available toxicological data is still far from sufficient to explain the cause-and-effect. Platelets can regulate a variety of physiological and pathological processes, and the epidemiological study has indicated a positive association between PM exposure and the increased number of circulative platelets. As one of the target organs for PM pollution, the lung has been found to be involved in the storage of platelet progenitor cells (i.e. megakaryocytes) and thrombopoiesis. Whether PM exposure influences thrombopoiesis or not is thus explored in the present study by investigating the differentiation of megakaryocytes upon PM treatment.
resultsThe results showed that PM exposure promoted the thrombopoiesis in an exposure concentration-dependent manner. PM exposure induced the megakaryocytic maturation and development by causing cell morphological changes, occurrence of DNA ploidy, and alteration in the expressions of biomarkers for platelet formation. The proteomics assay demonstrated that the main metabolic pathway regulating PM-incurred alteration of megakaryocytic maturation and thrombopoiesis was the mitochondrial oxidative phosphorylation (OXPHOS) process. Furthermore, airborne PM sample promoted-thrombopoiesis from megakaryocytes was related to particle size, but independent of sampling filters.
conclusionThe findings for the first time unveil the potential perturbation of haze exposure in thrombopoiesis from megakaryocytes by regulating mitochondrial OXPHOS. The substantial evidence on haze particle-incurred hematotoxicity obtained herein provided new insights for assessing the hazardous health risks from PM pollution.
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