Airborne particulate matters induce thrombopoiesis from megakaryocytes through regulating mitochondrial oxidative phosphorylation
文献类型:期刊论文
作者 | Jin, Xiaoting; Yu, Hongyan; Wang, Baoqiang; Sun, Zhendong; Zhang, Ze; Liu, Qian S.; Zheng, Yuxin; Zhou, Qunfang; Jiang, Guibin![]() |
刊名 | PARTICLE AND FIBRE TOXICOLOGY
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出版日期 | 2021-05-13 |
卷号 | 18期号:1页码:- |
关键词 | Airborne fine particulate matters Thrombopoiesis Megakaryocyte Differentiation Mitochondrial oxidative phosphorylation |
ISSN号 | 1743-8977 |
英文摘要 | Background Although 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. Results The 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. Conclusion The 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. |
WOS研究方向 | Toxicology |
源URL | [http://ir.rcees.ac.cn/handle/311016/45652] ![]() |
专题 | 生态环境研究中心_环境化学与生态毒理学国家重点实验室 |
作者单位 | 1.Qingdao Univ, China Sch Publ Hlth, Qingdao 266071, Peoples R China 2.Univ Chinese Acad Sci, Sch Environm, Hangzhou Inst Adv Study, Hangzhou 310000, Peoples R China 3.Univ Chinese Acad Sci, Coll Resources & Environm, Beijing 100049, Peoples R China 4.Chinese Acad Sci, Res Ctr Ecoenvironm Sci, State Key Lab Environm Chem & Ecotoxicol, Beijing 100085, Peoples R China 5.Jianghan Univ, Inst Environm & Hlth, Wuhan 430056, Peoples R China |
推荐引用方式 GB/T 7714 | Jin, Xiaoting,Yu, Hongyan,Wang, Baoqiang,et al. Airborne particulate matters induce thrombopoiesis from megakaryocytes through regulating mitochondrial oxidative phosphorylation[J]. PARTICLE AND FIBRE TOXICOLOGY,2021,18(1):-. |
APA | Jin, Xiaoting.,Yu, Hongyan.,Wang, Baoqiang.,Sun, Zhendong.,Zhang, Ze.,...&Jiang, Guibin.(2021).Airborne particulate matters induce thrombopoiesis from megakaryocytes through regulating mitochondrial oxidative phosphorylation.PARTICLE AND FIBRE TOXICOLOGY,18(1),-. |
MLA | Jin, Xiaoting,et al."Airborne particulate matters induce thrombopoiesis from megakaryocytes through regulating mitochondrial oxidative phosphorylation".PARTICLE AND FIBRE TOXICOLOGY 18.1(2021):-. |
入库方式: OAI收割
来源:生态环境研究中心
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