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Airborne particulate matters induce thrombopoiesis from megakaryocytes through regulating mitochondrial oxidative phosphorylation
Particle and Fibre Toxicology ( IF 10 ) Pub Date : 2021-05-13 , DOI: 10.1186/s12989-021-00411-4
Xiaoting Jin 1, 2 , Hongyan Yu 2 , Baoqiang Wang 2 , Zhendong Sun 1, 3 , Ze Zhang 2 , Qian S Liu 1 , Yuxin Zheng 2 , Qunfang Zhou 1, 3, 4, 5 , Guibin Jiang 1, 3, 4
Affiliation  

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. 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. 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.

中文翻译:

空气中颗粒物通过调节线粒体氧化磷酸化诱导巨核细胞血小板生成

尽管空气中细颗粒物 (PM) 污染已被证明是肺部和心血管疾病的独立危险因素,但其目前可用的毒理学数据仍远不足以解释其因果关系。血小板可以调节多种生理和病理过程,流行病学研究表明 PM 暴露与循环血小板数量增加之间存在正相关。肺作为PM污染的靶器官之一,已被发现参与血小板祖细胞(即巨核细胞)的储存和血小板生成。因此,本研究通过研究 PM 治疗后巨核细胞的分化来探讨 PM 暴露是否影响血小板生成。结果表明,PM暴露以暴露浓度依赖性方式促进血小板生成。PM暴露通过引起细胞形态变化、DNA倍性的发生和血小板形成生物标志物表达的改变来诱导巨核细胞的成熟和发育。蛋白质组学分析表明,调节 PM 引起的巨核细胞成熟和血小板生成改变的主要代谢途径是线粒体氧化磷酸化 (OXPHOS) 过程。此外,空气中 PM 样品促进巨核细胞的血小板生成与颗粒大小有关,但与采样过滤器无关。这些发现首次揭示了通过调节线粒体 OXPHOS 对巨核细胞血小板生成中雾霾暴露的潜在扰动。
更新日期:2021-05-13
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