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DOI | 10.1289/EHP8792 |
Air Pollution Particulate Matter Exposure and Chronic Cerebral Hypoperfusion and Measures of White Matter Injury in a Murine Model | |
Qinghai Liu; Kristina Shkirkova; Krista Lamorie-Foote; Michelle Connor; Arati Patel; Robin Babadjouni; Mikko Huuskonen; Axel Montagne; Hans Baertsch; Hongqiao Zhang; Jiu-Chiuan Chen; Wendy J. Mack; Brian P. Walcott; Berislav V. Zlokovic; Constantinos Sioutas; Todd E. Morgan; Caleb E. Finch; William J. Mack | |
2021-08-23 | |
发表期刊 | Environmental Health Perspectives
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出版年 | 2021 |
英文摘要 | AbstractBackground:Exposure to ambient air pollution particulate matter (PM) is associated with increased risk of dementia and accelerated cognitive loss. Vascular contributions to cognitive impairment are well recognized. Chronic cerebral hypoperfusion (CCH) promotes neuroinflammation and blood–brain barrier weakening, which may augment neurotoxic effects of PM. Objectives:This study examined interactions of nanoscale particulate matter (nPM; fine particulate matter with aerodynamic diameter ) and CCH secondary to bilateral carotid artery stenosis (BCAS) in a murine model to produce white matter injury. Based on other air pollution interactions, we predicted synergies of nPM with BCAS. Methods:nPM was collected using a particle sampler near a Los Angeles, California, freeway. Mice were exposed to 10 wk of reaerosolized nPM or filtered air (FA) for 150 h. CCH was induced by BCAS surgery. Mice (C57BL/6J males) were randomized to four exposure paradigms: a) FA, b) nPM, c) , and d) . Behavioral outcomes, white matter injury, glial cell activation, inflammation, and oxidative stress were assessed. Results:The joint group exhibited synergistic effects on white matter injury (2.3× the additive nPM and scores) with greater loss of corpus callosum volume on T2 magnetic resonance imaging (MRI) (30% smaller than FA group). Histochemical analyses suggested potential microglial-specific inflammatory responses with synergistic effects on corpus callosum C5 immunofluorescent density and whole brain nitrate concentrations (2.1× and 3.9× the additive nPM and effects, respectively) in the joint exposure group. Transcriptomic responses (RNA-Seq) showed greater impact of than individual additive effects, consistent with changes in proinflammatory pathways. Although nPM exposure alone did not alter working memory, the cohort demonstrated impaired working memory when compared to the group. Discussion:Our data suggest that nPM and CCH contribute to white matter injury in a synergistic manner in a mouse model. Adverse neurological effects may be aggravated in a susceptible population exposed to air pollution. https://doi.org/10.1289/EHP8792 |
领域 | 资源环境 |
URL | 查看原文 |
引用统计 | |
文献类型 | 期刊论文 |
条目标识符 | http://119.78.100.173/C666/handle/2XK7JSWQ/336537 |
专题 | 资源环境科学 |
推荐引用方式 GB/T 7714 | Qinghai Liu,Kristina Shkirkova,Krista Lamorie-Foote,et al. Air Pollution Particulate Matter Exposure and Chronic Cerebral Hypoperfusion and Measures of White Matter Injury in a Murine Model[J]. Environmental Health Perspectives,2021. |
APA | Qinghai Liu.,Kristina Shkirkova.,Krista Lamorie-Foote.,Michelle Connor.,Arati Patel.,...&William J. Mack.(2021).Air Pollution Particulate Matter Exposure and Chronic Cerebral Hypoperfusion and Measures of White Matter Injury in a Murine Model.Environmental Health Perspectives. |
MLA | Qinghai Liu,et al."Air Pollution Particulate Matter Exposure and Chronic Cerebral Hypoperfusion and Measures of White Matter Injury in a Murine Model".Environmental Health Perspectives (2021). |
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