In utero exposure to diesel exhaust air pollution promotes adverse intrauterine conditions, resulting in weight gain, altered blood pressure, and increased susceptibility to heart failure in adult mice.
In utero exposure to diesel exhaust air pollution promotes adverse intrauterine conditions, resulting in weight gain, altered blood pressure, and increased susceptibility to heart failure in adult mice.
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DOI：
10.1371/journal.pone.0088582
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发表时间：
2014
期刊：
影响因子：
3.7
通讯作者：
Chin MT
中科院分区：
文献类型：
--
作者：
Weldy CS;Liu Y;Liggitt HD;Chin MT
暴露于细颗粒空气污染（PM2.5）与心血管疾病发病率和死亡率密切相关。怀孕期间暴露于PM2.5会导致出生体重下降，相关的宫内不良状况也可能会增加成年后患心血管疾病的风险。在这里，我们调查了子宫内暴露于柴油机废气（DE）空气污染的可能性，柴油机废气是城市PM2.5的主要来源，促进不利的子宫内条件和影响成人对疾病的易感性。我们将妊娠雌性C57 Bl/6 J小鼠从胚胎日（E）0.5至17.5暴露于DE（≤ 300 µg/m3 PM2.5，6小时/天，5天/周）。在E17.5时，收集胚胎进行重量分析，并评估吸收证据。胎盘组织进行病理学检查，以评估损伤程度，炎性细胞浸润和氧化应激。此外，允许暴露于DE的一些母鼠在过滤空气（FA）条件下生育幼仔并抚养后代。在10周龄时，测量体重和血压。在12周龄时，通过超声心动图评估心脏功能。然后在横主动脉缩窄手术后确定压力超负荷诱导心力衰竭的易感性。我们发现，在子宫内暴露于DE增加胚胎吸收，并促进胎盘出血，局灶性坏死，迷路血管间隙压实，炎性细胞浸润和氧化应激。此外，我们观察到子宫内DE暴露增加了体重，但违反直觉地降低了血压，而成年雄性小鼠的基线心脏功能没有任何变化。重要的是，我们观察到这些小鼠对压力超负荷诱导的心力衰竭的易感性增加，这表明子宫内暴露于DE“重新编程”心脏对衰竭的易感性增加。这些观察结果提供了重要的数据表明，发育暴露于空气污染可能会强烈影响成人心血管疾病的易感性。
Exposure to fine particulate air pollution (PM2.5) is strongly associated with cardiovascular morbidity and mortality. Exposure to PM2.5 during pregnancy promotes reduced birthweight, and the associated adverse intrauterine conditions may also promote adult risk of cardiovascular disease. Here, we investigated the potential for in utero exposure to diesel exhaust (DE) air pollution, a major source of urban PM2.5, to promote adverse intrauterine conditions and influence adult susceptibility to disease. We exposed pregnant female C57Bl/6J mice to DE (≈300 µg/m3 PM2.5, 6 hrs/day, 5 days/week) from embryonic day (E) 0.5 to 17.5. At E17.5 embryos were collected for gravimetric analysis and assessed for evidence of resorption. Placental tissues underwent pathological examination to assess the extent of injury, inflammatory cell infiltration, and oxidative stress. In addition, some dams that were exposed to DE were allowed to give birth to pups and raise offspring in filtered air (FA) conditions. At 10-weeks of age, body weight and blood pressure were measured. At 12-weeks of age, cardiac function was assessed by echocardiography. Susceptibility to pressure overload-induced heart failure was then determined after transverse aortic constriction surgery. We found that in utero exposure to DE increases embryo resorption, and promotes placental hemorrhage, focal necrosis, compaction of labyrinth vascular spaces, inflammatory cell infiltration and oxidative stress. In addition, we observed that in utero DE exposure increased body weight, but counterintuitively reduced blood pressure without any changes in baseline cardiac function in adult male mice. Importantly, we observed these mice to have increased susceptibility to pressure-overload induced heart failure, suggesting this in utero exposure to DE ‘reprograms’ the heart to a heightened susceptibility to failure. These observations provide important data to suggest that developmental exposure to air pollution may strongly influence adult susceptibility to cardiovascular disease.
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影响因子：
10.4
作者：
Janssen BG;Munters E;Pieters N;Smeets K;Cox B;Cuypers A;Fierens F;Penders J;Vangronsveld J;Gyselaers W;Nawrot TS
通讯作者：
Nawrot TS
影响因子：
3.3
作者：
Bagley HN;Wang Y;Campbell MS;Yu X;Lane RH;Joss-Moore LA
通讯作者：
Joss-Moore LA
影响因子：
8.3
作者：
Eriksson, J;Forsén, T;Barker, D
通讯作者：
Barker, D
DOI：
10.1007/978-94-007-0265-3_47
发表时间：
2011-01-01
期刊：
TRANSIENT RECEPTOR POTENTIAL CHANNELS
影响因子：
--
作者：
Doerr, Janka;Fecher-Trost, Claudia
通讯作者：
Fecher-Trost, Claudia
影响因子：
3.8
作者：
Campen, Matthew J.;Lund, Amie K.;McDonald, Jacob D.
通讯作者：
McDonald, Jacob D.