We investigated whether the effects of PM10 on BP are mediated by microRNAs.
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PM10 exposure was associated with increased systolic and diastolic BP.
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Nine blood miRNAs were associated with PM10 levels 48 h after exposure.
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miR-101 mediated the effects of particle exposure on diastolic BP.
Abstract
Aims
Exposure to particulate air pollution is associated with increased blood pressure (BP), a well-established risk factor for cardiovascular disease. To elucidate the mechanisms underlying this relationship, we investigated whether the effects of particulate matter of less than 10 μm in aerodynamic diameter (PM10) on BP are mediated by microRNAs.
Methods and results
We recruited 90 obese individuals and we assessed their PM10 exposure 24 and 48 h before the recruitment day. We performed multivariate linear regression models to investigate the effects of PM10 on BP. Using the TaqMan® Low-Density Array, we experimentally evaluated and technically validated the expression levels of 377 human miRNAs in peripheral blood. We developed a mediated moderation analysis to estimate the proportion of PM10 effects on BP that was mediated by miRNA expression.
PM10 exposure 24 and 48 h before the recruitment day was associated with increased systolic BP (β=1.22 mmHg, P=0.019; β=1.24 mmHg, P=0.019, respectively) and diastolic BP (β=0.67 mmHg, P=0.044; β=0.91 mmHg, P=0.007, respectively). We identified nine miRNAs associated with PM10 levels 48 h after exposure. A conditional indirect effect (CIE=−0.1431) of PM10 on diastolic BP, which was mediated by microRNA-101, was found in individuals with lower values of mean body mass index.
Conclusions
Our data provide evidence that miRNAs are a molecular mechanism underlying the BP-related effects of air pollution exposure, and indicate miR-101 as epigenetic mechanism to be further investigated.