The placenta is the bridge that connects the developing fetus and mother and is the place where nutrient uptake, waste elimination and gas exchange occurs. Epidemiological studies indicate that fetal stress, such as gestational PM2.5 (particulate matter (PM) with diameter ≤ 2.5 μm) exposure, is a risk factor for abnormal placenta development that could induce adverse effects on the fetus. In the present study, PM samples were collected in Taiyuan. Then, pregnant C57BL/6 mice were treated with 3 mg/kg b.w. PM2.5 every other day starting on GD0.5, and were sacrificed at embryonic day 13.5 (E13.5), E15.5 and E18.5, and placentas were collected for placenta histopathological analysis and gene expression evaluation at the transcription or translation level. Our results showed that gestational exposure to PM2.5 significantly reduced the ratio of the mean area of labyrinthine (lab) layer/total area of placentas at E18.5. However, no significant difference was observed at E13.5 and E15.5. Interestingly, genes essential for this process were altered at E13.5 and E18.5 but not E15.5. Furthermore, gestational PM2.5 exposure decreased the mean area of maternal blood sinuses and fetal blood vessels and suppressed protein expression of CD31 in the PM2.5 group only at E18.5, while protein expression of CD34 in the PM2.5 group was similar to that in the control group at all time points. Finally, gestational exposure to PM2.5 activated mitogen-activated protein kinase (MAPK) pathways at E13.5 and E18.5 but not E15.5. Taking these results together, gestational exposure to PM2.5 leads to histopathological changes and vascularization injuries of the placenta, and this response may be associated with activation of the MAPK pathway.
Keywords: Gestational PM(2.5) exposure; MAPK pathway; Placenta development; Vessel development.
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