Low-dose aspirin treatment enhances the adhesion of preeclamptic decidual mesenchymal stem/stromal cells and reduces their production of pro-inflammatory cytokines

Preeclampsia (pe) is a hypertensive disorder of human pregnancy. low-dose aspirin (acetylsalicylic acid) (60–150 mg/day) is used to prevent pe when taken early in pregnancy. the effect of aspirin on term pe remains uncertain. abnormal placentation is a hallmark of pe and leads to increased placental oxidative stress, which triggers the release of anti-angiogenic factors that cause local damage to the decidual vasculature. the damage subsequently spreads systemically and culminates in maternal clinical symptoms. decidua basalis mesenchymal stem/stromal cells (dmscs) reside in a vascular microenvironment. in pe, dmscs are exposed to abnormally high levels of oxidative stress and circulating inflammatory factors from the maternal blood. we previously showed that colony-forming unit ability and resistance to oxidative stress in dmscs are reduced in mscs derived from term pe pregnancies (pe-dmscs). the action, if any, of aspirin on term pe-dmscs has not been reported. in this study, aspirin (5 μg/ml) was found to significantly increase pe-dmsc adhesion compared to untreated pe-dmscs and gestation-matched control dmscs (p value < 0.001) but had no effect on pe-dmsc proliferation. elisa analysis showed that aspirin significantly decreased the production of inflammatory cytokines ifn-γ (p value < 0.05) and il-8 (p value < 0.001) in pe-dmscs. in addition, aspirin treatment increased the antioxidant capacity of pe-dmscs compared with the untreated group (p value < 0.05). this study is the first to reveal a novel, beneficial action of aspirin on pe-dmscs from term pe pregnancies by improving their adhesion, suppressing their production of pro-inflammatory cytokines production, and increasing their antioxidant capacity.