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Q&A

Basic Science

Poster Session 2

(627) Does the dosing of low-dose aspirin for preeclampsia prevention alter serum extracellular vesicle characteristics?

Tuesday, February 13, 2024
3:30 PM – 5:00 PM  
Location: Prince George's Exhibit Hall CDE, Lower Atrium Level
Objective: Extracellular vesicles (EVs) are essential for communication at the fetal-maternal interface. EVs represent the physiologic state of the cell at the time of its release. This study evaluated the changes in the serum EV characteristics and their protein cargo in women with preeclampsia (PE) treated with aspirin (ASA).

Study Design: Previously collected maternal samples from at-risk people receiving 81 mg vs. 162 mg aspirin, based on the development of PE or not. Samples were collected between 28-32 weeks (12-20 weeks after aspirin initiation). The optimal method of ultra-centrifugation (UC) followed by size exclusion chromatography was chosen for EV isolation and characterization. EVs from women not on ASA (control), on 81 mg, or 162 mg ASA were isolated and characterized (size and quantity [ZetaView], shape [transmission electron microscopy], markers [Exoview]). Mass spectrometry-based proteomics experiments are performed using a stochastic sampling approach (data-dependent acquisition) for EV proteome cargo analysis.

Results: Ultracentrifugation and size exclusion chromatography yielded EVs’ highest number and quality. EV size and concentrations among groups were similar (Fig. 1A-B). TEM images validated intact and expected EVs’ size and shape (Fig. 1C). Average gestational age at collection was 35 weeks for the control group (n=7), 29 weeks for 81 mg group (n=32), and 28 weeks for 162 mg group (n=13). ExoView analysis confirmed known EV markers of CD9, CD81, and CD63 (Fig. 1D) that were not different between groups. The proteomic analysis did not show any differences in total maternal serum EV proteins regardless of the dose of treatment or untreated groups.

Conclusion: Total serum EVs were not different between different doses of ASA-treated and untreated PE groups, as our current approach did not distinguish between fetal vs. maternal EVs. PE is a disease of the placenta and vasculature and therefore, we postulate that placental-specific (fetal) EV characterization is required to identify prognostic markers of ASA treatment.