(207) Microplastic-Exposed endometrial stromal cells exhibit mitochondrial dysfunction during decidualization, potentially impairing pregnancy outcomes

Objective:
The widespread use of plastics has led to increasing exposure to microplastics (MP), raising concerns about their potential impact on reproductive health. Decidualization, the differentiation of human endometrial stromal cells (hESCs), is essential for establishing a receptive endometrium and maintaining a healthy maternal-fetal interface. Disruption of this process by MP exposure could impair implantation and lead to adverse pregnancy outcomes. Mitochondrial dysfunction may be a key mediator of this effect, but the underlying mechanisms remain poorly understood. This study investigates the impact of MP exposure on decidualization of hESCs, focusing on mitochondrial dysfunction as a possible mechanism.

Study Design:
MP (polyvinyl chloride :PVC), in micro (< 25 µm) were used to investigate the toxic effects and potential mechanisms of MP on decidualization of hESCs. Morphological and functional changes were assessed in vitro using immunofluorescence staining, electron microscopy, quantitative real-time polymerase chain reaction, Western blotting, and microarray analysis.

Results:
The results showed that exposure to PVC had significant biological effects, inhibiting the decidualization of hESCs in vitro, both morphologically and functionally. Electron microscopy revealed mitochondrial abnormality and immunofluorescence staining showed functional impairement of mitochondria. In addition, Microarray analysis exhibited that PVC-exposed decidualized stromal cells (DSCs) showed a reduction in the expression of genes related with Ca2+ fluxes between ER and mitochondria in ESC.

Conclusion:

Conclusion: This study demonstrated that PVC inhibits the decidualization of hESCs and induces the mitochondrial dysfunction in DSCs. It is suggested that mitochondrial dysfunction in decidualization of hESCs caused by PVC may be one of the mechanisms potentially compromising the maternal-fetal interface and leading to adverse pregnancy outcomes (Grant Number: NRF-2022R1I1A1A01064011 and RS-2024-00342487)