PCB118 Is Associated with Impaired Decidualization and Angiogenesis Through miR-542-3p-Mediated Regulation of ILK Signaling.

2,3',4,4',5-Pentachlorobiphenyl (PCB118) is a persistent environmental pollutant associated with adverse female reproductive outcomes; however, its effects on uterine function and epigenetic regulation remain incompletely understood. This study investigated whether PCB118 disrupts uterine decidualization and angiogenesis through miRNA-mediated regulatory pathways. Human endometrial stromal cells (HESCs) and human umbilical vein endothelial cells (HUVECs) were exposed to an environmentally relevant, non-cytotoxic concentration of PCB118. Decidualization and angiogenesis were evaluated in vitro, and underlying mechanisms were investigated using molecular and miRNA-based approaches. In vivo validation of miR-542-3p expression was performed in pregnant mice following PCB118 exposure. PCB118 exposure was associated with reduced expression of decidualization markers, including prolactin (PRL) and insulin-like growth factor-binding protein 1 (IGFBP-1), as well as impaired angiogenic capacity in HUVECs. PCB118 treatment was accompanied by increased miR-542-3p expression, which was associated with decreased integrin-linked kinase (ILK) levels and changes in transforming growth factor beta 1 (TGF-β1) and total Smad2 protein abundance. ILK overexpression partially restored decidualization and angiogenesis-related phenotypes, supporting a functional involvement of ILK in these processes. Consistently, elevated miR-542-3p expression was observed in murine endometrial tissues following PCB118 exposure, suggesting physiological relevance in vivo. PCB118 exposure is associated with impaired decidualization and angiogenesis, potentially involving dysregulation of the miR-542-3p/ILK signaling axis, suggesting a potential role for epigenetic modulation in PCB118-associated reproductive dysfunction.