Preeclampsia and intrauterine growth restriction, multisystemic disorders characterized by a shallow trophoblast invasion, have been associated with maternal cadmium (Cd) exposure. The molecular mechanisms of this association remain unknown. Cell adhesion and matrix metalloproteinase production are essential for an adequate trophoblast invasion. Thus, the aim of this study was to determine the effect of Cd exposure on invasion, adhesion, and matrix metalloproteinase-9 (MMP-9) production in the trophoblast-derived HTR-8/SVneo cell line. Cultured HTR-8/SVneo trophoblast cells were incubated with different concentrations of CdCl₂ for 6 h. Cell invasion was determined by the transwell assay, while cell adhesion was examined on collagen type I. MMP-9 release and activity were measured by ELISA and zymography, respectively. MMP-9 mRNA expression was detected by reverse-transcription polymerase chain reaction, while intracellular MMP-9 protein was assessed by Western blotting. Cd exposure significantly decreased the invasion and adhesion of HTR-8/SVneo cells. Also, MMP-9 levels and activity in the culture medium were significantly reduced after Cd incubation. In contrast, MMP-9 mRNA expression and intracellular protein levels were significantly increased. These data indicate that Cd reduces trophoblast cells invasiveness by inhibiting cell adhesion and MMP-9 secretion.

先兆子痫和宫内生长受限，以浅层滋养细胞侵袭为特征的多系统疾病，与母体镉 (Cd) 暴露有关。这种关联的分子机制仍然未知。细胞粘附和基质金属蛋白酶的产生对于足够的滋养层侵袭是必不可少的。因此，本研究的目的是确定镉暴露对滋养层衍生的 HTR-8/SVneo 细胞系中侵袭、粘附和基质金属蛋白酶 9 (MMP-9) 产生的影响。培养的 HTR-8/SVneo 滋养层细胞与不同浓度的 CdCl ₂孵育6 小时。细胞侵袭由 transwell 测定确定，而细胞粘附在 I 型胶原蛋白上进行检查。MMP-9 的释放和活性分别通过 ELISA 和酶谱法测量。通过逆转录聚合酶链反应检测 MMP-9 mRNA 表达，而通过蛋白质印迹评估细胞内 MMP-9 蛋白。Cd暴露显着降低了HTR-8/SVneo细胞的侵袭和粘附。此外，Cd 孵育后培养基中的 MMP-9 水平和活性显着降低。相比之下，MMP-9 mRNA 表达和细胞内蛋白水平显着增加。这些数据表明，Cd 通过抑制细胞粘附和 MMP-9 分泌来降低滋养层细胞的侵袭性。