Mechanical forces on trophoblast motility and its potential role in spiral artery remodeling during pregnancy

Xie, Baozhen; Wu, Hui; Li, Jing; Lv, Xiaoli; Zhou, Yuexi; Yu, Qing-Ying; Cui, Shichao; Zeng, Lihua; Li, Jingwei; Huang, Xian; Gao, Jie; Luo, Songping

doi:10.1016/j.placenta.2022.03.013

Cited by 1 publication

(1 citation statement)

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“…These results confirm that the invasion of trophoblast cells under hypoxic conditions has a clear effect on vessel morphology. Although spiral arteries expand in vivo [34,38], our study showed shrinkage of the HUVEC vessel mainly due to the direction of trophoblast invasion and that blood perfusion was difficult to fully realize on the chip, as reported in other studies [39,40]. However, our results show the same tight junction weakening and morphological changes in the HUVEC vessels, similar to what has previously been reported in in vivo systems [41][42][43].…”

Section: Huvec Vessel Remodeling By Trophoblast Invasionsupporting

confidence: 86%

A Microphysiological Model to Mimic the Placental Remodeling during Early Stage of Pregnancy under Hypoxia-Induced Trophoblast Invasion

Jeong,

Fuwad,

Yoon

et al. 2024

Biomimetics

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Placental trophoblast invasion is critical for establishing the maternal–fetal interface, yet the mechanisms driving trophoblast-induced maternal arterial remodeling remain elusive. To address this gap, we developed a three-dimensional microfluidic placenta-on-chip model that mimics early pregnancy placentation in a hypoxic environment. By studying human umbilical vein endothelial cells (HUVECs) under oxygen-deprived conditions upon trophoblast invasion, we observed significant HUVEC artery remodeling, suggesting the critical role of hypoxia in placentation. In particular, we found that trophoblasts secrete matrix metalloproteinase (MMP) proteins under hypoxic conditions, which contribute to arterial remodeling by the degradation of extracellular matrix components. This MMP-mediated remodeling is critical for facilitating trophoblast invasion and proper establishment of the maternal–fetal interface. In addition, our platform allows real-time monitoring of HUVEC vessel contraction during trophoblast interaction, providing valuable insights into the dynamic interplay between trophoblasts and maternal vasculature. Collectively, our findings highlight the importance of MMP-mediated arterial remodeling in placental development and underscore the potential of our platform to study pregnancy-related complications and evaluate therapeutic interventions.

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