Fig. 8: ST6GALNAC6 rescues impaired invasiveness of RPL-derived EVT cells in a microfluidic implantation-on-chip model. | Cell Death & Disease

Fig. 8: ST6GALNAC6 rescues impaired invasiveness of RPL-derived EVT cells in a microfluidic implantation-on-chip model.

From: Deficient extravillous trophoblast invasion caused by impaired sialylation–Siglec-7 interaction contributes to recurrent pregnancy loss

Fig. 8: ST6GALNAC6 rescues impaired invasiveness of RPL-derived EVT cells in a microfluidic implantation-on-chip model.

A Microfluidic implantation-on-a-chip model was established by seeding EVT cells into the fetal chamber and HUVEC cells into the maternal chamber. A layer of low-growth-factor matrigel containing NK-92MI cells was introduced into the central chamber to mimic the decidual–trophoblast interface. Figure created with BioRender.com (https://BioRender.com/x60p1q7). B EVT cells displayed increased invasion depth and area over time within the chip-based implantation model. C, D Recombinant ST3GAL4 and ST6GALNAC6 were added individually or in combination to RPL-derived EVT cells. The matrigel was supplemented with either Siglec-7⁺ or Siglec-7⁻ NK-92MI cells. Images were acquired after 24 h using an Olympus confocal microscope. Quantification revealed that ST6GALNAC6, alone or in combination with ST3GAL4, significantly enhanced the invasion depth and area of RPL EVT cells. ST3GAL4 alone had a minimal effect. All glycosyltransferase treatments improved invasiveness in the presence of Siglec-7⁺ NK cells. The data are presented as the means ± SDs. Statistical analysis was performed via one-way ANOVA. *P < 0.05, **P < 0.01, ***P < 0.001, ns not significant.

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