Figure 6.

The expression of AXL in decidua of normal pregnancy and sPE patients

(A and B) Representative images and quantification of AXL intensity in the decidual tissue of normal pregnancies (NP) and severe preeclampsia (sPE). (a, b) AXL; (c, d) vimentin. Dec, decidual cell-enriched area; T, trophoblast cell-enriched area. (C) Relative expression of AXL mRNA to GAPDH in utero-fetal interfaces of NP and sPE. (D) Western blotting showed that the protein level of AXL was decreased in sPE utero-fetal interfaces. GAPDH was used as the loading control. (E) Western blotting results were quantified and are shown in bar graphs (NP vs. sPE, 17 vs. 16). (F) Pathway model in which Axl knockout leads to insufficient placental trophoblast invasion through STAT3-CORIN-ANP signaling, thus causing maternal preeclamptic symptoms. Our study highlights the role of aberrant interactions between the maternal decidua and fetal placenta in the pathogenesis of PE. Data are presented as means ± SDs. Scale bars, 0.2 mm; ∗p < 0.05; ∗∗p < 0.01.