Table 1.
Clinical Characteristics of Participants.
Fig 1.
The characteristics of fetal origin AECs. Scale bar = 50μm.
(A) Fetal origin AECs from a healthy pregnant woman, and a pregnant woman with PE. AECs marker cytokeratin-7 was visualized by Alexa Fluor® 488 goat anti-Rabbit secondary antibody (green). And nuclei were counter stained with 4’,6-diamidino-2-phenylindole (DAPI). (B) RT-QPCR analysis was used to determine Oct4, Nanog, and Sox-2, which are indicating their stem-like potential. (lane 1, human fibroblast as a negative control; lane 2–4, normal AECs; lane 5–7, patient AECs; and lane 8, iPSC from normal AECs). RT-QPCR was performed 35 cycles, and GAPDH was used as the internal control, and performed 25 cycles.
Fig 2.
Gene-ontology analysis of DEGs between PE and normal pregnancy.
(A) Main categories of increased or decreased genes in PE on the basis of their cellular components. (B) Main categories of increased or decreased genes in PE on the basis of their biological processes. The numbers indicate involved genes. (F-statistic p<0.05).
Table 2.
Pathways associated with preeclampsia subjects generated by DAVID.
Fig 3.
Information regarding gene function using gene ontology from KEGG pathway database.
The numbers indicate involved genes. (F-statistic p<0.05).
Table 3.
Pathways upregulated in preeclampsia subjects generated by DAVID.
Table 4.
Pathways downregulated in preeclampsia subjects generated by DAVID.
Fig 4.
Validation for mRNA quantification of ECM-related and biological adhesion molecules.
(A) The relative expression levels for COL16A1, ITGB2, and LAMA3 were significantly up-regulated, but ITGA1, ITGA3, ITGA6, MMP-1, MMP-3, MMP-10 and MMP-11 were significantly down-regulated in AEC from patients with PE. (B) COL6A1, COL6A2, COL14A1, FN1, LAMA2, THBS2, and THBS3 were up- or down-regulated, but not significant in AEC from patients with PE.