Transcriptome analysis on mesenchymal stromal cells derived from placenta and blood in preeclampsia

Abstract

Preeclampsia (PE) is a hypertensive pregnancy disorder accompanied by proteinuria, maternal organ dysfunction, and abnormal placental angiogenesis. The expression differences of genes in decidua basalis and peripheral blood–derived mesenchymal stromal cells (MSCs) are effective in preeclampsia. It was aimed to investigate whether angiogenesis-related MSC transcripts previously implicated in placental vascular dysfunction exhibit differential expression in decidua-derived and peripheral blood–derived MSCs in preeclampsia. Methods: This study covers messenger RNA (mRNA) expression analysis of MSCs from decidua (hDMSCs) (n = 14) and peripheral blood (n = 14) (PBMSCs) obtained from a total of 28 samples containing placenta and peripheral blood samples of PE patients (n = 7, 37.6 ± 1.53 weeks) and a healthy group (n = 7, 38 ± 0.92 weeks). Vascular endothelial growth factor A (VEGFAA), metallopeptidase inhibitor 1 (TIMP1), ephrin A3 (EFNA3), and thrombospondin type-1 domain-containing protein 7A (THSD7A) were analyzed for gene expression levels using droplet digital polymerase chain reaction (ddPCR) due to its high sensitivity rate to detect small amounts of samples. Results: In hDMSC samples, expression levels of VEGFAA (fold change (FC) = 5.16), TIMP-1 (FC = 1.68), and EFNA3 (FC = 1.57) were downregulated, and THSD7A was upregulated (FC = 2.56) compared to the healthy group; however, they are not statistically significant. In PBMSC samples, VEGFAA (FC = 4.2), EFNA3 (FC = 1.39), and THSD7A (FC = 1.06) levels were upregulated, while TIMP-1 (FC = 2.4) was downregulated in preeclamptic samples. Vascular endothelial growth factor A was significantly (P < .05) increased (AUC = 0.95, P = .019) in PBMSC of preeclampsia patients. Conclusion: It was aimed to show the relation of MSC-related genes, angiogenesis, and preeclampsia. Vascular endothelial growth factor A elevation in PBMSCs suggests a potential systemic angiogenic response in preeclampsia, rather than concluding its primacy in fetoplacental development. Overall, the findings suggest that MSC-related angiogenic alterations may contribute to the pathophysiology of PE, supporting the need for larger studies to validate these preliminary observations. Cite this article as: Kumral Z, Gümüşoğlu Acar E, Sevgin K, et al. Transcriptome analysis on mesenchymal stromal cells derived from placenta and blood in preeclampsia. Cerrahpaşa Med J 2026, 50, 0015, doi: 10.5152/cjm.2026.26015.