Differential expressions of stromal cell-derived factor-1α and vascular endothelial growth factor in the placental bed of pregnancies complicated by preeclampsia

SC Kim, SH Moon, DH Lee, MJ Park… - Hypertension in …, 2014 - Taylor & Francis
SC Kim, SH Moon, DH Lee, MJ Park, BS Joo, KS Lee
Hypertension in Pregnancy, 2014Taylor & Francis
Objective: The aim of this study is to examine the differential expression of stromal cell-
derived factor-1α (SDF-1α)/CXCR4 and vascular endothelial growth factor (VEGF) in the
third trimester placental bed of normotensive controls and preeclamptic patients. Methods:
Placental bed tissues were collected from 15 patients with preeclampsia (PE) and 15
gestational-matched normotensive controls at the time of their cesarean delivery. Placental
bed expressions of SDF-1α, CXCR4 and VEGF were evaluated by reverse transcriptase …
Objective: The aim of this study is to examine the differential expression of stromal cell-derived factor-1α (SDF-1α)/CXCR4 and vascular endothelial growth factor (VEGF) in the third trimester placental bed of normotensive controls and preeclamptic patients. Methods: Placental bed tissues were collected from 15 patients with preeclampsia (PE) and 15 gestational-matched normotensive controls at the time of their cesarean delivery. Placental bed expressions of SDF-1α, CXCR4 and VEGF were evaluated by reverse transcriptase-polymerase chain reaction (RT-PCR), real-time PCR and immunohistochemical staining. Results: No statistical difference was found between the PE and the normotensive control group with respect to their age and parity, gravidity and body mass index. The placental bed expressions of SDF-1α/CXCR4 and VEGF were significantly decreased in the PE group compared with the normotensive control group. Conclusions: This study showed decreased expressions of SDF-1α/CXCR4 and VEGF in the third trimester placental bed of pregnancies with PE. This result suggests that decreased expressions of SDF-1α/CXCR4 and VEGF in the placental bed could be associated with the pathogenesis of PE.
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