Abstract
Background. Mitofusin 2 (Mfn2) is a novel mitochondrial protein that is implicated in cellular proliferation and metabolism; however, the role of Mfn2 in preeclampsia (PE) remains unknown. This study aimed to explore the relationship between Mfn2 and PE. Method. Preeclamptic and normal pregnancies were enrolled in a comparative study. The expression of Mfn2 in placenta was detected by qRT-PCR. And the mitochondrial function was detected by ATP assay. Then TEV-1 cells were cultured in hypoxic conditions. mRNA and protein expressions of Mfn2 were detected by qRT-PCR and western blot separately. Cells' viability was detected by MTT. And the mitochondrial function was detected by ATP and mitochondrial membrane potential (MMP) assay. We further knocked down the Mfn2 gene in TEV-1 cells and evaluated the cells' viability. Results. Mfn2 and ATP expressions were significantly decreased in preeclamptic placentae compared to normal placentae. Mfn2 expression level and the viability of TEV-1 cells were reduced during hypoxic conditions. TEV-1 cells' viability, ATP, and MMP levels were also significantly decreased after knockdown of the Mfn2 gene. Conclusions. These results suggest that defects in Mfn2 could cause mitochondrial dysfunction and decrease trophoblastic cells' viability. Therefore, Mfn2 may be functionally involved in the pathogenesis of PE.
Highlights
PE is one of the leading causes of maternal and perinatal mortality and morbidity, which affects approximately 5–8% of all pregnancies, there is a great degree of variation across regions [1]
The results revealed that the Mitofusin 2 (Mfn2) mRNA expression and ATP levels in the villous tissue of the PE group were notably lower than in the control group (Figure 1)
These findings suggest that expression of Mfn2 mRNA decreased in the placental villous tissues of patients with PE
Summary
PE is one of the leading causes of maternal and perinatal mortality and morbidity, which affects approximately 5–8% of all pregnancies, there is a great degree of variation across regions [1]. Some researchers have hypothesized that mitochondrial defects may cause the impairment of trophoblasts that leads to the severe placental disorder observed in PE [3,4,5]. This hypothesis provides potential new preventative strategies for PE. Mfn expression level and the viability of TEV-1 cells were reduced during hypoxic conditions. TEV-1 cells’ viability, ATP, and MMP levels were significantly decreased after knockdown of the Mfn gene. These results suggest that defects in Mfn could cause mitochondrial dysfunction and decrease trophoblastic cells’ viability. Mfn may be functionally involved in the pathogenesis of PE
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