Abnormal maternal trophoblast invasion is a common finding in preeclampsia pregnancy. A hypoxic environment develops in the placenta after the 10th week of pregnancy and exerts a major influence over trophoblast activity. In the present study, we investigated expression of miR-222 and apoptosis-related BCL2L11 in preeclampsia placenta and in primary placenta mesenchymal stem cells (MSCs) under hypoxia. The results demonstrate that miR-222 is upregulated in the placenta of preeclampsia patients, along with the downregulation of BCL2L11 in both mRNA and protein levels. In vitro results demonstrate that miR-222 is upregulated either in preeclampsia placenta tissues or in the MSCs under hypoxia. Western blotting showed downregulation of BCL2L11 in the trophoblasts under hypoxia, along with an increased MSC apoptosis. miR-222 was also confirmed to downregulate BCL2L11 expression via targeting the 3' untranslated region (UTR) of the BCL2L11 gene. miR-222 inhibitor transfection markedly ameliorated expression and transcriptional activity of BCL2L11. Altogether, the present study found that upregulation of miR-222 promotes apoptosis of mesenchymal stem cells in preeclampsia patients in response to hypoxia, via targeting BCL2L11. This suggests that a key regulatory role of miR-222 is in preeclampsia progression.
Keywords: Apoptosis; BCL2L11; hypoxia; miR-222; preeclampsia.
IJCEP Copyright © 2018.