Objectives: Abnormal decidualization is a contributing factor for the development of preeclampsia. BCL-2/adenovirus E1B 19KD interacting protein 3 (BNIP3) has been identified as an apoptosis regulator in many tumors. Furthermore, our previous studies showed that both BNIP3 and cleaved-caspase 3 were significantly decreased in the decidual tissue of preeclampsia. Therefore, we hypothesized that BNIP3 might affect the development of preeclampsia by regulating both decidualization and apoptosis of decidual cells.
Method: BNIP3 expression in human decidua and its function during decidualization were investigated using in-vitro cultured human endometrial stromal cells (hESCs) and primary hESCs using real-time PCR, western blotting, immunohistochemistry, siRNA techniques, and flow cytometry.
Results: The levels of BNIP3 mRNA and protein in the decidua of female preeclampsia patients were lower than those of women with normal pregnancy. The expression of BNIP3 was upregulated after in-vitro decidualization and knock down of BNIP3 with small interfering RNA (siRNA) significantly reduced the transcription of decidualization markers. In addition, BNIP3 knockdown upregulated p-mTOR and p-p70s6k as well as decreased apoptosis, whereas rapamycin (which is an inhibitor of mTOR) reversed apoptosis.
Conclusion: This study indicates that BNIP3 is particularly important for decidualization and may contribute to both the occurrence and development of preeclampsia via mTOR/p70s6k/BCL-2 signaling pathways.
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