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Year : 2019  |  Volume : 3  |  Issue : 1  |  Page : 36-41

Lin28B expression in reduced uterine perfusion pressure rat model

Department of Obstetrics and Gynecology, Shengjing Hospital; Key Laboratory of Maternal-Fetal Medicine; Key Laboratory of Obstetrics and Gynecology of Higher Education, China Medical University, Shenyang 110004, Liaoning, China

Correspondence Address:
Chong Qiao
Department of Obstetrics and Gynecology, Shengjing Hospital, China Medical University, 39 Huaxiang Road, Tiexi District, Shenyang 110004, Liaoning
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/2096-2924.255987

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Objective: Preeclampsia (PE) is a serious complication of pregnancy. Placental ischemia could be an initiating event, but the molecular mechanisms underlying PE are unclear. Lin28B, a paralog of Lin28 RNA-binding protein, is predominantly expressed in human placenta, and decreased Lin28B expression may play a role in PE by reducing trophoblast invasion. The current study was intended to verify whether Lin28B plays a role in the pathogenesis of PE in rat model for reduced uterine perfusion pressure (RUPP). Methods: We used RUPP rat model. The changes in blood pressure, 24-h urine protein excretion, and fetal development in RUPP rats were recorded and compared to those of normal pregnant (NP) rats. Furthermore, the expression of Lin28B mRNA and protein in placenta was determined using quantitative real-time polymerase chain reaction, Western blotting, and immunohistochemistry. Results: The blood pressure, 24-h urine protein excretion, and embryo absorption rate were significantly increased in RUPP rats on the 20th day of gestational period compared with the NP rats (P < 0.001). However, there was no difference in the weight of placenta in RUPP versus NP rats (P > 0.05). The expression levels of Lin28B mRNA and protein in the placenta of RUPP rats were also significantly decreased in comparison to NP rats (P < 0.001). Conclusion: Our results show that the expression of Lin28B in the placenta of RUPP rats is different from that in NP rats, thus suggesting a role of Lin28B in the pathogenesis of preeclampsia.

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