Abstract
Long non-coding RNAs (lncRNAs) are key regulatory molecules that are involved in a variety of biological processes and human diseases. Their impact on early onset preeclampsia remains unclear. In this study, we tested the expression of RPAIN (transcript variant 12 of RPA interacting protein, a non-coding RNA, NR_027683.1) in placenta tissues derived from 25 pregnant women with PE and 15 healthy pregnant women using quantitative real-time PCR. The effect of RPAIN on trophoblast proliferation, invasion, and apoptosis and the underlying mechanisms were examined in trophoblast cell lines (HTR-8/SVneo). The results showed that RPAIN expression levels were significantly increased in early onset preeclamptic placentas compared to normal controls. The proliferation and invasive abilities of the trophoblast cells were significantly inhibited, and the apoptosis abilities of the trophoblast cells were significantly promoted when RPAIN was overexpressed. In addition, the overexpression of RPAIN inhibited the expression of complement protein C1q. Furthermore, C1q overexpression rescued the decreased cell invasion and enhanced cell apoptosis in RPAIN-overexpressing trophoblast cells. Our results suggest that increased RPAIN levels may contribute to the development of preeclampsia through regulating trophoblast invasion and apoptosis via C1q. Therefore, we proposed RPAIN as a novel lncRNA molecule, which might contribute to the development of PE (preeclampsia) and might compose a potential diagnostic and therapeutic target for this disease.
Highlights
Preeclampsia is a pregnancy-specific syndrome that affects 3–5% of pregnancies and is traditionally diagnosed by the combined presentation of high blood pressure and proteinuria [1]
Based on a Long non-coding RNAs (lncRNAs) microarray analysis, we found that lncRNA RPAIN was overexpressed in preeclampsia placenta tissues
Accumulating evidence has indicated that lncRNAs participate in preeclampsia
Summary
Preeclampsia is a pregnancy-specific syndrome that affects 3–5% of pregnancies and is traditionally diagnosed by the combined presentation of high blood pressure and proteinuria [1]. Preeclampsia is one of the main causes of maternal, foetal and neonatal mortality, especially in low-income and middle-income countries [2, 3]. This syndrome is generally defined as the new onset of hypertension in association with proteinuria or multiple organ complications at or after the 20th week of gestation. The primary mechanism of preeclampsia remains unknown, considerable evidence indicates that the preeclampsia placenta is characterized by an abnormal trophoblast invasion, deficient maternal spiral artery modification, and increased apoptosis of trophoblastic cells [9,10,11]
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