Long non-coding RNA RPAIN regulates the invasion and apoptosis of trophoblast cell lines via complement protein C1q.
Long non-coding RNA RPAIN regulates the invasion and apoptosis of trophoblast cell lines via complement protein C1q.
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长链非编码RNA RPAIN通过补体蛋白C1q调节滋养层细胞系的侵袭和凋亡
DOI：
10.18632/oncotarget.13826
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发表时间：
2017-01-31
期刊：
影响因子：
--
通讯作者：
Long W
中科院分区：
文献类型：
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作者：
Song X;Rui C;Meng L;Zhang R;Shen R;Ding H;Li J;Li J;Long W
长链非编码RNA（lncRNA）是参与多种生物过程和人类疾病的关键调控分子。它们对早发性先兆子痫的影响尚不清楚。在这项研究中，我们使用定量实时PCR检测了来自25名患有PE的孕妇和15名健康孕妇的胎盘组织中RPAIN（RPA相互作用蛋白的转录变体12，非编码RNA，NR_027683.1）的表达。在滋养层细胞系（HTR-8/SVneo）中检测RPAIN对滋养层细胞增殖、侵袭和凋亡的作用及其潜在机制。结果显示，与正常对照相比，早发性先兆子痫胎盘中RPAIN表达水平显著增加。RPAIN过表达可显著抑制滋养层细胞的增殖和侵袭能力，促进滋养层细胞的凋亡能力。此外，RPAIN的过表达抑制补体蛋白C1 q的表达。此外，C1 q的过度表达挽救了细胞侵袭力的下降和增强细胞凋亡的RPAIN过表达的滋养层细胞。我们的研究结果表明，增加RPAIN水平可能有助于先兆子痫的发展，通过调节滋养细胞的侵袭和凋亡，通过C1 q。因此，我们提出RPAIN作为一种新的lncRNA分子，它可能有助于PE（先兆子痫）的发展，并可能构成这种疾病的潜在诊断和治疗靶点。
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.