Drum Tower Clinical Medical College, Nanjing Medical University, and the Department of Obstetrics and Gynecology, Nanjing Drum Tower Hospital, Nanjing, China.
Am J Obstet Gynecol. 2010 May;202(5):466.e1-7. doi: 10.1016/j.ajog.2010.01.057.
The aim of this study was to characterize the molecular mechanism of preeclampsia (PE) development through miR-155.
PE and normal placentas were used to measure miR-155 and cysteine-rich protein 61 (CYR61) expression. CYR61 3' untranslated region was validated as the target of miR-155 using in vitro transfections. miR-155 and CYR61 expression levels were assessed by real-time reverse transcription polymerase chain reaction or Western blot.
An inverse correlation was found between miR-155 and CYR61 expression levels, with miR-155 up-regulated and CYR61 down-regulated in PE tissues. Luciferase assays and CYR61 transfection assays experimentally validated that miR-155 efficiently targets the 3' untranslated region of CYR61.
This study reported for the first time that overexpression of miR-155 contributes to PE development by targeting and down-regulating angiogenic regulating factor CYR61, leading to pathological alterations. This finding not only characterizes a new mechanism for the disease but also provides a potential therapeutic target.
本研究旨在通过 miR-155 来阐明子痫前期（PE）发展的分子机制。
采用 PE 和正常胎盘来检测 miR-155 和富含半胱氨酸蛋白 61（CYR61）的表达。通过体外转染验证 CYR61 的 3'非翻译区（UTR）是 miR-155 的靶标。采用实时逆转录聚合酶链反应或 Western blot 来评估 miR-155 和 CYR61 的表达水平。
miR-155 与 CYR61 的表达水平呈负相关，PE 组织中 miR-155 上调，而 CYR61 下调。荧光素酶测定和 CYR61 转染实验证实 miR-155 能有效靶向 CYR61 的 3'UTR。
本研究首次报道，通过靶向和下调血管生成调节因子 CYR61，导致病理改变，miR-155 的过表达有助于 PE 的发展。这一发现不仅阐明了该疾病的新机制，还为潜在的治疗靶点提供了依据。
