OBJECTIVE: The aim of this study was to characterize the molecular mechanism of preeclampsia (PE) development through miR-155. STUDY DESIGN: 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. RESULTS: 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. CONCLUSION: 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. Copyright (c) 2010 Mosby, Inc. All rights reserved.
OBJECTIVE: The aim of this study was to characterize the molecular mechanism of preeclampsia (PE) development through miR-155. STUDY DESIGN: 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. RESULTS: 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. CONCLUSION: 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. Copyright (c) 2010 Mosby, Inc. All rights reserved.
Authors: Daniel A Enquobahrie; Dejene F Abetew; Tanya K Sorensen; David Willoughby; Kumaravel Chidambaram; Michelle A Williams Journal: Am J Obstet Gynecol Date: 2010-11-20 Impact factor: 8.661