期刊论文详细信息
Reproductive Biology and Endocrinology
MicroRNA-181a is involved in the regulation of human endometrial stromal cell decidualization by inhibiting Krüppel-like factor 12
Research
Yali Hu1  Lijun Ding1  Zhenyu Diao1  Yue Jiang1  Qun Zhang1  Xin Zhen1  Guijun Yan1  Haixiang Sun1  Hui Zhang2  Bai Xue2 
[1] Reproductive Medicine Center, Department of Obstetrics and Gynecology, Nanjing Drum Tower Hospital, Nanjing University Medical School, 210008, Nanjing, Jiangsu, China;Reproductive Medicine Center, Drum Tower Clinic Medical College of Nanjing Medical University, 210029, Nanjing, Jiangsu, China;
关键词: MicroRNA-181a;    KLF12;    Human endometrial stromal cell;    Decidualization;   
DOI  :  10.1186/s12958-015-0019-y
 received in 2014-11-11, accepted in 2015-03-14,  发布年份 2015
来源: Springer
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【 摘 要 】

BackgroundThe transformation of endometrium into decidua is essential for normal implantation of the blastocyst. However, the post-transcriptional regulation and the miRNAs involved in decidualization remain poorly understood. Here, we examined microRNA-181a (miR-181a) expression in decidualized human endometrial stromal cell (hESC). In addition, we investigated the functional effect of miR-181a on hESC decidualization in vitro.MethodsQuantitative real-time PCR (qRT-PCR) was used to detect the profile of miR-181a in decidualized hESC. qRT-PCR, enzyme-linked fluorescent assay, and immunofluorescence assay were performed to investigate decidualization marker genes’ expression after enhancing or inhibition of miR-181a expression in hESC. Luciferase reporter assay, western blotting, qRT-PCR, and immunofluorescence assay were carried out to identify the relationship between miR-181a and Krüppel-like factor 12 (KLF12).ResultsmiR-181a expression levels increased dramatically in hESC treated with 8-Br-cAMP and MPA. Increased miR-181a expression promoted hESC decidualization-related gene expression and morphological transformation; conversely, inhibition of miR-181a expression compromised hESC decidualization in vitro. Further analysis confirmed that miR-181a interacted with the 3′ untranslated region of the transcription factor KLF12 and down-regulated KLF12 at the transcriptional and translational levels. KLF12 overexpression abolished miR-181a-induced decidualization.ConclusionsOur findings suggest that miR-181a plays a functionally important role in human endometrial stromal cell decidualization in vitro by inhibiting KLF12.

【 授权许可】

Unknown   
© Zhang et al.; licensee BioMed Central. 2015. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly credited. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.

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