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
Yali Hu1  Guijun Yan1  Haixiang Sun1  Xin Zhen1  Lijun Ding1  Zhenyu Diao1  Bai Xue2  Yue Jiang1  Hui Zhang2  Qun Zhang1 
[1] Reproductive Medicine Center, Department of Obstetrics and Gynecology, Nanjing Drum Tower Hospital, Nanjing University Medical School, Nanjing 210008, Jiangsu, China;Reproductive Medicine Center, Drum Tower Clinic Medical College of Nanjing Medical University, Nanjing 210029, Jiangsu, China
关键词: Decidualization;    Human endometrial stromal cell;    KLF12;    MicroRNA-181a;   
Others  :  1157033
DOI  :  10.1186/s12958-015-0019-y
 received in 2014-11-11, accepted in 2015-03-14,  发布年份 2015
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【 摘 要 】

Background

The 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.

Methods

Quantitative 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).

Results

miR-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.

Conclusions

Our 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】

   
2015 Zhang et al.; licensee BioMed Central.

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