| 论文题目: | A MicroRNA Signature in Gestational Diabetes Mellitus Associated with Risk of Macrosomia |
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| 作者: | Li Jiandong, Song Liping, Zhou Ling, Wu Jiaoxiang, Sheng Chunjie, Chen Huiming, Liu Yanjun*, Gao Shijuan*, and Huang Wenlin*. |
| 联系作者: | Liu, Yanjun* Gao, Shijuan* Huang, Wenlin* |
| 刊物名称: | Cell Physiol Biochem |
| 期: | 1 |
| 卷: | 37 |
| 页: | 243-52 |
| 年份: | |
| 影响因子: | 2.871 |
| 论文下载: | 下载地址 |
| 摘要: | BACKGROUND/AIMS: MicroRNA (miRNA) is a small non-coding RNA molecule that functions in regulation of gene expression by targeting mRNA to affect its stability and/or translation. The aim of this study was to evaluate the miRNAs involvement in gestational diabetes mellitus (GDM), a well known risk factor for fetal overgrowth. METHODS: Differential microRNA expression in placental tissues of normal controls and women with GDM were identified by miRNA micorarray analysis and further confirmed by quantitative real-time PCR (qRT-PCR) on an independent set of normal and GDM placental tissues. Target genes of microRNAs were bioinformatically predicted and verified in vitro by Western blotting. RESULTS: Our results uncovered 9 miRNAs that were significantly deregulated in GDM samples: miR-508-3p was up-regulated and miR-27a, miR-9, miR-137, miR-92a, miR-33a, miR-30d, miR-362-5p and miR-502-5p were down-regulated. Bioinformatic approaches revealed that the microRNAs signature identifies gene targets involved in EGFR (epidermal growth factor receptor)-PI3K (phosphoinositide 3-Kinase)-Akt (also known as protein kinase B) pathway, a signal cascade which plays important roles in placental development and fetal growth. We found that the protein levels of EGFR, PI3K and phospho-Akt were up-regulated and PIKfyve (a FYVE finger-containing phosphoinositide kinase), a negative regulator of EGFR signaling, was down-regulated significantly in GDM tissues. We also confirmed PIKfyve was a direct target of miR-508-3p. CONCLUSION: Our data identified a miRNA signature involvement in GDM which may contribute to macrosomia through enhancing EGFR signaling. |
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