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鉴定和验证妊娠期糖尿病胎盘中胎儿-胎盘动脉内皮细胞的 miRNA-mRNA 调控网络。

Identification and validation of the miRNA-mRNA regulatory network in fetoplacental arterial endothelial cells of gestational diabetes mellitus.

机构信息

Department of Pediatrics, The First Affiliated Hospital of Jinan University, Guangzhou, Guangdong, China.

出版信息

Bioengineered. 2021 Dec;12(1):3503-3515. doi: 10.1080/21655979.2021.1950279.

DOI:10.1080/21655979.2021.1950279
PMID:34233591
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8806558/
Abstract

Gestational diabetes mellitus (GDM) increases the risk of fetal heart malformations, though little is known about the mechanism of hyperglycemia-induced heart malformations. Thus, we aimed to reveal the global landscape of miRNAs and mRNAs in GDM-exposed fetoplacental arterial endothelial cells (dAECs) and establish regulatory networks for exploring the pathophysiological mechanism of fetal heart malformations in maternal hyperglycemia. Gene Expression Omnibus (GEO) datasets were used, and identification of differentially expressed miRNAs (DEMs) and genes (DEGs) in GDM was based on a previous sequencing analysis of dAECs. A miRNA-mRNA network containing 20 DEMs and 65 DEGs was established using DEMs altered in opposite directions to DEGs. In an in vivo study, we established a streptozotocin-induced pregestational diabetes mellitus (PGDM) mouse model and found the fetal cardiac wall thickness in different regions to be dramatically increased in the PGDM grouValidation of DEMs and DEGs in the fetal heart showed significantly upregulated expression of let-7e-5p, miR-139-5p and miR-195-5p and downregulated expression of SGOL1, RRM2, RGS5, CDK1 and CENPA. In summary, we reveal the miRNA-mRNA regulatory network related to fetal cardiac development disorders in offspring, which may shed light on the potential molecular mechanisms of fetal cardiac development disorders during maternal hyperglycemia.

摘要

妊娠期糖尿病（GDM）增加了胎儿心脏畸形的风险，但对于高血糖引起的心脏畸形的机制知之甚少。因此，我们旨在揭示 GDM 暴露的胎盘中动脉内皮细胞（dAEC）中 miRNA 和 mRNAs 的全局图谱，并建立调控网络，以探索母体高血糖胎儿心脏畸形的病理生理机制。使用基因表达综合数据库（GEO）数据集，并基于之前对 dAECs 的测序分析来鉴定 GDM 中的差异表达 miRNA（DEMs）和基因（DEGs）。使用与 DEGs 变化方向相反的 DEMs 建立包含 20 个 DEMs 和 65 个 DEGs 的 miRNA-mRNA 网络。在体内研究中，我们建立了链脲佐菌素诱导的孕前糖尿病（PGDM）小鼠模型，并发现 PGDM 组不同区域的胎儿心壁厚度显著增加。在胎儿心脏中验证 DEMs 和 DEGs 的表达显示，let-7e-5p、miR-139-5p 和 miR-195-5p 的表达显著上调，而 SGOL1、RRM2、RGS5、CDK1 和 CENPA 的表达下调。总之，我们揭示了与后代胎儿心脏发育障碍相关的 miRNA-mRNA 调控网络，这可能为母体高血糖时胎儿心脏发育障碍的潜在分子机制提供线索。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6128/8806558/edec4b946519/KBIE_A_1950279_F0005_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6128/8806558/560ec61a0657/KBIE_A_1950279_UF0001_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6128/8806558/fe922bddb647/KBIE_A_1950279_F0001_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6128/8806558/213d83996c66/KBIE_A_1950279_F0002_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6128/8806558/08fa44e7bf47/KBIE_A_1950279_F0003_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6128/8806558/4bdad69a1c92/KBIE_A_1950279_F0004_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6128/8806558/edec4b946519/KBIE_A_1950279_F0005_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6128/8806558/560ec61a0657/KBIE_A_1950279_UF0001_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6128/8806558/fe922bddb647/KBIE_A_1950279_F0001_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6128/8806558/213d83996c66/KBIE_A_1950279_F0002_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6128/8806558/08fa44e7bf47/KBIE_A_1950279_F0003_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6128/8806558/4bdad69a1c92/KBIE_A_1950279_F0004_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6128/8806558/edec4b946519/KBIE_A_1950279_F0005_OC.jpg

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