{"title":"Impact of gestational and type 2 diabetes on fetal endothelial cell miRNA expression","authors":"Samar Sultan , Reham Sabeeh","doi":"10.1016/j.jdiacomp.2025.109106","DOIUrl":null,"url":null,"abstract":"<div><h3>Aims</h3><div>Fetal exposure to hyperglycemia <em>in utero</em> have been suggested to induce epigenetic changes through expression of various miRNAs, and cause dysfunctional endothelium connected with elevated risk of cardiovascular disease (CVD) in offspring during early adulthood. In this study, we investigated whether hyperglycemia-induced changes in the expression of 28 fetal endothelial microRNAs (miRNAs) are associated with endothelial dysfunction and CVD.</div></div><div><h3>Methods</h3><div>Differentially expressed miRNAs in TaqMan miRNA human arrays were quantified using qPCR.</div></div><div><h3>Results</h3><div>The expression of miR-140-3p, miR-1307-5p, miR-342-3p, and miR-16-5p was significantly reduced in human umbilical vein endothelial cells (HUVECs) from females with gestational diabetes (GDM-UVECs) compared with that of the control group. Meanwhile, in type 2 diabetes (T2D-HUVECs), miR-126-3p and miR-27a-5p were significantly reduced, while miR-27b-3p was significantly increased. Furthermore, miR-29b-3p expression was upregulated in both GDM– and T2D-HUVECs compared with that in the control. The expression of fibroblast growth factor 11 (<em>FGF11</em>) mRNA—a target of dysregulated miR-342-3p—was downregulated in GDMHUVECs compared with that in the control.</div></div><div><h3>Conclusions</h3><div>Altered miRNA and target <em>FGF11</em> mRNA expression may contribute mechanistically to endothelial dysfunction in diabetic HUVECs when maintained under normal glucose conditions for several passages.</div></div>","PeriodicalId":15659,"journal":{"name":"Journal of diabetes and its complications","volume":"39 9","pages":"Article 109106"},"PeriodicalIF":2.9000,"publicationDate":"2025-06-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Journal of diabetes and its complications","FirstCategoryId":"3","ListUrlMain":"https://www.sciencedirect.com/science/article/pii/S105687272500159X","RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q3","JCRName":"ENDOCRINOLOGY & METABOLISM","Score":null,"Total":0}
引用次数: 0
Abstract
Aims
Fetal exposure to hyperglycemia in utero have been suggested to induce epigenetic changes through expression of various miRNAs, and cause dysfunctional endothelium connected with elevated risk of cardiovascular disease (CVD) in offspring during early adulthood. In this study, we investigated whether hyperglycemia-induced changes in the expression of 28 fetal endothelial microRNAs (miRNAs) are associated with endothelial dysfunction and CVD.
Methods
Differentially expressed miRNAs in TaqMan miRNA human arrays were quantified using qPCR.
Results
The expression of miR-140-3p, miR-1307-5p, miR-342-3p, and miR-16-5p was significantly reduced in human umbilical vein endothelial cells (HUVECs) from females with gestational diabetes (GDM-UVECs) compared with that of the control group. Meanwhile, in type 2 diabetes (T2D-HUVECs), miR-126-3p and miR-27a-5p were significantly reduced, while miR-27b-3p was significantly increased. Furthermore, miR-29b-3p expression was upregulated in both GDM– and T2D-HUVECs compared with that in the control. The expression of fibroblast growth factor 11 (FGF11) mRNA—a target of dysregulated miR-342-3p—was downregulated in GDMHUVECs compared with that in the control.
Conclusions
Altered miRNA and target FGF11 mRNA expression may contribute mechanistically to endothelial dysfunction in diabetic HUVECs when maintained under normal glucose conditions for several passages.
期刊介绍:
Journal of Diabetes and Its Complications (JDC) is a journal for health care practitioners and researchers, that publishes original research about the pathogenesis, diagnosis and management of diabetes mellitus and its complications. JDC also publishes articles on physiological and molecular aspects of glucose homeostasis.
The primary purpose of JDC is to act as a source of information usable by diabetes practitioners and researchers to increase their knowledge about mechanisms of diabetes and complications development, and promote better management of people with diabetes who are at risk for those complications.
Manuscripts submitted to JDC can report any aspect of basic, translational or clinical research as well as epidemiology. Topics can range broadly from early prediabetes to late-stage complicated diabetes. Topics relevant to basic/translational reports include pancreatic islet dysfunction and insulin resistance, altered adipose tissue function in diabetes, altered neuronal control of glucose homeostasis and mechanisms of drug action. Topics relevant to diabetic complications include diabetic retinopathy, neuropathy and nephropathy; peripheral vascular disease and coronary heart disease; gastrointestinal disorders, renal failure and impotence; and hypertension and hyperlipidemia.