ArticleDiabetes, metabolic syndrome and obesity : targets and therapy2019
mRNAs expression profiles of high glucose-induced memory in human umbilical vein endothelial cells.
Article in Diabetes, metabolic syndrome and obesity : targets and therapy, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 7 citations in OpenAlex.
- Putative Novel miR-1133 Is Associated with Oxidative Stress in Hyperglycemia-Induced Endothelial Cells.Biomedicines · 2026Article
- Sustained ROS scavenging and pericellular oxygenation by lignin composites rescue HIF-1α and VEGF levels to improve diabetic wound neovascularization and healing.Acta biomaterialia · 2025Article
- Profile analysis of differentially expressed long non‑coding RNAs in metabolic memory induced by high glucose in human umbilical vein endothelial cells.Experimental and therapeutic medicine · 2023Article
- RNF6 Targeted by miR-26a-5p Protects Pancreatic β-Cell Function Against Type 2 Diabetes.Diabetes, metabolic syndrome and obesity : targets and therapy · 2022Article
- Bioinformatic Reconstruction and Analysis of Gene Networks Related to Glucose Variability in Diabetes and Its Complications.International journal of molecular sciences · 2020Article
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
purposeA long-term "memory" of hyperglycemic stress, even when glycemia is normalized, has been previously reported in endothelial cells. However, the molecular mechanism of "metabolic memory" (MM) remains unknown. In this report, we sought to screen at the whole transcriptome level the genes that participate in MM.
methodsIn the present research, RNA sequencing was used to determine the protein-coding mRNA expression profiles of human umbilical vein endothelial cells (HUVECs) under normal-glucose concentration (LG), high-glucose concentration (HG), and MM. A series of bioinformatic analyses was performed. HG-induced MM-involved up-regulated genes (up-HGMMGs) and HG-induced MM-involved down-regulated genes (down-HGMMGs) were identified. Afterward, based on up-HGMMGs and down-HGMMGs, the biological functions and signaling pathways were analyzed using Gene Ontology (GO) and the Kyoto Encyclopedia of Genes and Genomes (KEGG). In addition, several of the identified genes were validated by RT-qPCR.
resultsA total of 726 HGMMGs were identified, including 210 down- and 516 up-HGMMGs, which were enriched in the cell cycle (hsa04110), oocyte meiosis (hsa04114), p53 signaling pathway (hsa04115), and oxidative phosphorylation (hsa00190), among others. The protein-protein-interaction (PPI) network consisted of 462 nodes and 2656 connections, and four main modules were identified by MCODE. The cell cycle (hsa04110), oocyte meiosis (hsa04114), p53 signaling pathway (hsa04115), and oxidative phosphorylation (hsa00190), among others, could be potential therapeutic targets of HG-induced MM in endothelial cells. The real-time PCR results validated the RNA-seq data.
conclusionThis study identified crucial mRNAs related to MM-persistent injury in endothelial cells even after switching the cells from high- glucose to normal glucose levels. Further research focusing on these mRNA may unravel new ways to modify MM in diabetes.
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