Project description:This study aimed to elucidate the mechanisms underlying the anti-diabetic effects of Mathurameha against high glucose-induced endothelial dysfunction by SWATH-MS. The EA.hy926 cells were treated with normal glucose, high glucose, or high glucose plus Mathurameha for 24 h. Proteins were extracted and resolved on 12% SDS-PAGE. Coomassie blue-stained gel were excised in the whole lane and subjected to in-gel tryptic digestion and SWATH-MS.
Project description:RNA-seq was performed on 4-week high glucose (25mM D-glucose) treated human retinal microvascular endothelial cells (HRMECs) and control (5mM D-glucose) passage-matched cells.
Project description:Here, the effects of high glucose levels on influenza severity were investigated using an in vitro model of the pulmonary epithelial-endothelial barrier. We show that compared to low glucose levels, high glucose conditions prior to influenza A virus infection increased virus-induced barrier damage. Increased barrier damage was not associated with increased cell death nor increased virus replication, but rather an increased pro-inflammatory response in endothelial cells and the subsequent damage of the epithelial junctional complex.
Project description:Human valvular endothelial cells were co-cultured with THP-1 monocytes in high glucose (33mM) or normal glucose (5mM) levels for 2 hours. Afterwards cells were lysed and total cellular RNA was extracted using TRIzol reagent.
Project description:To observe the effects on cell programming that isolevulgandin adduct formation has on endothelial cells, we increased ROS with glucose oxidase
Project description:Purpose: To investigate the potential target genes associated with diabetic condition in mouse cavernous endothelial cells (MCECs) for diabetic induced erectile dysfunction (ED) treatment. Materials and Methods: Mouse cavernous tissue was embedded into Matrigel and sprouted cells were subcultivated for other studies. To mimic diabetic condition, the MCECs were exposed to normal-glucose (NG, 5 mmoL) and high-glucose (HG, 30 mmoL) condition for 72 hours. RNA-sequencing assay was performed to evaluate gene expression profiling and RT-PCR was used for sequencing data validation.
Project description:Artificially sweetened beverages containing noncaloric monosaccharides were suggested as healthier alternatives to sugar-sweetened beverages. Nevertheless, the potential detrimental effects of these noncaloric monosaccharides on blood vessel function remain inadequately understood. Presently, we have established a zebrafish model that exhibits significant excessive angiogenesis induced by high glucose. Utilizing this model, we observed that glucose and noncaloric monosaccharides could induce excessive formation of blood vessels, especially intersegmental vessels (ISVs). The excessively branched vessels were observed to be formed by ectopic activation of quiescent endothelial cells (ECs) into tip cells. Single-cell transcriptomic sequencing analysis of the endothelial cells in the embryos exposed to high glucose revealed an augmented ratio of capillary ECs, proliferating ECs, and a series of upregulated proangiogenic genes.
Project description:To investigate the overall gene expression pattern and explore potential drug targets of diabetic retinopathy, we used high glucose media to treat the main endothelial cells in retina, ARPE-19 cells, and then performed the gene expression profiling analysis containing mRNA and LncRNA information.
Project description:Regulation of endothelial nutrient transport is poorly understood. Vascular endothelial growth factor (VEGF)-B signaling in endothelial cells promotes uptake and transcytosis of fatty acids (FA) from the bloodstream to the underlying tissue, advancing pathological lipid accumulation and lipotoxicity in diabetic complications. Here we demonstrate a VEGF-B dependent obstruction of endothelial glucose transport attributed to plasma membrane lipid alterations affecting glucose transporter 1 function, which was independent of FA uptake. Specifically, VEGF-B signaling impaired recycling of low-density lipoprotein receptor to the plasma membrane, leading to reduced cholesterol uptake and membrane cholesterol loading, decreasing endothelial glucose uptake capacity. Inhibiting VEGF-B in vivo was accordingly linked to reconstitution of membrane cholesterol and induction of glucose uptake, of particular relevance for conditions inferring insulin resistance and diabetic complications. In summary, our study reveals a novel mechanism of action for VEGF-B in endothelial nutrient uptake and highlights the impact of membrane cholesterol for the regulation of endothelial glucose transport.
