scholarly journals Downregulation of Lysyl Oxidase Protects Retinal Endothelial Cells From High Glucose–Induced Apoptosis

2017 ◽  
Vol 58 (5) ◽  
pp. 2725 ◽  
Author(s):  
Dongjoon Kim ◽  
Robert P. Mecham ◽  
Philip C. Trackman ◽  
Sayon Roy
Keyword(s):  
Endothelial Cells ◽  
High Glucose ◽  
Lysyl Oxidase ◽  
Retinal Endothelial Cells ◽  
Induced Apoptosis

MiR-126 targets IL-17A to enhance proliferation and inhibit apoptosis in high-glucose-induced human retinal endothelial cells

2020 ◽  
Vol 98 (2) ◽  
pp. 277-283 ◽  
Author(s):  
Xiujuan Chen ◽  
Xuequn Yu ◽  
Xinxiang Li ◽  
Li Li ◽  
Fang Li ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
High Glucose ◽  
Molecular Mechanisms ◽  
Caspase 3 ◽  
Vision Loss ◽  
Retinal Endothelial Cells ◽  
Interleukin 17A ◽  
Novel Target ◽  
Induced Apoptosis

Diabetic retinopathy (DR) is a common complication of diabetes mellitus (DM), which results in vision loss. This study explored the role of miR-126 in high-glucose-induced human retinal endothelial cells (HRECs) and its underlying molecular mechanisms. The results showed that the expression levels of miR-126 and interleukin-17A (IL-17A) in high-glucose-induced HRECs were downregulated and upregulated, respectively. Functionally, overexpression of miR-126 promoted proliferation and suppressed apoptosis in high-glucose-induced HRECs, while IL-17A reversed the effects induced by miR-126. However, overexpression of IL-17A inhibited the proliferation and induced apoptosis, while knockdown of IL-17A accelerated the proliferation and repressed apoptosis. In addition, miR-126 repressed the expression of IL-17A, Bax, and caspase-3, while promoting the expression of survivin and phosphorylation of PI3K and AKT; restoration of IL-17A rescued these effects. Furthermore, IL-17A was identified as a target of miR-126. This indicates that miR-126 enhances proliferation and inhibits apoptosis in high-glucose-induced HRECs by activating the PI3K–AKT pathway, increasing survivin levels, and decreasing Bax and caspase-3 expression by targeting IL-17A, suggesting that miR-126 could be a novel target for preventing DR.

scholarly journals High Glucose-Induced Apoptosis Is Linked to Mitochondrial Connexin 43 Level in RRECs: Implications for Diabetic Retinopathy

Cells ◽  
2021 ◽  
Vol 10 (11) ◽  
pp. 3102
Author(s):  
Aravind Sankaramoorthy ◽  
Sayon Roy
Keyword(s):  
Endothelial Cells ◽  
Diabetic Retinopathy ◽  
High Glucose ◽  
Connexin 43 ◽  
Caspase 3 ◽  
Vision Loss ◽  
Mitochondrial Morphology ◽  
Mitochondrial Fragmentation ◽  
Retinal Endothelial Cells ◽  
Induced Apoptosis

Diabetic retinopathy (DR) is one of the most common causes of vision loss and blindness among the working-age population. High glucose (HG)-induced decrease in mitochondrial connexin 43 (mtCx43) level is known to promote mitochondrial fragmentation, cytochrome c release, and apoptosis in retinal endothelial cells associated with DR. In this study, we investigated whether counteracting HG-induced decrease in mtCx43 level would preserve mitochondrial integrity and prevent apoptosis. Rat retinal endothelial cells (RRECs) were grown in normal (N; 5 mM glucose) or HG (30 mM glucose) medium for 7 days. In parallel, cells grown in HG were transfected with Cx43 plasmid, or empty vector (EV), as control. Western blot (WB) analysis showed a significant decrease in mtCx43 level concomitant with increased cleaved caspase-3, Bax, cleaved PARP, and mitochondrial fragmentation in cells grown in HG condition compared to those grown in N medium. When cells grown in HG were transfected with Cx43 plasmid, mtCx43 level was significantly increased and resulted in reduced cleaved caspase-3, Bax, cleaved PARP and preservation of mitochondrial morphology with a significant decrease in the number of TUNEL-positive cells compared to those grown in HG alone. Findings from the study indicate a novel role for mtCx43 in regulating apoptosis and that maintenance of mtCx43 level could be useful in preventing HG-induced apoptosis by reducing mitochondrial fragmentation associated with retinal vascular cell loss in DR.

scholarly journals Sulodexide reduces glucose induced senescence in human retinal endothelial cells

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
A. Gericke ◽  
K. Suminska-Jasińska ◽  
A. Bręborowicz
Keyword(s):  
Endothelial Cells ◽  
High Glucose ◽  
Glucose Concentration ◽  
Chronic Exposure ◽  
Replicative Senescence ◽  
Population Doubling ◽  
Population Doubling Time ◽  
High Glucose Concentration ◽  
Retinal Endothelial Cells

AbstractChronic exposure of retinal endothelium cells to hyperglycemia is the leading cause of diabetic retinopathy. We evaluated the effect of high glucose concentration on senescence in human retinal endothelial cells (HREC) and modulation of that effect by Sulodexide. Experiments were performed on HREC undergoing in vitro replicative senescence in standard medium or medium supplemented with glucose 20 mmol/L (GLU) or mannitol 20 mnol/L (MAN). Effect of Sulodexide 0.5 LRU/mL (SUL) on the process of HREC senescence was studied. Glucose 20 mmol/L accelerates senescence of HREC: population doubling time (+ 58%, p < 0.001) β-galactosidase activity (+ 60%, p < 0.002) intracellular oxidative stress (+ 65%, p < 0.01), expression of p53 gene (+ 118%, p < 0.001). Senescent HREC had also reduced transendothelial electrical resistance (TEER) (− 30%, p < 0.001). Mannitol 20 mmol/L used in the same scenario as glucose did not induce HREC senescence. In HREC exposed to GLU and SUL, the senescent changes were smaller. HREC, which became senescent in the presence of GLU, demonstrated higher expression of genes regulating the synthesis of Il6 and VEGF-A, which was reflected by increased secretion of these cytokines (IL6 + 125%, p < 0.001 vs control and VEGF-A + 124% p < 0.001 vs control). These effects were smaller in the presence of SUL, and additionally, an increase of TEER in the senescent HREC was observed. Chronic exposure of HREC to high glucose concentration in medium accelerates their senescence, and that process is reduced when the cells are simultaneously exposed to Sulodexide. Additionally, Sulodexide decreases the secretion of IL6 and VEGF-A from senescent HREC and increases their TEER.

scholarly journals High Glucose Disrupts Mitochondrial Morphology in Retinal Endothelial Cells

2010 ◽  
Vol 177 (1) ◽  
pp. 447-455 ◽  
Author(s):  
Kyle Trudeau ◽  
Anthony J.A. Molina ◽  
Wen Guo ◽  
Sayon Roy
Keyword(s):  
Endothelial Cells ◽  
High Glucose ◽  
Mitochondrial Morphology ◽  
Retinal Endothelial Cells
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