Role of the Polyol Pathway in High Glucose–Induced Apoptosis of Retinal Pericytes and Proliferation of Endothelial Cells

2008 ◽  
Vol 49 (7) ◽  
pp. 3216 ◽  
Author(s):  
Yoshihiro Takamura ◽  
Takeshi Tomomatsu ◽  
Eri Kubo ◽  
Syousai Tsuzuki ◽  
Yoshio Akagi
Keyword(s):  
Endothelial Cells ◽  
High Glucose ◽  
Polyol Pathway ◽  
Retinal Pericytes ◽  
Induced Apoptosis

scholarly journals SENP1-Mediated Desumoylation of DBC1 Inhibits Apoptosis Induced by High Glucose in Bovine Retinal Pericytes

2016 ◽  
Vol 2016 ◽  
pp. 1-11
Author(s):  
Jian Gao ◽  
Xia Chen ◽  
Qing Gu ◽  
Xiaoxiao Liu ◽  
Xun Xu
Keyword(s):  
Diabetic Retinopathy ◽  
High Glucose ◽  
Molecular Mechanisms ◽  
Characteristic Change ◽  
High Concentration ◽  
Retinal Pericytes ◽  
Specific Protease ◽  
Induced Apoptosis ◽  
Pericyte Loss

Pericyte loss is an early characteristic change in diabetic retinopathy, but its precise molecular mechanisms have not been elucidated. This study investigated the role of SENP1 in pericyte loss in diabetic retinopathy. We demonstrated that a high concentration of glucose inhibited the expression of the Sentrin/SUMO-specific protease 1 (SENP1), which resulted in an increase in DBC1 sumoylation in bovine retinal pericytes (BRPCs). Furthermore, SENP1 overexpression attenuated hyperemia-induced apoptosis of BPRCs, and SENP1 knockdown aggravated this effect. We also provide evidence that DBC1 sumoylation/desumoylation is involved in the SENP1-regulated apoptosis of BRPCs under high glucose conditions. Understanding the role of SENP1 in the pathogenesis of high glucose induced pericyte loss could help elucidate important targets for future pharmacological interventions.

The role of polyol pathway in glucose-induced apoptosis of cultured retinal pericytes

2003 ◽  
Vol 60 (1) ◽  
pp. 1-9 ◽  
Author(s):  
Kazuma Miwa ◽  
Jiro Nakamura ◽  
Yoji Hamada ◽  
Keiko Naruse ◽  
Eitaro Nakashima ◽  
...  
Keyword(s):  
Polyol Pathway ◽  
Retinal Pericytes ◽  
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 Protective Pleiotropic Effect of Flavonoids on NAD+Levels in Endothelial Cells Exposed to High Glucose

2015 ◽  
Vol 2015 ◽  
pp. 1-7 ◽  
Author(s):  
Daniëlle M. P. H. J. Boesten ◽  
Saskia N. I. von Ungern-Sternberg ◽  
Gertjan J. M. den Hartog ◽  
Aalt Bast
Keyword(s):  
Endothelial Cells ◽  
Enzyme Activity ◽  
Aldose Reductase ◽  
High Glucose ◽  
Umbilical Vein ◽  
Polyol Pathway ◽  
Pleiotropic Effect ◽  
Protective Role ◽  
Parp Activation

NAD+is important for oxidative metabolism by serving as an electron transporter. Hyperglycemia decreases NAD+levels by activation of the polyol pathway and by overactivation of poly(ADP-ribose)-polymerase (PARP). We examined the protective role of three structurally related flavonoids (rutin, quercetin, and flavone) during high glucose conditions in anin vitromodel using human umbilical vein endothelial cells (HUVECs). Additionally we assessed the ability of these flavonoids to inhibit aldose reductase enzyme activity. We have previously shown that flavonoids can inhibit PARP activation. Extending these studies, we here provide evidence that flavonoids are also able to protect endothelial cells against a high glucose induced decrease in NAD+. In addition, we established that flavonoids are able to inhibit aldose reductase, the key enzyme in the polyol pathway. We conclude that this protective effect of flavonoids on NAD+levels is a combination of the flavonoids ability to inhibit both PARP activation and aldose reductase enzyme activity. This study shows that flavonoids, by a combination of effects, maintain the redox state of the cell during hyperglycemia. This mode of action enables flavonoids to ameliorate diabetic complications.

Icariin Attenuates High Glucose-Induced Apoptosis, Oxidative Stress, and Inflammation in Human Umbilical Venous Endothelial Cells

Planta Medica ◽  
2019 ◽  
Vol 85 (06) ◽  
pp. 473-482 ◽  
Author(s):  
Si Sun ◽  
Le Liu ◽  
Xiaojun Tian ◽  
Yanghongyun Guo ◽  
Yingkang Cao ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Endothelial Dysfunction ◽  
High Glucose ◽  
Vascular Endothelial Cells ◽  
Reactive Oxygen Species Generation ◽  
Vascular Complications ◽  
Flavonoid Glycoside ◽  
Inflammatory Factors ◽  
Diabetic Vascular Complications ◽  
Induced Apoptosis

AbstractEndothelial dysfunction is closely associated with diabetic complications. Icariin, a flavonoid glycoside isolated from the Epimedium plant species, exhibits antidiabetic properties. However, its impact on endothelial function remains poorly understood, particularly under hyperglycemia. In this study, we investigated the potential protective effect of icariin on high glucose-induced detrimental effects on vascular endothelial cells. Human umbilical venous endothelial cells were incubated in media containing 5.5 mM glucose (normal glucose) or 25 mM glucose (high glucose) in the presence or absence of 50 µM icariin for 72 h. We found that high glucose markedly induced cell apoptosis, enhanced reactive oxygen species generation, and elevated expression levels of inflammatory factors and cell adhesion molecules, which were greatly subdued by icariin supplementation. In conclusion, icariin exerted a beneficial effect on high glucose-induced endothelial dysfunction. This new finding provides a promising strategy for future treatment of diabetic vascular complications.

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