scholarly journals Inhibition of glutathione synthesis in brain endothelial cells lengthens S-phase transit time in the cell cycle: Implications for proliferation in recovery from oxidative stress and endothelial cell damage

Redox Biology ◽  
2013 ◽  
Vol 1 (1) ◽  
pp. 131-139 ◽  
Author(s):  
Carmina Buşu ◽  
Wei Li ◽  
Gloria Caldito ◽  
Tak Yee Aw
Keyword(s):  
Oxidative Stress ◽  
Cell Cycle ◽  
Endothelial Cells ◽  
Endothelial Cell ◽  
Transit Time ◽  
Cell Damage ◽  
S Phase ◽  
Brain Endothelial Cells ◽  
Endothelial Cell Damage ◽  
Glutathione Synthesis

Reactive oxygen species downregulate glucose transport system in retinal endothelial cells

2011 ◽  
Vol 300 (4) ◽  
pp. C927-C936 ◽  
Author(s):  
Rosa Fernandes ◽  
Ken-ichi Hosoya ◽  
Paulo Pereira
Keyword(s):  
Oxidative Stress ◽  
Endothelial Cells ◽  
Plasma Membrane ◽  
Endothelial Cell ◽  
Glucose Transport ◽  
Glucose Transporter ◽  
Cell Damage ◽  
Proteasome Inhibition ◽  
Glucose Transporter 1 ◽  
Retinal Endothelial Cells

Retinal endothelial cells are believed to play an important role in the pathogenesis of diabetic retinopathy. In previous studies, we and others demonstrated that glucose transporter 1 (GLUT1) is downregulated in response to hyperglycemia. Increased oxidative stress is likely to be the event whereby hyperglycemia is transduced into endothelial cell damage. However, the effects of sustained oxidative stress on GLUT1 regulation are not clearly established. The objective of this study is to evaluate the effect of increased oxidative stress on glucose transport and on GLUT1 subcellular distribution in a retinal endothelial cell line and to elucidate the signaling pathways associated with such regulation. Conditionally immortalized rat retinal endothelial cells (TR-iBRB) were incubated with glucose oxidase, which increases the intracellular hydrogen peroxide levels, and GLUT1 regulation was investigated. The data showed that oxidative stress did not alter the total levels of GLUT1 protein, although the levels of mRNA were decreased, and there was a subcellular redistribution of GLUT1, decreasing its content at the plasma membrane. Consistently, the half-life of the protein at the plasma membrane markedly decreased under oxidative stress. The proteasome appears to be involved in GLUT1 regulation in response to oxidative stress, as revealed by an increase in stabilization of the protein present at the plasma membrane and normalization of glucose transport following proteasome inhibition. Indeed, levels of ubiquitinated GLUT1 increase as revealed by immunoprecipitation assays. Furthermore, data indicate that protein kinase B activation is involved in the stabilization of GLUT1 at the plasma membrane. Thus subcellular redistribution of GLUT1 under conditions of oxidative stress is likely to contribute to the disruption of glucose homeostasis in diabetes.

scholarly journals Comparison of the Changes in Corneal Endothelial Cells after Pars Plana and Anterior Chamber Ahmed Valve Implant

2015 ◽  
Vol 2015 ◽  
pp. 1-7 ◽  
Author(s):  
Ji Won Seo ◽  
Jong Yeon Lee ◽  
Dong Heun Nam ◽  
Dae Yeong Lee
Keyword(s):  
Endothelial Cells ◽  
Endothelial Cell ◽  
Anterior Chamber ◽  
Cell Damage ◽  
Corneal Endothelial Cells ◽  
Refractory Glaucoma ◽  
Endothelial Cell Damage ◽  
Significant Difference ◽  
Pars Plana

Purpose. To compare the changes in corneal endothelial cells after pars plana Ahmed glaucoma valve (AGV) implantation with those after the anterior chamber AGV implantation for refractory glaucoma.Methods. The medical records of 18 eyes with pars plana implantation of AGV (ppAGV) were reviewed retrospectively and were compared with 18 eyes with the anterior chamber AGV (acAGV) implant. The preoperative and postoperative endothelial cells, intraocular pressure (IOP), and postoperative complications during the follow-up in both groups were compared.Results. The average follow-up was 18 months. The postoperative endothelial cells in the ppAGV and acAGV groups were 2044 ± 303 and 1904 ± 324, respectively(P=0.25). The average percentage decrease in the endothelial cells in the ppAGV and acAGV groups at 18 months was 12.5% and 18.4%, respectively, and showed significant difference between the 2 groups(P=0.01). No difference in IOP control and the number of postoperative glaucoma medications was observed between the 2 groups.Conclusions. Endothelial cell damage in the ppAGV group for refractory glaucoma appeared to be lower than that in the acAGV group. Therefore, pars plana implantation of AGV may be preferred as it may have lower level of endothelial cell damage while maintaining similar level of IOP control.

Effects of helium on inflammatory and oxidative stress-induced endothelial cell damage

2015 ◽  
Vol 337 (1) ◽  
pp. 37-43 ◽  
Author(s):  
Kirsten F. Smit ◽  
Raphaela P Kerindongo ◽  
Anita Böing ◽  
Rienk Nieuwland ◽  
Markus W. Hollmann ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Endothelial Cell ◽  
Cell Damage ◽  
Endothelial Cell Damage ◽  
And Oxidative Stress

scholarly journals Relationship between Candida albicans Virulence during Experimental Hematogenously Disseminated Infection and Endothelial Cell Damage In Vitro

2004 ◽  
Vol 72 (1) ◽  
pp. 598-601 ◽  
Author(s):  
Angela A. Sanchez ◽  
Douglas A. Johnston ◽  
Carter Myers ◽  
John E. Edwards ◽  
Aaron P. Mitchell ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Candida Albicans ◽  
Endothelial Cell ◽  
Cell Damage ◽  
Endothelial Cell Damage ◽  
Disseminated Infection ◽  
Lethal Infection ◽  
Cell Lining ◽  
Wild Type Parent

ABSTRACT Candida albicans must penetrate the endothelial cell lining of the vasculature to invade the deep tissues during a hematogenously disseminated infection. We compared 27 C. albicans mutants with their wild-type parent for their capacity to damage endothelial cells in vitro and cause a lethal infection in mice following tail vein inoculation. Of 10 mutants with significantly impaired capacity to damage endothelial cells, all had attenuated virulence. Therefore, the endothelial cell damage assay can be used as a screen to identify some virulence factors relevant to hematogenously disseminated candidiasis.

Oxidative stress-induced endothelial cell damage in thyroidectomized rat

2012 ◽  
Vol 64 (5) ◽  
pp. 481-485 ◽  
Author(s):  
Ayse Basak Engin ◽  
Aylin Sepici-Dincel ◽  
Ipek Isik Gonul ◽  
Atilla Engin
Keyword(s):  
Oxidative Stress ◽  
Endothelial Cell ◽  
Cell Damage ◽  
Endothelial Cell Damage

scholarly journals Vitamin D ameliorated endothelial cell damage induced by diabetes via regulation of lncRNA MEG3 in human umbilical vein endothelial cells

2020 ◽  
Author(s):  
Hua Wei ◽  
Qiongfang Zhang ◽  
Jun Li ◽  
Jing Yang ◽  
Bin Huang ◽  
...  
Keyword(s):  
Vitamin D ◽  
Endothelial Cells ◽  
Endothelial Cell ◽  
Cell Damage ◽  
Umbilical Vein ◽  
Nuclear Volume ◽  
Endothelial Cell Damage ◽  
Tnf Α ◽  
Gene And Protein Expression ◽  
Umbilical Vein Endothelial Cells

IntroductionThe purpose of this study was to investigate long non-coding RNA (lncRNA) maternally expressed gene 3 (MEG3) effects in vitamin D (Vit. D) treatment in endothelial cell damage induced by diabetes.Material and methodsWe used human umbilical vein endothelial cells (HUVECs) as a research objective in our study and used high glucose in a diabetic cell model. We evaluated cell apoptosis by flow cytometry, inflammatory factors (IL-6, IL-1β and TNF-α) concentrations by ELISA assay, relative gene and protein expression by RT-qPCR and WB assay, and NF-κB(p65) nuclear volume by cellular immunofluorescence.ResultsCompared with the NC (normal control) group, the cell apoptosis rate was significantly increased, inflammatory factor (IL-6, IL-1β and TNF-α) concentrations were significantly up-regulated, lncRNA MEG3 gene expression was significantly depressed, Toll-like receptor 4 (TLR4), myeloid differentiation factor 88 (MyD88) and nuclear factor B p65 (NF-κB(p65)) gene and protein expression levels were significantly increased and NF-κB(p65) nuclear volume was significantly up-regulated (p < 0.001, respectively). With Vit. D supplementation, compared with the Model group, Vit. D improved endothelial cell damage induced by diabetes, while lncRNA MEG3 was significantly increased and the TLR4/MyD88/NF-κB(p65) pathway was significantly depressed dose-dependently (all p < 0.05). With sh-MEG3 transfection, the Vit. D treatment effects were significantly reduced.ConclusionsVit. D improved endothelial cell damage induced by diabetes via lncRNA MEG3 up-regulation in vitro study.

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