Simultaneous Measurement of Endothelial Cell Damage, Elastase Release, and Chemiluminescence Response During Interaction Between Polymorphonuclear Leukocytes and Endothelial Cells

1991 ◽  
pp. 281-293
Author(s):  
E. Jonas ◽  
A. Dwenger ◽  
B. Lueken ◽  
U. Böhme
Keyword(s):  
Endothelial Cells ◽  
Endothelial Cell ◽  
Simultaneous Measurement ◽  
Polymorphonuclear Leukocytes ◽  
Cell Damage ◽  
Endothelial Cell Damage

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.

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.

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.

Endothelial Cell Damage in Sarcoidosis and Neurosarcoidosis: Autoantibodies to Endothelial Cells

1995 ◽  
Vol 35 (2) ◽  
pp. 108-112 ◽  
Author(s):  
Naoyuki Tsukada ◽  
Nobuo Yanagisawa ◽  
Ichiro Mochizuki
Keyword(s):  
Endothelial Cells ◽  
Endothelial Cell ◽  
Cell Damage ◽  
Endothelial Cell Damage

scholarly journals The Comparison of the Protective Effects of α- and β-Antithrombin against Vascular Endothelial Cell Damage Induced by Histone in Vitro

TH Open ◽  
2017 ◽  
Vol 01 (01) ◽  
pp. e3-e10 ◽  
Author(s):  
Toshiaki Iba ◽  
Tetsuya Sasaki ◽  
Kazutoshi Ohshima ◽  
Koichi Sato ◽  
Isao Nagaoka ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Endothelial Cell ◽  
Cell Viability ◽  
Cell Damage ◽  
Immunofluorescent Staining ◽  
Vascular Endothelial ◽  
Protective Effects ◽  
Histone H4 ◽  
Endothelial Cell Damage

AbstractAntithrombin is a promising option for the treatment of sepsis, and vascular endothelium is an important target for this fatal condition. Here, we aimed to evaluate the protective effects of different glycoforms of antithrombin on histone-induced endothelial cell damage and explore the responsible mechanisms in an experimental model in vitro. Endothelial cells were treated in vitro using histone H4 to induce cellular damage. Various doses of either α- or β-antithrombin were used as treatment interventions, and both cell viability and the levels of lactate dehydrogenase (LDH) in the medium were assessed. Endothelial cell damage was also assessed using microscopic examination and immunofluorescent staining with anti-syndecan-4 and anti-antithrombin antibodies. As a result, both glycoforms of antithrombin significantly improved cell viability when administered at a physiological dose (150 μg/mL). Cellular injury as evaluated using the LDH level was significantly suppressed by β-antithrombin at a supranormal dose (600 μg/mL). Microscopic observation suggested that β-antithrombin suppressed the endothelial cell damage more efficiently than α-antithrombin. β-Antithrombin suppressed the intensity of syndecan-4 staining which became evident after treatment with histone H4, more prominently than α-antithrombin. The distribution of antithrombin was identical to that of syndecan-4. In conclusion, both α- and β-antithrombin can protect vascular endothelial cells from histone H4-induced damage, although the effect was stronger for β-antithrombin. The responsible mechanisms might involve the binding of antithrombin to the glycocalyx on the endothelial surface. These results provide a theoretical basis for the application of antithrombin to the prevention and treatment of sepsis-related endothelial damage.

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