The Measurement of Intraocular Biomarkers in Various Stages of Proliferative Diabetic Retinopathy Using Multiplex xMAP Technology

Rušňák, Štěpán; Vrzalová, Jindra; Sobotova, Marketa; Hecová, Lenka; Ricarova, Renata; Topolčan, Ondřej

doi:10.1155/2015/424783

Cited by 33 publications

(32 citation statements)

References 18 publications

(22 reference statements)

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“…The overexpression of t-PA and PAI induces extracellular matrix destruction and the degradation of the basement membrane of vascular endothelial cells [ 96 , 97 ]. Increased VEGF levels may induce the expression of various inflammatory factors, such as transforming growth factor beta-1 (TGF- β 1) and interleukin 6 (IL-6) that accelerate PDR progression [ 98 ]. Heparan sulfate is an important component of the blood-retinal barrier stroma.…”

Section: Angiogenesis and Vegf Roles During Dr Pathogenesismentioning

confidence: 99%

The Oxidative Stress and Mitochondrial Dysfunction during the Pathogenesis of Diabetic Retinopathy

Yiang

Lai

et al. 2018

Oxidative Medicine and Cellular Longevity

154

110

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Diabetic retinopathy is one of the most serious microvascular complications induced by hyperglycemia via five major pathways, including polyol, hexosamine, protein kinase C, and angiotensin II pathways and the accumulation of advanced glycation end products. The hyperglycemia-induced overproduction of reactive oxygen species (ROS) induces local inflammation, mitochondrial dysfunction, microvascular dysfunction, and cell apoptosis. The accumulation of ROS, local inflammation, and cell death are tightly linked and considerably affect all phases of diabetic retinopathy pathogenesis. Furthermore, microvascular dysfunction induces ischemia and local inflammation, leading to neovascularization, macular edema, and neurodysfunction, ultimately leading to long-term blindness. Therefore, it is crucial to understand and elucidate the detailed mechanisms underlying the development of diabetic retinopathy. In this review, we summarized the existing knowledge about the pathogenesis and current strategies for the treatment of diabetic retinopathy, and we believe this systematization will help and support further research in this area.

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Section: Angiogenesis and Vegf Roles During Dr Pathogenesismentioning

confidence: 99%

The Oxidative Stress and Mitochondrial Dysfunction during the Pathogenesis of Diabetic Retinopathy

Yiang

Lai

et al. 2018

Oxidative Medicine and Cellular Longevity

154

110

View full text Add to dashboard Cite

show abstract

“…Among newborns who weighed < 1000 g, those who received/needed oxygen for more than 6 h had higher MCP-1 concentrations in blood collected on day 3 than their peers who received oxygen for a shorter amount of time (even after adjusting for potential confounders) [ 58 ]. In addition, several studies documented elevated levels of MCP-1 in the vitreous humor of patients with retinopathy [ 59 , 60 ], and in animal models, MCP-1 was shown to be involved in the induction of the retinal neovascularization possibly by modulating or attracting macrophages/microglia during the ischemic phase of retinopathy [ 61 , 62 ].…”

Section: Introductionmentioning

confidence: 99%

Retinopathy of prematurity: inflammation, choroidal degeneration, and novel promising therapeutic strategies

Rivera

Holm

Austeng

et al. 2017

J Neuroinflammation

111

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Retinopathy of prematurity (ROP) is an important cause of childhood blindness globally, and the incidence is rising. The disease is characterized by initial arrested retinal vascularization followed by neovascularization and ensuing retinal detachment causing permanent visual loss. Although neovascularization can be effectively treated via retinal laser ablation, it is unknown which children are at risk of entering this vision-threatening phase of the disease. Laser ablation may itself induce visual field deficits, and there is therefore a need to identify targets for novel and less destructive treatments of ROP. Inflammation is considered a key contributor to the pathogenesis of ROP. A large proportion of preterm infants with ROP will have residual visual loss linked to loss of photoreceptor (PR) and the integrity of the retinal pigment epithelium (RPE) in the macular region. Recent studies using animal models of ROP suggest that choroidal degeneration may be associated with a loss of integrity of the outer retina, a phenomenon so far largely undescribed in ROP pathogenesis. In this review, we highlight inflammatory and neuron-derived factors related to ROP progression, as well, potential targets for new treatment strategies. We also introduce choroidal degeneration as a significant cause of residual visual loss following ROP. We propose that ROP should no longer be considered an inner retinal vasculopathy only, but also a disease of choroidal degeneration affecting both retinal pigment epithelium and photoreceptor integrity.

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“…Diabetes cataracts (DC) has become the primary cause of visual loss and blindness with diabetes reaching global epidemic proportions [1][2]. It is well known that the primary damage of environmental or genetic factors of lens epithelial cell (LEC) may cause the abnormal differentiation and damage of cells in lens expressed as the opacity of lens tissues eventually and which resulted in cataracts [3][4].…”

Section: Introductionmentioning

confidence: 99%

Interaction of AR and iNOS in lens epithelial cell: A new pathogenesis and potential therapeutic targets of diabetic cataract

Liu

Huang

et al. 2017

Archives of Biochemistry and Biophysics

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Although there is significant interest in revealing the role of aldose reductase (AR) and inducible nitric oxide synthase (iNOS) in diabetic cataract (DC), the interaction of AR and iNOS remains unknown. The aim of this study is to investigate the pathogenesis mechanisms and explore as a new potential therapeutic targets for DC. This study investigated the interaction of AR-iNOS through the methods of enzyme kinetics, molecular docking and molecular dynamics simulation, co-immunoprecipitation and fluorescence resonance energy transfer (FRET). The IC50 of AR for inhibition of iNOS activity is 0.04 μM, and the IC50 of iNOS for inhibition of AR activity is 0.042 μM through enzyme kinetics; the interface showed that ARG99 on AR and GLU317 on iNOS played the key roles in the interaction of AR-iNOS predicted by molecular docking and molecular dynamics simulation. Co-immunoprecipitation of protein complexes in human lens epithelial cell (HLEC) demonstrated that AR could association with iNOS in cell; and the interaction distance of AR-iNOS was 6.50 ± 0.22 nm detected by FRET. This study exhibited a direct inhibition interaction between AR and iNOS in HLECs. It is the first report of inhibition interaction between AR and iNOS, suggesting a new pathophysiological mechanism and providing a new insight into the therapeutic mechanism of DC.

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The Measurement of Intraocular Biomarkers in Various Stages of Proliferative Diabetic Retinopathy Using Multiplex xMAP Technology

Cited by 33 publications

References 18 publications

The Oxidative Stress and Mitochondrial Dysfunction during the Pathogenesis of Diabetic Retinopathy

The Oxidative Stress and Mitochondrial Dysfunction during the Pathogenesis of Diabetic Retinopathy

Retinopathy of prematurity: inflammation, choroidal degeneration, and novel promising therapeutic strategies

Interaction of AR and iNOS in lens epithelial cell: A new pathogenesis and potential therapeutic targets of diabetic cataract

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