Recent advances in understanding the biochemical and molecular mechanism of diabetic retinopathy

Ola, Mohammad Shamsul; Nawaz, Mohd Imtiaz; Siddiquei, Mohammad Mairaj; Al-Amro, Saleh A.; El‐Asrar, Ahmed M. Abu

doi:10.1016/j.jdiacomp.2011.11.004

Cited by 147 publications

(132 citation statements)

References 119 publications

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“…This phenomenon has been defined as 'metabolic memory' [2,3] and remains poorly understood and a major challenge in treating diabetes. Accumulating studies have reported the altered expression of inflammatory genes during diabetic retinopathy [4]. These retinal inflammatory mediators may be activated for several months after the reinstitution of glycaemic control following a period of poor control [5,6].…”

Section: Introductionmentioning

confidence: 99%

miR-23b-3p induces the cellular metabolic memory of high glucose in diabetic retinopathy through a SIRT1-dependent signalling pathway

Zhao

et al. 2015

Diabetologia

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Aims/hypothesis The mechanisms underlying the cellular metabolic memory induced by high glucose remain unclear. Here, we sought to determine the effects of microRNAs (miRNAs) on metabolic memory in diabetic retinopathy. Methods The miRNA microarray was used to examine human retinal endothelial cells (HRECs) following exposure to normal glucose (N) or high glucose (H) for 1 week or transient H for 2 days followed by N for another 5 days (H→N). Levels of sirtuin 1 (SIRT1) and acetylated-nuclear factor κB (Ac-NF-κB) were examined following transfection with miR-23b-3p inhibitor or with SIRT1 small interfering (si)RNA in the H→N group, and the apoptotic HRECs were determined by flow cytometry. Retinal tissues from diabetic rats were similarly studied following intravitreal injection of miR-23b-3p inhibitor. Chromatin immunoprecipitation (ChIP) analysis was performed to detect binding of NF-κB p65 to the potential binding site of the miR-23b-27b-24-1 gene promoter in HRECs. Results High glucose increased miR-23b-3p expression, even after the return to normal glucose. Luciferase assays identified SIRT1 as a target mRNA of miR-23b-3p. Reduced miR-23b-3p expression inhibited Ac-NF-κB expression by rescuing SIRT1 expression and also relieved the effect of metabolic memory induced by high glucose in HRECs. The results were confirmed in the retina using a diabetic rat model of metabolic memory. High glucose facilitated the recruitment of NF-κB p65 and promoted transcription of the miR-23b-27b-24-1 gene, which can be suppressed by decreasing miR-23b-3p expression. Conclusions/interpretation These studies identify a novel mechanism whereby miR-23b-3p regulates high-glucoseinduced cellular metabolic memory in diabetic retinopathy through a SIRT1-dependent signalling pathway.

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Section: Introductionmentioning

confidence: 99%

miR-23b-3p induces the cellular metabolic memory of high glucose in diabetic retinopathy through a SIRT1-dependent signalling pathway

Zhao

et al. 2015

Diabetologia

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“…[33] Cytokines such as IL-6 and TNF-α have many pro-atherosclerotic actions, including promoting leukocyte recruitment to the endothelium by inducing adhesion molecule and Chemoattractants synthesis and increasing capillary permeability. [34] Such cytokines may be produced by the endothelium, smooth muscle cells, and macrophages at the site of atherosclerosis and contribute to a systemic acute-phase response, and/or cytokinemia and augmented acute-phase reactants inherent to type 2 diabetes may promote arterial disease [28] .…”

Section: Methodsmentioning

confidence: 99%

Role of Adiponectin in Development and Progression of Diabetic Complications

Ismail¹

2016

jmscr

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“…s0085 2.2.3 Pathways p0680 Hyperglycemia has been considered the key initiator of retinal damage associated with DR by activation or dysregulation of several (glycolytic, protein kinase C (PKC), polyol, poly-(ADP)-ribose polymerase (PARP), and hexosamine) pathways. All these converge to increase the production of ROS, which induces apoptosis and inflammatory responses and promotes angiogenesis (Ola et al, 2012). It also induces the diacylglycerol (DAG) pathway de novo, initiating its synthesis through actions of phospholipase C. The elevated level of DAG has been linked to vascular dysfunctions and pathogenesis of DR (Geraldes and King, 2010).…”

Section: Protective Compounds In Diabetic Retinopathymentioning

confidence: 99%

“…The progression of axonal atrophy and axoglial disjunction in the optic nerve in 12-month diabetic Bio-Breeding/Worcester (BB/ W) rats is a polyol pathway-related mechanism activated by hyperglycemia and galactosemia. Hexosamine has been shown to impair insulin signaling in retina , therefore being also considered as a potential pathway implicated in DR (Ola et al, 2012). The high glucose and the diabetic state stimulate different pathways to produce excess levels of ROS.…”

Section: P0690mentioning

confidence: 99%

Neuropeptides, Trophic Factors, and Other Substances Providing Morphofunctional and Metabolic Protection in Experimental Models of Diabetic Retinopathy

Szabadfi

Pintér

Reglődi

et al. 2014

International Review of Cell and Molecular Biology

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Recent advances in understanding the biochemical and molecular mechanism of diabetic retinopathy

Cited by 147 publications

References 119 publications

miR-23b-3p induces the cellular metabolic memory of high glucose in diabetic retinopathy through a SIRT1-dependent signalling pathway

miR-23b-3p induces the cellular metabolic memory of high glucose in diabetic retinopathy through a SIRT1-dependent signalling pathway

Role of Adiponectin in Development and Progression of Diabetic Complications

Neuropeptides, Trophic Factors, and Other Substances Providing Morphofunctional and Metabolic Protection in Experimental Models of Diabetic Retinopathy

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