High-Mobility Group Box-1 and Endothelial Cell Angiogenic Markers in the Vitreous from Patients with Proliferative Diabetic Retinopathy

El‐Asrar, Ahmed M. Abu; Nawaz, Mohd Imtiaz; Kangave, Dustan; Abouammoh, Marwan; Mohammad, Ghulam

doi:10.1155/2012/697489

Cited by 29 publications

(48 citation statements)

References 48 publications

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“…As mentioned previously, numerous studies have documented marked increases in vitreous VEGF levels in DME and PDR [12][13][14][15][16][17][18][19][20][21]. The rule of vitreous/plasma concentration ≥ 1 certainly applies to VEGF, where levels in DME and retinal tissue surrounding the macula is partially ablated by multiple hemorrhage, proteins from the blood contaminate these vitreal samples PDR vitreous can be many fold those found in plasma [17].…”

Section: Vitreous Levels Of Angiogenesis Factors In Diabetic Retinopathymentioning

confidence: 99%

“…Additional cytokines and growth factors have been observed to be elevated in the vitreous of DME and PDR patients including: interleukin-1beta (IL-1β) [ [145], granulocyte-colony stimulating factor (G-CSF) [15], macrophage-colony stimulating factor (M-CSF) [89], and platelet factor 4 (PF-4, CXCL4) [21]. However, it is important to consider the how plasma extravasation and hemorrhage may be influencing the inflammatory milieu of the vitreous, especially in PDR patients.…”

Section: Additional Cytokines In Drmentioning

confidence: 99%

“…In 1994, Aiello and co-workers demonstrated that VEGF protein levels are markedly upregulated in the vitreous fluid of DR patients [12]. This seminal report, and numerous subsequent studies, demonstrated that the mean vitreous VEGF concentrations in patients with DME and PDR are often increased to more than 10-times normal levels [12][13][14][15][16][17][18][19][20][21]. Furthermore, VEGF levels are significantly higher in the vitreous of patients with active PDR than in those with inactive or quiescent PDR, characterized by regressed or non-perfused neo-vessels and lack of active hemorrhage [19,20,22,23].…”

Section: Introductionmentioning

confidence: 99%

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Angiogenic Factors and Cytokines in Diabetic Retinopathy

Abcouwer¹

2011

J Clin Cell Immunol

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Diabetic retinopathy (DR) is a sight-threatening complication of both type-1 and type-2 diabetes. The recent success of treatments inhibiting the function of vascular endothelial growth factor (VEGF) demonstrates that specific targeting of a growth factor responsible for vascular permeability and growth is an effective means of treating DRtargets involved in the control of retinal vascular function. However, additional treatment options and preventative measures are still needed and these require a greater understanding of the pathological mechanisms leading to the disturbance of retinal tissue homeostasis in DR. Although severe DR can be treated as a vascular disease, abundant data suggests that inflammation is also occurring in the diabetic retina.Thus, anti-inflammatory therapies may also be useful for treatment and prevention of DR. Herein, the evidence for altered expression of angiogenic factors and cytokines in DR is reviewed and possible mechanisms by which the expression of VEGF and cytokines may be increased in the diabetic retina are examined. In addition, the potential role for microglial activation in diabetic retinal neuroinflammation is explored.

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Section: Vitreous Levels Of Angiogenesis Factors In Diabetic Retinopathymentioning

confidence: 99%

Section: Additional Cytokines In Drmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Angiogenic Factors and Cytokines in Diabetic Retinopathy

Abcouwer¹

2011

J Clin Cell Immunol

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“…Numerous studies have reported increased levels of pro-angiogenic factors and cytokines in the vitreous of DR patients, particularly those with severe diabetic macular edema and PDR [21][22][23][24][25][26][27][28].…”

Section: Discussionmentioning

confidence: 99%

Diffusion-weighted magnetic resonance imaging in diabetic retinopathy

Burulday¹,

Örnek²,

İnal³

et al. 2018

Med-Science

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Diabetic retinopathy (DR) is a complication of diabetes mellitus (DM) that may causes blindness. The vitreous is an extracellular matrix and it may have changes through liquefaction and syneresis in patients with DM, even in those without apparent DR. Diffusion-weighted imaging (DWI) is a new technique provide tissue contrast relying on difference with the diffusion of water molecules among tissues, which can be measured by the apparent diffusion coefficient (ADC) value. We aimed to investigate the vitreous of patients in different stages of DR using diffusion-weighted imaging technique. This prospective study included a group of 100 patients with DR and 100 members of an age-and gender-matched control group. All groups were tested using a head coil in conduction with a Achieva 1.5T magnetic resonans imaging (MRI) system (Philips Medical Systems, Best, The Netherlands). The mean ADC values were calculated and used for statistical comparisons. Mean duration of diabetes was 12.22±10.13 years in patients. Compared to controls, both eyes of the DR group had statistically and significantly lower values of ADC (p=0.025 and p=0.002, respectively). No significant correlations were found among the ADC values and central macular thickness, disease duration and stage of DR (all p>0.05) in patients. Mean ADC values revealed no significant differences among the subgroups of patients at different stages of DR (all p>0.05). Decreased ADCs in the vitreous of diabetes patients seem to be associated with the presence of diabetic retinopathy.

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“…GA has also been shown to bind to and inhibit mitogenic, chemoattractant, and cytokine-like activities of HMGB1 [11] . We demonstrated increased levels of HMGB1 in the vitreous samples from patients with proliferative diabetic retinopathy (PDR) [12] and the in situ localization of the expression of HMGB1 and RAGE in vascular endothelial cells and stromal cells in fibrovascular epiretinal membranes from patients with PDR [13] . Furthermore, we demonstrated that diabetes induced significant upregulation of the expression of HMGB1, RAGE, activated extracellular signal-regulated kinase 1 and 2 (ERK1/2) and activated nuclear factor-κB in the retinas of rats and mice and that intravitreal administration of HMGB1 in normal rats mimics the effect of diabetes [14] .…”

mentioning

confidence: 99%

High-Mobility Group Box-1 Protein Mediates the Regulation of Signal Transducer and Activator of Transcription-3 in the Diabetic Retina and in Human Retinal Müller Cells

et al. 2016

Self Cite

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Purpose: The expression of high-mobility group box-1 (HMGB1) and signal transducer and activator of transcription-3 (STAT-3) is upregulated in the diabetic retina. We hypothesized that the activation of STAT-3 is under the control of HMGB1. Methods: Retinas from 1-month-old diabetic rats and from normal rats intravitreally injected with HMGB1 and human retinal Müller glial cells (MIO-M1) stimulated with HMGB1 or high glucose were studied by Western blot analysis and immunofluorescence. We also studied the effect of the HMGB1 inhibitor glycyrrhizin (GA) on high-glucose-induced pSTAT-3 nuclear translocation and upregulation in Müller cells and on pSTAT-3 expression in the retinas of diabetic rats (n = 7-10 in each group). In addition, we studied the effect of STAT-3 inhibitor on the HMGB1-induced induction of vascular endothelial growth factor (VEGF) by Müller cells and human retinal microvascular endothelial cell (HRMEC) migration. Results: Treatment of retinal Müller cells with recombinant HMGB1 induced nuclear translocation of pSTAT-3 but did not alter pSTAT-3 expression. High glucose induced a significant upregulation of HMGB1 and pSTAT-3 upregulation and nuclear translocation in retinal Müller cells. GA co-treatment normalized the high-glucose-induced upregulation of HMGB1 and pSTAT-3 upregulation and nuclear translocation in Müller cells. Intravitreal administration of HMGB1 in normal and diabetic rats upregulated pSTAT-3 expression in the retina. GA attenuated the diabetes-induced upregulation of pSTAT-3 in the retina. The STAT-3 inhibitor attenuated HMGB1-induced VEGF upregulation by Müller cells and HRMEC migration. Conclusions: The results suggest a role for HMGB1 in the modulation of STAT-3 expression in the diabetic retina.

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High-Mobility Group Box-1 and Endothelial Cell Angiogenic Markers in the Vitreous from Patients with Proliferative Diabetic Retinopathy

Cited by 29 publications

References 48 publications

Angiogenic Factors and Cytokines in Diabetic Retinopathy

Angiogenic Factors and Cytokines in Diabetic Retinopathy

Diffusion-weighted magnetic resonance imaging in diabetic retinopathy

High-Mobility Group Box-1 Protein Mediates the Regulation of Signal Transducer and Activator of Transcription-3 in the Diabetic Retina and in Human Retinal Müller Cells

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