Interleukin‐8, monocyte chemoattractant protein‐1 and IL‐10 in the vitreous fluid of patients with proliferative diabetic retinopathy

Hernández, Cristina; Segura, Rosa; Fonollosa, Alex; Carrasco, Esther; Francisco, Gemma; Simó, Rafael

doi:10.1111/j.1464-5491.2005.01538.x

Cited by 161 publications

(134 citation statements)

References 27 publications

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“…In recent years evidence has accumulated indicating that inflammation is an important event in the pathogenesis of diabetic retinopathy [26][27][28]. In the present study, vitreous levels of several components of the complement system (C4b, factor B, C3 and C9) have been found, for the first time, to be simultaneously increased in PDR patients relative to control subjects.…”

Section: Discussionsupporting

confidence: 58%

Proteomic analysis of human vitreous fluid by fluorescence-based difference gel electrophoresis (DIGE): a new strategy for identifying potential candidates in the pathogenesis of proliferative diabetic retinopathy

Garcia-Ramírez

Canals

Hernández³

et al. 2007

Diabetologia

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151

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Aims/hypothesis The aim of this study was to compare the protein profile of vitreous fluid from diabetic patients with proliferative diabetic retinopathy (PDR) with that from nondiabetic patients with idiopathic macular holes (MH). The mRNA of proteins differentially produced was also assessed in the retinas from diabetic and non-diabetic donors. Materials and methods Vitreous humour from type 1 diabetic patients with PDR (n=8) and from non-diabetic patients with MH (n=10) closely matched in terms of age were studied. The comparative proteomic analysis was performed using fluorescence-based difference gel electrophoresis (DIGE). Differentially produced proteins (abundance ratio >1.4, p<0.05) were identified by mass spectrometry. Expressions of mRNA were measured by real-time RT-PCR in retinas from ten human eyes obtained at post-mortem (five eyes from diabetic subjects and five eyes from non-diabetic subjects). Results Eight proteins were highly produced in PDR patients in comparison with non-diabetic subjects: zinc-α 2 -glycoprotein (ZAG), apolipoprotein (apo) A1, apoH, fibrinogen A, and the complement factors C3, C4b, C9 and factor B). We found three proteins that were underproduced in PDR subjects: pigment epithelial derived factor (PEDF), interstitial retinol-binding protein (IRBP) and inter-α-trypsin inhibitor heavy chain (ITIH2). There was no overlap in the vitreous levels of the above-mentioned proteins between PDR patients and non-diabetic control subjects. The differential production of ZAG, C3, factor B, PEDF and IRBP was further confirmed by western blot, and was in agreement with mRNA levels detected in the retina. Conclusions/interpretation Proteomic analysis by DIGE, which permits an accurate quantitative comparison, was useful in identifying new potential candidates involved in the pathogenesis of PDR.

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Section: Discussionsupporting

confidence: 58%

Proteomic analysis of human vitreous fluid by fluorescence-based difference gel electrophoresis (DIGE): a new strategy for identifying potential candidates in the pathogenesis of proliferative diabetic retinopathy

Garcia-Ramírez

Canals

Hernández³

et al. 2007

Diabetologia

Self Cite

151

135

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“…82 Concordantly, elevation in the intra-vitreous levels of two pro-inflammatory cytokines Interleukin-8 and MCP-1 was observed in diabetic patients with proliferative DR compared with non-diabetic subjects. 83 Interestingly, intra-vitreous levels of cytokines were correlated with proliferative DR activity, suggesting that these cytokines may be pathogenically important in proliferative DR. 83 To this end, our group demonstrated that the presence of Ectodermal dysplasia 1 (ED-1)-positive cells in the retina, which indicate microglial activation, is increased in SHR rats, mainly in diabetic SHR rats, and this increment was accompanied by an increase in ICAM-1 and the NF-kB p65 transcription factor. 84 …”

Section: Contribution Of Inflammation and Oxidative Stress To Dr And mentioning

confidence: 97%

The contribution of hypertension to diabetic nephropathy and retinopathy: the role of inflammation and oxidative stress

2011

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Diabetes and hypertension frequently coexist and constitute the most notorious combination for the pathogenesis of diabetic nephropathy and retinopathy. Large clinical trials have clearly demonstrated that tight control of glycemia and/or blood pressure significantly reduces the incidence and progression of diabetic retinopathy (DR) and nephropathy. However, the mechanism by which hypertension interacts with diabetes to induce and/or exacerbate nephropathy and retinopathy is very unclear. Substantial evidence implicates the involvement of chronic inflammation and oxidative stress in the pathogenesis of DR and nephropathy. In addition, hypertension causes oxidative stress and inflammation in the kidney and retina. In the present review, we summarized data obtained from our research along with those from other groups to better understand the role of hypertension in the pathogenesis of diabetic nephropathy and retinopathy. It is suggested that oxidative stress and inflammation may be common denominators of kidney and retinal damage in the concomitant presence of diabetes and hypertension.

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“…Apart from its intrinsic deleterious effect, IL-1β has been shown to stimulate several pro-inflammatory cytokines such as IL-6, IL-8 and monocyte chemotactic protein 1 (MCP-1) [26,27], which, in turn, have also been involved in both PDR and DMO [28][29][30]. It is well known that IL-1β participates in the breakdown of the inner BRB, which is constituted by retinal capillaries [31][32][33].…”

Section: Discussionmentioning

confidence: 99%

Fenofibric acid prevents retinal pigment epithelium disruption induced by interleukin-1β by suppressing AMP-activated protein kinase (AMPK) activation

et al. 2011

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Aims/hypothesis The mechanisms involved in the beneficial effects of fenofibrate on the development and progression of diabetic macular oedema (DMO) remain to be elucidated. To shed light on this issue we have explored the effect of fenofibric acid on the barrier function of human retinal pigment epithelium (RPE) cells. Methods ARPE-19 cells (a human RPE line) were cultured for 18 days under standard conditions and under conditions leading to the disruption of the monolayer (D-glucose, 25 mmol/l, with IL-1β, 10 ng/ml, added at days 16 and 17). Fenofibric acid, 25 μmol/l and 100 μmol/l, was added on the last 3 days of the experiment (one application/day). RPE cell permeability was evaluated by measuring apicalbasolateral movements of FITC-dextran (40 kDa). The production of tight junction proteins and AMP-activated protein kinase (AMPK) phosphorylation was assessed by western blot. Immunohistochemical studies of tight junction proteins and small interfering RNA transfection to AMPK were also performed in ARPE-19 monolayers. Results Treatment of ARPE-19 cells with fenofibric acid significantly reduced the increment of permeability and the breakdown of the ARPE-19 cell monolayer induced by Dglucose, 25 mmol/l, and IL-1β, 10 ng/ml, in a dose-dependent manner. This effect was unrelated to changes in the content of tight junction proteins. Fenofibric acid prevented the activation of AMPK induced by IL-1β and the hyperpermeability induced by IL-1β was blocked by silencing AMPK. Conclusions/interpretation Disruption of RPE induced by IL-1β is prevented by fenofibric acid through its ability to suppress AMPK activation. This mechanism could be involved in the beneficial effects of fenofibrate on DMO development.

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Interleukin‐8, monocyte chemoattractant protein‐1 and IL‐10 in the vitreous fluid of patients with proliferative diabetic retinopathy

Cited by 161 publications

References 27 publications

Proteomic analysis of human vitreous fluid by fluorescence-based difference gel electrophoresis (DIGE): a new strategy for identifying potential candidates in the pathogenesis of proliferative diabetic retinopathy

Proteomic analysis of human vitreous fluid by fluorescence-based difference gel electrophoresis (DIGE): a new strategy for identifying potential candidates in the pathogenesis of proliferative diabetic retinopathy

The contribution of hypertension to diabetic nephropathy and retinopathy: the role of inflammation and oxidative stress

Fenofibric acid prevents retinal pigment epithelium disruption induced by interleukin-1β by suppressing AMP-activated protein kinase (AMPK) activation

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