Elevated intravitreal interleukin-6 levels in patients with proliferative diabetic retinopathy

Mocan, Mehmet Cem; Kadayıfçılar, Sibel; Eldem, Bora

doi:10.3129/i06-070

Cited by 78 publications

(47 citation statements)

References 19 publications

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“…20,21 However, under severe insults, including hypoxic/ischemic injury, microglia become overactivated and function as a prominent source of cytotoxic oxidant stress and proinflammatory factors. [22][23][24] In this regard, microglial overactivation can contribute to the production of IL-1β, tumor necrosis factor-α, and IL-6 found in high concentrations in tissues of patients and animals with vasoproliferative retinopathy, [25][26][27] and have been linked to the development of ischemic retinopathies in humans 28 and animal models. 27,29,30 IL-1β exerts its biological effects by interacting with the IL-1 receptor type I (IL-1RI), which is composed of a ligand-binding unit and a signaling unit named the accessory protein .…”

mentioning

confidence: 99%

Microglia and Interleukin-1β in Ischemic Retinopathy Elicit Microvascular Degeneration Through Neuronal Semaphorin-3A

Rivera

Sitaras

Noueihed

et al. 2013

ATVB

123

134

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Objective-Proinflammatory cytokines contribute to the development of retinal vasculopathies. However, the role of these factors and the mechanisms by which they elicit their effects in retina are not known. We investigated whether activated microglia during early stages of ischemic retinopathy produces excessive interleukin-1β (IL-1β), which elicits retinal microvascular degeneration not directly but rather by triggering the release of the proapoptotic/repulsive factor semaphorin-3A (Sema3A)

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mentioning

confidence: 99%

Microglia and Interleukin-1β in Ischemic Retinopathy Elicit Microvascular Degeneration Through Neuronal Semaphorin-3A

Rivera

Sitaras

Noueihed

et al. 2013

ATVB

123

134

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“…Yoshimura et al [25] have reported the increased levels of vitreal VEGF, IL-6, IL-8 and MCP-1 in PDR. Previous studies also reported increased vitreous levels of VEGF [26,27], IL-6 [21][22][23]25,27], IL-8 [23][24][25]28], and MCP-1 [25,26,28] in PDR.…”

Section: Discussionmentioning

confidence: 99%

“…No significant correlation was found between adipocytokines and FBG. Mocan et al [21] determined the correlation between the vitreous levels of IL-6 and FBG, but they did not find significant correlation between the circulating levels of IL-6 and FBG.…”

Section: Discussionmentioning

confidence: 99%

Effect of Adipose Tissue-Derived Inflammatory and Proangiogenic Cytokines on Proliferative Diabetic Retinopathy

Yabanoglu¹

2014

Turk J Bioch

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Objective: To determine the vitreous and serum concentrations of TNF-α, IL-6, VEGF, IL-1β, IL-8, IL-17, MCP-1, IL-1Ra, IL-10 in patients with proliferative diabetic retinopathy (PDR) and to investigate the effect of adipose tissue on the pathogenesis of PDR. Methods: Twenty-two patients with PDR were prospectively evaluated. Seven cadavers and 11 patients with idiopathic epiretinal membrane or macular hole served as the controls. Multiplex bead array technology was employed to assess the concentrations of the cytokines. Results: The intravitreal levels of VEGF, IL-8, IL-6 were significantly higher in PDR group than control groups. In PDR group, the levels of IL-17, IL-8, IL-6 were significantly elevated in the vitreous, whereas the intravitreal levels of IL-10, IL-1Ra were found to be significantly lower than the serum concentrations. No significant correlation was found between cytokine levels and body mass index (BMI), fasting blood glucose (FBG), or glycated haemoglobin (HbA1c) of diabetic patients. Conclusion:In PDR the balance between the intravitreal pro-and anti-inflammatory adipocytokines is disturbed in favor of proinflammatory and proangiogenic cytokines in the vitreous humour. This study supports the role of adipocytokines in vascular pathology in PDR. It seems that PDR is a local inflammatory disease. However, obesity may not be the root of the inflammatory mediators in PDR.

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“…Therefore, we sought a repositioning strategy to target fibrosis. The elevated IL-6 levels that remained after Retisert implantation (and in stage IV disease) were an attractive target (Supplemental Figure 2C and Figure 3, A and B), since IL-6 is linked to many fibrotic diseases (21-28), including ocular fibrosis associated with proliferative diabetic retinopathy (29) and proliferative vitreoretinopathy (30). Tocilizumab, which targets IL-6 (anti-IL-6), is used to treat severe cases of rheumatoid arthritis, systemic juvenile idiopathic arthritis, and is currently in trial for the treatment of systemic sclerosis (28,31).…”

Section: L I N I C a L M E D I C I N Ementioning

confidence: 99%

Therapeutic drug repositioning using personalized proteomics of liquid biopsies

Vélez¹,

Bassuk²,

Colgan³

et al. 2017

JCI Insight

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IntroductionAfter spending several billion dollars and a decade or more in development and clinical trial, only approximately 10% of new drugs show efficacy and reach the market for patient use. This apparent inefficiency, however, masks enormous opportunities to repurpose existing drugs to treat diseases for which they were not originally intended, especially diseases with limited therapeutic options (1, 2). Therapies for inflammatory diseases are an attractive choice for drug repositioning because of the complexity of the immune response, the hit-or-miss nature of treatment (which is often by trial and error), and the number of traditional drugs and new biologics for inflammatory diseases.Determining which drugs to reposition, however, is not trivial. Among a heterogeneous patient population that seems affected by the same autoimmune condition, one cannot be sure if the disease is in fact the same, or at what progressive stage a patient is presenting. Currently, most predictions of patients that would benefit from drug repositioning are drawn from retrospective computational methods, genomic analyses, BACKGROUND. In patients with limited response to conventional therapeutics, repositioning of already approved drugs can bring new, more effective options. Current drug repositioning methods, however, frequently rely on retrospective computational analyses and genetic testing -time consuming methods that delay application of repositioned drugs. Here, we show how proteomic analysis of liquid biopsies successfully guided treatment of neovascular inflammatory vitreoretinopathy (NIV), an inherited autoinflammatory disease with otherwise poor clinical outcomes.

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Elevated intravitreal interleukin-6 levels in patients with proliferative diabetic retinopathy

Cited by 78 publications

References 19 publications

Microglia and Interleukin-1β in Ischemic Retinopathy Elicit Microvascular Degeneration Through Neuronal Semaphorin-3A

Microglia and Interleukin-1β in Ischemic Retinopathy Elicit Microvascular Degeneration Through Neuronal Semaphorin-3A

Effect of Adipose Tissue-Derived Inflammatory and Proangiogenic Cytokines on Proliferative Diabetic Retinopathy

Therapeutic drug repositioning using personalized proteomics of liquid biopsies

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