Chemokines in proliferative diabetic retinopathy and proliferative vitreoretinopathy

Asrar, A. Abu El; Struyf, Sofie; Kangave, Dustan; Geboes, Karel; Damme, Jo Van

doi:10.1111/j.1755-3768.2008.5323.x

Cited by 77 publications

(112 citation statements)

References 42 publications

(69 reference statements)

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“…Increasing evidence indicates that inflammation is an important component of the pathogenesis of these retinopathies (1,2). Numerous proinflammatory molecules such as NO synthase 2 (NOS2), 3 cyclooxygenase-2 (COX-2), chemokines, and adhesion molecules have been implicated in the development of retinopathies (1)(2)(3)(4)(5)(6)(7)(8)(9)(10). However, we have an incomplete grasp on how these mechanisms of retinal injury are activated.…”

mentioning

confidence: 99%

CD40 Mediates Retinal Inflammation and Neurovascular Degeneration

Portillo

Grol

Zheng

et al. 2008

The Journal of Immunology

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Retinopathies are major causes of visual impairment. We used a model of ischemic retinopathy to examine the role of CD40 in the pathogenesis of retinal injury. Retinal inflammation, loss of ganglion cells, and capillary degeneration were markedly attenuated in ischemic retinas of CD40−/− mice. Up-regulation of NOS2 and COX2 after retinal ischemia were blunted in CD40−/− mice. NOS2-COX-2 up-regulation in ischemic retinas from wild-type mice was at least in part explained by recruitment of NOS2+COX-2+ leukocytes. Up-regulation of KC/CXCL1 and ICAM-1 also required CD40. Retinal endothelial and Muller cells expressed CD40. Stimulation of these cells through CD40 caused ICAM-1 up-regulation and KC/CXCL1 production. Bone marrow transplant experiments revealed that leukocyte infiltration, ganglion cell loss, and up-regulation of proinflammatory molecules after retinal ischemia were dependent on CD40 expression in the retina and not peripheral blood leukocytes. These studies identified CD40 as a regulator of retinal inflammation and neurovascular degeneration. They support a model in which CD40 stimulation of endothelial and Muller cells triggers adhesion molecule up-regulation and chemokine production, promoting the recruitment of leukocytes that express NOS2/COX-2, molecules linked to neurovascular degeneration.

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confidence: 99%

CD40 Mediates Retinal Inflammation and Neurovascular Degeneration

Portillo

Grol

Zheng

et al. 2008

The Journal of Immunology

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“…MCP-1 levels in vitreous humor are significantly elevated in patients with proliferative diabetic retinopathy, and correlates with extent of activity [22] and clinical staging of retinopathy [23]. Another report observed a strong association between MCP-1, IL-6 and IL-8 in patients with vitreoretinal diseases (including proliferative diabetic retinopathy and macular oedema), implying a common inflammatory pathway [24].…”

Section: Mcp-1 In Diabetic Retinopathymentioning

confidence: 95%

Review Article - MCP-1: A Potential Target for Diabetic Microvascular Complications?

Yap¹

2017

UNOAJ

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MCP-1 is a potent chemokine with the ability to mobilize and stimulate leucocytes, especially monocytes and macrophages. It is increasingly recognized as an important player in the inflammatory process that is diabetic nephropathy. In this article, we describe its role in inducing renal injury by outlining key studies in animal models and clinical studies of diabetic nephropathy, its association with diabetic retinopathy, as well as its potential use as a prognostic biomarker and as a therapeutic target in the clinical setting. IntroductionMonocyte Chemoattractant Protein-1 (MCP-1) was first identified as a chemoattractant cytokine by Matsushima in 1989 [1], using conditioned media from a human myelomonocytic cell line. DNA cloning and sequencing of MCP-1 was completed that

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“…Chronic inflammation develops in the retinal microvasculature under sustained hyperglycemia (Abu El-Asrar et al, 1992;Meleth et al, 2005) and is implicated in the pathogenesis of diabetic retinopathy. Proliferative DR (PDR) is followed by recurrent vitreous hemorrhages, traction retinal detachment, retinal and vitreous fibrosis, and optic nerve atrophy, which finally lead to severe visual impairments (Abu El-Asrar et al, 2006;Bhavsar, 2006;Lim et al, 2008). Retinal neovascularization (RNV) is the most striking characteristic of PDR (Du et al, 2014) and involves various angiogenic factors such as cytokines, inflammatory cells, and growth factors (Adamis, 2002;Abu El-Asrar et al, 2006;Patel et al, 2006).…”

Section: Introductionmentioning

confidence: 99%

“…Proliferative DR (PDR) is followed by recurrent vitreous hemorrhages, traction retinal detachment, retinal and vitreous fibrosis, and optic nerve atrophy, which finally lead to severe visual impairments (Abu El-Asrar et al, 2006;Bhavsar, 2006;Lim et al, 2008). Retinal neovascularization (RNV) is the most striking characteristic of PDR (Du et al, 2014) and involves various angiogenic factors such as cytokines, inflammatory cells, and growth factors (Adamis, 2002;Abu El-Asrar et al, 2006;Patel et al, 2006). Previous studies have also emphasized the role of vascular endothelial growth factor (VEGF) and other factors with angiogenic properties in the pathogenesis of PDR (Citirik et al, 2012;Mohan et al, 2012;Pennock and Kazlauskas, 2012).…”

Section: Introductionmentioning

confidence: 99%

Tumor necrosis factor-like weak inducer of apoptosis association with proliferative diabetic retinopathy and promotes proliferation and collagen synthesis in retinal ARPE-19 cells

Chen

2016

Genet. Mol. Res.

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Chemokines in proliferative diabetic retinopathy and proliferative vitreoretinopathy

Cited by 77 publications

References 42 publications

CD40 Mediates Retinal Inflammation and Neurovascular Degeneration

CD40 Mediates Retinal Inflammation and Neurovascular Degeneration

Review Article - MCP-1: A Potential Target for Diabetic Microvascular Complications?

Tumor necrosis factor-like weak inducer of apoptosis association with proliferative diabetic retinopathy and promotes proliferation and collagen synthesis in retinal ARPE-19 cells

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