Expression of CXCL8, CXCR1, and CXCR2 in Neurons and Glial Cells of the Human and Rabbit Retina

Goczalik, Iwona; Ulbricht, Elke; Hollborn, Margrit; Raap, Maik; Uhlmann, Susann; Weick, Michael; Pannicke, Thomas; Wiedemann, Peter; Bringmann, Andreas; Reichenbach, Andreas; Francke, Mike

doi:10.1167/iovs.08-1887

Cited by 48 publications

(30 citation statements)

References 45 publications

(57 reference statements)

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“…Müller cells were shown to express IL-8 (CXCL8), a proinflammatory chemokine that adheres to CXCL1 receptors. An upregulation of CXCL8 and CXCL1/ CXCL2 receptors in Müller cells and microglial cells has been found in retinas and vitreous of human and rabbit PVR eyes [20,21]. Other cytokines were found to be elevated in PVR eyes in a more recent study indicating an inflammatory mechanism in the development of PVR [23].…”

Section: Discussionmentioning

confidence: 99%

Systemic corticosteroids reduce the risk of cellophane membranes after retinal detachment surgery: a prospective randomized placebo-controlled double-blind clinical trial

Koerner

Koerner-Stiefbold

Garweg

2012

Graefes Arch Clin Exp Ophthalmol

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Section: Discussionmentioning

confidence: 99%

Systemic corticosteroids reduce the risk of cellophane membranes after retinal detachment surgery: a prospective randomized placebo-controlled double-blind clinical trial

Koerner

Koerner-Stiefbold

Garweg

2012

Graefes Arch Clin Exp Ophthalmol

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“…37 IL-8 is a pluripotent chemokine that induces chemotaxis and phagocytosis that aids in the scavenging of cellular debris and also induces inflammation. 38 Goczalik et al 39 showed that the expression of the IL-8 receptor in the glial cells of retinas with PVR and in the PVR membranes suggests a role for IL-8 in the initiation of reactive gliosis. Therefore, it is possible that IL-6 and IL-8 can modulate the subretinal environment after RD.…”

Section: Discussionmentioning

confidence: 99%

Toxic effects of extracellular histones and their neutralization by vitreous in retinal detachment

Kawano

Ito

Yamada³

et al. 2014

Laboratory Investigation

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Histones are DNA-binding proteins and are involved in chromatin remodeling and regulation of gene expression. Histones can be released after tissue injuries, and the extracellular histones cause cellular damage and organ dysfunction. Regardless of their clinical significance, the role and relevance of histones in ocular diseases are unknown. We studied the role of histones in eyes with retinal detachment (RD). Vitreous samples were collected during vitrectomy, and the concentration of histone H3 was measured by enzyme-linked immunosorbent assay. The location of the histones and related molecules was examined in a rat RD model. The release of histones and their effects on rat retinal progenitor cells R28 and ARPE-19 were evaluated in vitro. In addition, the protective role of the vitreous body against histones was tested. The intravitreal concentration of histones was higher in eyes with RD (mean, 30.9±9.8 ng/ml) than in control eyes (below the limit of detection, Po0.05). In the rat RD model, histone H3 was observed on the outer side of the detached retina and was associated with photoreceptor death. Histone H3 was released from cultured R28 by oxidative stress. Histones at a concentration 10 mg/ml induced the production of interleukin-8 in ARPE-19 cells (2.5-fold increase, Po0.05) that was mediated through the ERK1/2-and p38 MAPK-dependent pathways and Toll-like receptor 4. Histones were toxic to cells at concentrations of Z20 mg/ml. Vitreous body or hyaluronan decreased toxicity of histones by inhibiting diffusion of histones. These results indicate that histones are released from retinas with RD and may modulate the subretinal microenvironment by functioning as damage-associated molecular pattern molecules, thereby inducing proinflammatory cytokines or cell toxicity. In addition, the important role of the vitreous body and hyaluronan in protecting the retina from these toxic effects is suggested.

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“…This finding indicates that cells of the neural retina are also able to produce CCL2 and Il-8 in the presence of Ab. Under pathological conditions, RMG cells produce CCL2, as well as IL-8 (Yoshida et al, 2004;Goczalik et al, 2008). Retinal Mü ller glial cell-derived CCL2 and ⁄ or IL-8 may therefore participate in the development of retinal inflammation.…”

Section: Role Of Inflammation In the Subretinal Ab-induced Rmg Cell Gmentioning

confidence: 99%

Distinct effects of inflammation on gliosis, osmohomeostasis, and vascular integrity during amyloid beta‐induced retinal degeneration

et al. 2012

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SummaryIn normal retinas, amyloid-b (Ab) accumulates in the subretinal space, at the interface of the retinal pigment epithelium, and the photoreceptor outer segments. However, the molecular and cellular effects of subretinal Ab remain inadequately elucidated. We previously showed that subretinal injection of Ab(1-42) induces retinal inflammation, followed by photoreceptor cell death. The retinal Mü ller glial (RMG) cells, which are the principal retinal glial cells, are metabolically coupled to photoreceptors. Their role in the maintenance of retinal water ⁄ potassium and glutamate homeostasis makes them important players in photoreceptor survival. This study investigated the effects of subretinal Ab(1-42) on RMG cells and of Ab(1-42)-induced inflammation on retinal homeostasis. RMG cell gliosis (upregulation of GFAP, vimentin, and nestin) on day 1 postinjection and a proinflammatory phenotype were the first signs of retinal alteration induced by Ab(1-42). On day 3, we detected modifications in the protein expression patterns of cyclooxygenase 2 (COX-2), glutamine synthetase (GS), Kir4.1 [the inwardly rectifying potassium (Kir) channel], and aquaporin (AQP)-4 water channels in RMG cells and of the photoreceptor-associated AQP-1. The integrity of the blood-retina barrier was compromised and retinal edema developed. Ab(1-42) induced endoplasmic reticulum stress associated with sustained upregulation of the proapoptotic factors of the unfolded protein response and persistent photoreceptor apoptosis. Indomethacin treatment decreased inflammation and reversed the Ab(1-42)-induced gliosis and modifications in the expression patterns of COX-2, Kir4.1, and AQP-1, but not of AQP-4 or GS. Nor did it improve edema. Our study pinpoints the adaptive response to Ab of specific RMG cell functions.

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Expression of CXCL8, CXCR1, and CXCR2 in Neurons and Glial Cells of the Human and Rabbit Retina

Cited by 48 publications

References 45 publications

Systemic corticosteroids reduce the risk of cellophane membranes after retinal detachment surgery: a prospective randomized placebo-controlled double-blind clinical trial

Systemic corticosteroids reduce the risk of cellophane membranes after retinal detachment surgery: a prospective randomized placebo-controlled double-blind clinical trial

Toxic effects of extracellular histones and their neutralization by vitreous in retinal detachment

Distinct effects of inflammation on gliosis, osmohomeostasis, and vascular integrity during amyloid beta‐induced retinal degeneration

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