Toll-like receptor 3 activation drives the inflammatory response in oxygen-induced retinopathy in rats

Min, Cai; Zhang, Xuedong; Li, Yingyuan; Xu, Haiyan

doi:10.1136/bjophthalmol-2014-305690

Cited by 20 publications

(15 citation statements)

References 21 publications

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“…A role for inflammation in the development of pathological retinal neovascularization in DR was also seen in the rat model of oxygen-induced retinopathy (OIR), which utilizes hypoxia to generate neovascularization and capillary non-perfusion, thus mimicking what it seen in human patients with PDR. Gene expression of NF-κB and protein expression of IL-6 and TNF-α were significantly increased in the retinas of OIR rats compared to controls [ 121 ]. Taken together, studies in the OIR models strongly support an interconnection between vascular alterations and inflammation, not only in the early stages of DR, but also in later stages of the disease, including neovascularization and edema.…”

Section: Role Of Inflammation In Diabetic Retinopathymentioning

confidence: 99%

Role of Inflammation in Diabetic Retinopathy

Rübsam

Parikh

Fort

2018

IJMS

561

471

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Diabetic retinopathy is a common complication of diabetes and remains the leading cause of blindness among the working-age population. For decades, diabetic retinopathy was considered only a microvascular complication, but the retinal microvasculature is intimately associated with and governed by neurons and glia, which are affected even prior to clinically detectable vascular lesions. While progress has been made to improve the vascular alterations, there is still no treatment to counteract the early neuro-glial perturbations in diabetic retinopathy. Diabetes is a complex metabolic disorder, characterized by chronic hyperglycemia along with dyslipidemia, hypoinsulinemia and hypertension. Increasing evidence points to inflammation as one key player in diabetes-associated retinal perturbations, however, the exact underlying molecular mechanisms are not yet fully understood. Interlinked molecular pathways, such as oxidative stress, formation of advanced glycation end-products and increased expression of vascular endothelial growth factor have received a lot of attention as they all contribute to the inflammatory response. In the current review, we focus on the involvement of inflammation in the pathophysiology of diabetic retinopathy with special emphasis on the functional relationships between glial cells and neurons. Finally, we summarize recent advances using novel targets to inhibit inflammation in diabetic retinopathy.

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Section: Role Of Inflammation In Diabetic Retinopathymentioning

confidence: 99%

Role of Inflammation in Diabetic Retinopathy

Rübsam

Parikh

Fort

2018

IJMS

561

471

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“…While generally not primary regulators of angiogenesis, mediators of inflammation may indeed influence angiogenesis through regulation of the factors we discussed. Inflammatory regulators described in the pathogenesis of both BPD and ROP include monocyte chemotactic protein 1 (MCP-1/CCL2), macrophage inflammatory protein 1 alpha (MIP-1α/CCL3), interleukin 6 (IL-6) ( 5 , 6 , 104 – 108 ), and macrophage inhibitory factor ( 109 – 111 ). Finally, factors such as arginase-2, NADPH oxidase and erythropoietin are also implicated in both BPD and ROP ( 107 , 112 – 118 ).…”

Section: Are Bpd and Rop Pathogenically Related? Conclusion And Suggmentioning

confidence: 99%

A Pathogenic Relationship of Bronchopulmonary Dysplasia and Retinopathy of Prematurity? A Review of Angiogenic Mediators in Both Diseases

et al. 2018

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Bronchopulmonary dysplasia (BPD) and retinopathy of prematurity (ROP) are common and significant morbidities of prematurely born infants. These diseases have in common altered and pathologic vascular formation in the face of incomplete organ development. Therefore, it is reasonable to question whether factors affecting angiogenesis could have a joint pathogenic role for both diseases. Inhibition or induced expression of a single angiogenic factor is unlikely to be 100% causative or protective of either of BPD or ROP. It is more likely that interactions of multiple factors leading to disordered angiogenesis are present, increasing the likelihood of common pathways in both diseases. This review explores this possibility by assessing the evidence showing involvement of specific angiogenic factors in the vascular development and maldevelopment in each disease. Theoretical interactions of specific factors mutually contributing to BPD and ROP are proposed and, where possible, a timeline of the proposed relationships between BPD and ROP is developed. It is hoped that future research will be inspired by the theories put forth in this review to enhance the understanding of the pathogenesis in both diseases.

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“…Ischemia plays an important role in various retinal diseases, including age-related macular degeneration (AMD), diabetic retinopathy, glaucoma and retinal vein occlusion. These diseases are leading causes of blindness worldwide (Cai et al, 2015 ). Due to their complexity, the exact pathogenesis is still unclear.…”

Section: Introductionmentioning

confidence: 99%

Optic Nerve Degeneration after Retinal Ischemia/Reperfusion in a Rodent Model

Renner

Stute

Alzureiqi

et al. 2017

Front. Cell. Neurosci.

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Retinal ischemia is a common pathomechanism in many ocular disorders such as age-related macular degeneration (AMD), diabetic retinopathy, glaucoma or retinal vascular occlusion. Several studies demonstrated that ischemia/reperfusion (I/R) leads to morphological and functional changes of different retinal cell types. However, little is known about the ischemic effects on the optic nerve. The goal of this study was to evaluate these effects. Ischemia was induced by raising the intraocular pressure (IOP) in one eye of rats to 140 mmHg for 1 h followed by natural reperfusion. After 21 days, histological as well as quantitative real-time PCR (qRT-PCR) analyses of optic nerves were performed. Ischemic optic nerves showed an infiltration of cells and also degeneration with signs of demyelination. Furthermore, a migration and an activation of microglia could be observed histologically as well as on mRNA level. In regard to macroglia, a trend toward gliosis could be noted after ischemia induction by vimentin staining. Additionally, an up-regulation of glial fibrillary acidic protein (GFAP) mRNA was found in ischemic optic nerves. Counting of oligodendrocyte transcription factor 2 positive (Olig2+) cells revealed a decrease of oligodendrocytes in the ischemic group. Also, myelin basic protein (MBP) and myelin oligodendrocyte glycoprotein (MOG) mRNA expression was down-regulated after induction of I/R. On immunohistological level, a decrease of MOG was detectable in ischemic optic nerves as well. In addition, SMI-32 stained neurofilaments of longitudinal optic nerve sections showed a strong structural damage of the ischemic optic nerves in comparison to controls. Consequently, retinal ischemia impacts optic nerve degeneration. These findings could help to better understand the course of destruction in the optic nerve after an ischemic insult. Especially for therapeutic studies, the optic nerve is important because of its susceptibility to be damaged as a result to retinal ischemic injury and also its connecting function between the eye and the brain. So, future drug screenings should target not only the retina, but also the functionality and structure of the optic nerve. In the future, these results could lead to the development of new therapeutic strategies for treatment of ischemic injury.

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Toll-like receptor 3 activation drives the inflammatory response in oxygen-induced retinopathy in rats

Abstract: Our results suggest that upregulation of the TLR3 signalling pathway is involved in the pro-inflammatory response in OIR rat retinas.

Cited by 20 publications

References 21 publications

Role of Inflammation in Diabetic Retinopathy

Role of Inflammation in Diabetic Retinopathy

A Pathogenic Relationship of Bronchopulmonary Dysplasia and Retinopathy of Prematurity? A Review of Angiogenic Mediators in Both Diseases

Optic Nerve Degeneration after Retinal Ischemia/Reperfusion in a Rodent Model

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