Pentraxin 3 and Other Inflammatory Factors in Central Retinal Vein Occlusion and Macular Edema

Noma, Hidetaka; Mimura, Tatsuya; Masahara, Hidetaka; Shimada, Katsunori

doi:10.1097/iae.0b013e3182993d74

Cited by 27 publications

(32 citation statements)

References 49 publications

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“…The levels of VEGF, sVEGFR-2, soluble ICAM-1 (sICAM-1), MCP-1 and PTX3 were measured in vitreous samples from the same eye and in plasma samples by enzyme-linked immunosorbent assay using kits for human VEGF, sVEGFR-2, sICAM-1, MCP-1 and PTX3 (VEGF, sVEGFR-2 and MCP-1: R & D Systems, Minneapolis, Minn., USA; sICAM-1: Bender Med Systems, Burlingame, Calif., USA; PTX3: Perseus Proteomics Inc., Tokyo, Japan) [6,7]. The VEGF kit was able to detect 2 of the 4 VEGF isoforms (VEGF 121 and VEGF 165 ), probably because these 2 shorter isoforms are secreted and the 2 longer isoforms are cell-associated.…”

Section: Methodsmentioning

confidence: 99%

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Role of Inflammation in Diabetic Macular Edema

et al. 2014

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Vitreous fluid levels of vascular endothelial growth factor (VEGF), soluble VEGF receptor (sVEGFR)-2, soluble intercellular adhesion molecule (sICAM)-1, monocyte chemotactic protein (MCP)-1 and pentraxin 3 (PTX3) were measured by enzyme-linked immunosorbent assay in 36 patients with diabetic macular edema (DME) and 15 patients with macular hole (MH). Aqueous flare values were measured with a laser flare meter, and macular edema was examined by optical coherence tomography. Vitreous fluid levels of VEGF, sVEGFR-2, sICAM-1, MCP-1 and PTX3 were significantly higher in the patients with DME than in those with MH. There was a significant correlation between the vitreous fluid level of sVEGFR-2 and the levels of sICAM-1, MCP-1 and PTX3. The aqueous flare value was significantly correlated with the vitreous fluid levels of sVEGFR-2, sICAM-1, MCP-1 and PTX3. These findings suggest that inflammatory factors may induce an increase in vascular permeability and disrupt the blood-aqueous barrier in DME patients.

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Section: Methodsmentioning

confidence: 99%

“…Recently, we reported that the vitreous fluid levels of long pentraxin 3 (PTX3) and soluble VEGFR (sVEGFR)-2 were significantly higher in patients with retinal vein occlusion and macular edema than in controls [6,7]. However, the relations among vitreous inflammatory factors and sVEGFR-2 have not been investigated in patients with DME.…”

Section: Introductionmentioning

confidence: 99%

Role of Inflammation in Diabetic Macular Edema

et al. 2014

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“…Importantly, vitreous levels of mediators such as VEGF and IL-6 correlated independently with vascular permeability and the severity of macular edema. 9 Resident microglia are important contributors to inflammation after injury. However, invading macrophages presumably also help clear debris and restore tissue integrity.…”

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confidence: 99%

Microglia Activation and Recruitment of Circulating Macrophages During Ischemic Experimental Branch Retinal Vein Occlusion

Ebneter

Kokona

Schneider

et al. 2017

Invest. Ophthalmol. Vis. Sci.

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METHODS. Experimental BRVO was induced in Balb/c mice and histologic changes were studied. Tissue hypoxia was visualized using pimonidazole hydrochloride. Monocyte-derived retinal cells were quantified using histology and flow cytometry. To investigate the dynamics of invading blood-borne macrophages, chimera mice were generated using bone marrow grafts from Cx3cr1 (gfp/gfp) mice to rescue lethally irradiated wild-type BALB/c mice. Longitudinal in vivo imaging was performed to monitor cell invasion. The levels of proinflammatory cytokines in the retina were quantified by quantitative real-time PCR.RESULTS. Histology showed disruption of tissue architecture and temporary swelling with marked hypoxia coinciding with increased VEGF-A and hypoxia inducible factor-1a (HIF-1a) expression and elevation of proinflammatory cytokines within 3 days after experimental BRVO, followed by thinning of the inner retinal layers at later time points. Proinflammatory cytokine levels were elevated. Activation of resident retinal microglia and recruitment of circulating macrophages in areas of hypoxic retina were evident early after the insult and peaked at day 7, remaining elevated for up to 28 days. Flow cytometry showed upregulation of CD68 and major histocompatibility complex class-II (MHC-II) expression at day 3, culminating at day 7.CONCLUSIONS. Experimental BRVO causes hypoxia and breakdown of the inner blood-retina barrier, followed by activation of microglia and invasion of macrophages from the systemic circulation. Consequently, treatments targeting microglia activation or macrophage recruitment might potentially mitigate the sequelae and attenuate degenerative changes induced by retinal vein occlusion.

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“…Given the above and the fact that vitreomacular traction may exacerbate macular oedema, vitrectomy alone has been studied as a means to release traction, remove angiogenic agents and improve oxygenation to the inner retina . A number of inflammatory mediators, including VEGF and agents within the interleukin and C‐reactive protein families have been isolated and directly correlated with increased macular oedema in eyes with RVO . Conversely, the anti‐inflammatory activity of pigment epithelium derived factor appears to be down‐regulated.…”

Section: Treatmentmentioning

confidence: 99%

“…[82][83][84][85] A number of inflammatory mediators, including VEGF and agents within the interleukin and C-reactive protein families have been isolated and directly correlated with increased macular oedema in eyes with RVO. 86,87 Conversely, the anti-inflammatory activity of pigment epithelium derived factor appears to be down-regulated. Given the increasing popularity of intravitreal injections in the treatment of macular oedema and the potential reduction in their efficacy postvitrectomy, this approach is likely to face continued scrutiny.…”

Section: Treatmentmentioning

confidence: 99%

The ABCs of RVO: A review of retinal venous occlusion

MacDonald¹

2014

Clinical and Experimental Optometry

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Retinal vein occlusions are important causes of loss of vision; indeed, they are the second most common retinal vascular disease, following diabetic retinopathy. For this reason alone, primary eye-care providers must be well versed in diagnosis and management. Risk factors, though not universally agreed upon, include but are not limited to advancing age, systemic hypertension, arteriolarsclerosis, diabetes, hyperlipidaemia, blood hyperviscosity, thrombophilia, ocular hypertension and glaucoma. Typically, visual loss is secondary to macular oedema and/or retinal ischaemia. Treatment modalities have included observation, systemic thrombolysis and haemodilution, radial optic neurotomy, chorioretinal anastomosis, vitrectomy, laser photocoagulation and intravitreal injection of anti-inflammatory and, most recently, anti-vascular endothelial growth factors.

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Pentraxin 3 and Other Inflammatory Factors in Central Retinal Vein Occlusion and Macular Edema

Abstract: These findings suggest the importance of VEGF, its signal transduction pathways, and the cytokine network and may be useful for understanding the mechanism of macular edema in CRVO and developing new treatments.

Cited by 27 publications

References 49 publications

Role of Inflammation in Diabetic Macular Edema

Role of Inflammation in Diabetic Macular Edema

Microglia Activation and Recruitment of Circulating Macrophages During Ischemic Experimental Branch Retinal Vein Occlusion

The ABCs of RVO: A review of retinal venous occlusion

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