Upregulation of Chemokine Expression in the Retinal Vasculature in Ischemia-Reperfusion Injury

Jo, Nobuo; Wu, Guey-Shuang; Rao, Narsing A.

doi:10.1167/iovs.02-1308

Cited by 86 publications

(52 citation statements)

References 26 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Treatment with anti-CCL4/ MIP-1ß delayed onset and reduced duration of AAU (Adamus et al, 2001). The retinal ischemia-reperfusion model showed an upregulation of CCL4/MIP-1beta in the retinal vessels and these results confirm that this chemokine may be involved in the inflammatory element of pathogenesis of retinal neovascularization (Jo et al, 2003).…”

Section: Discussionsupporting

confidence: 70%

CCL Chemokines Levels in Tear Fluid of Patients with Cystic Fibrosis

Mrugacz¹

2011

Human Genetic Diseases

View full text Add to dashboard Cite

Section: Discussionsupporting

confidence: 70%

CCL Chemokines Levels in Tear Fluid of Patients with Cystic Fibrosis

Mrugacz¹

2011

Human Genetic Diseases

View full text Add to dashboard Cite

“…Moreover, previous reports have shown that retinal ischaemia stimulates IL-8 and MCP-1 production, and both chemokines are involved in retinal neovascularization. [31][32][33][34] Although ischaemia as seen using FFA was one of the exclusion criteria, we cannot absolutely exclude that this was present in our patients. So retinal ischaemia may have also contributed to hyperproduction of IL-8 and MCP-1.…”

Section: Il-8 and Mcp-1 In Brvo Macular Oedemamentioning

confidence: 99%

Vitreous levels of interleukine-8 and monocyte chemoattractant protein-1 in macular oedema with branch retinal vein occlusion

Fonollosa¹,

García-Arumí

Santos

et al. 2010

Eye

View full text Add to dashboard Cite

Purpose To investigate whether interleukine-8 (IL-8) and monocyte chemoattractant protein-1 (MCP-1) are related with macular oedema in patients with branch retinal vein occlusions (BRVOs). Design Retrospective case-control study. Participants Nineteen patients who had macular oedema due to BRVO and nine patients with non-ischaemic ocular diseases (control group). Methods Macular oedema was examined by optical coherence tomography. Both venous blood and vitreous samples were obtained at the time of vitreoretinal surgery. IL-8 and MCP-1 levels in vitreous fluid and plasma were determined with enzyme-linked immunosorbent assay kits. Variables were compared with the Mann-Whitney U-test, Wilcoxon's signed-ranked test, and the v 2 -test, when appropriate. To examine correlations, Spearman's rank-order correlation coefficients were calculated. Statistical significance was set at Po0.05. Results The vitreous fluid levels of IL-8 (median: 63.5 pg/ml) and MCP-1 (median: 1522.4 pg/ml) were significantly higher in the patients with BRVO than in the control group (median: 5.1 and 746.5 pg/ml respectively; Po0.001 and o0.001 respectively). Vitreous IL-8 and MCP-1 were significantly correlated in patients with BRVO (P ¼ 0.009). Conclusions Both IL-8 and MCP-1 were elevated in the vitreous fluid of patients with BRVO and macular oedema. Both chemokines may contribute to the pathogenesis of macular oedema in patients with BRVO.

show abstract

“…2 MIP-1b was first isolated from the culture medium of LPS-activated macrophages, 3 and it recruited macrophages/microglia to the sites of injury in patients with arthritis, 4 sepsis, 5 and systemic sclerosis. 6 The upregulation of MIP-1b in the ischemic retina has been shown to occur in an ischemia-reperfusion injury model, 7 and its receptor, CCR5, is involved in the development of corneal NV. 8 However, it is not known what role the MIP-1b/CCR5 system has in the hypoxia-induced retinal NV.…”

mentioning

confidence: 99%

Bone marrow-derived monocyte lineage cells recruited by MIP-1β promote physiological revascularization in mouse model of oxygen-induced retinopathy

Ishikawa

Nakao

Sassa

et al. 2012

Laboratory Investigation

View full text Add to dashboard Cite

Recent clinical observations have indicated that vascular endothelial growth factor (VEGF) is a key factor that stimulates the development of preretinal pathological neovascularization (NV). However, it has not been established how intraretinal physiological revascularization of hypoxic avascular areas is regulated. Our earlier study on the gene expression profile of hypoxic retinas in a mouse model of oxygen-induced retinopathy (OIR) showed that macrophage inflammatory protein-1b (MIP-1b) was the most upregulated protein. The purpose of this study was to investigate the role played by MIP-1b in recruiting bone marrow-derived monocyte lineage cells (BM-MLCs) in a mouse model of OIR. Our results showed that MIP-1b was upregulated, and its receptor, CCR5, was expressed in BM-MLCs in the hypoxic inner retina. Neutralizing Ab against MIP-1b reduced the infiltration of BM-MLCs into the OIR retinas and increased the avascular area and preretinal neovascular tufts. A very strong significant correlation was found between the area of the preretinal neovascular tufts and the avascular area, regardless of the extent of BM-MLC infiltration into the OIR retinas. Additional treatment with VEGF-A-neutralizing Ab showed that the MIP-1b-regulated pathological NV strongly depended on VEGF-A, which was probably secreted by the hypoxic avascular retinas. These results indicate that MIP-1b is involved in the recruitment of BM-MLCs, which have a significant role in the physiological revascularization of hypoxic avascular retinas. Overall, these findings indicate that the MIP-1b induction of BM-MLCs might possibly be used to promote intraretinal revascularization and thus prevent the abnormal NV in ischemic vision-threatening retinal diseases. Tissue hypoxia is believed to be the common mechanism that initiates a series of events leading to compensatory angiogenesis. Hypoxia-induced retinal neovascularization (NV) is the main contributor to proliferative vascular diseases, such as diabetic retinopathy, retinopathy of prematurity, and retinal vein occlusion. These diseases can lead to irreversible damage to visual function.To determine the factors that are activated during retinal hypoxia, we performed a gene expression profile of hypoxic retinas obtained from a mouse model of oxygen-induced retinopathy (OIR) using gene microarray analyses. The results identified the functional set of genes that are related to the post-ischemic inflammation, neural and vascular development, and subsequent pathological NV. The most upregulated gene among the differentially expressed genes in hypoxic retinas was the macrophage inflammatory protein1b (MIP-1b) and not vascular endothelial growth factor A (VEGF-A) and other chemokines. 1 MIP-1b, also known as chemokine CC motif ligand 4, is a member of the CC chemokine family that are characterized by their ability to direct migration of leukocytes into inflamed tissues. 2 MIP-1b was first isolated from the culture medium of LPS-activated macrophages, 3 and it recruited macrophages/microglia to the sites of...

show abstract

Upregulation of Chemokine Expression in the Retinal Vasculature in Ischemia-Reperfusion Injury

Cited by 86 publications

References 26 publications

CCL Chemokines Levels in Tear Fluid of Patients with Cystic Fibrosis

CCL Chemokines Levels in Tear Fluid of Patients with Cystic Fibrosis

Vitreous levels of interleukine-8 and monocyte chemoattractant protein-1 in macular oedema with branch retinal vein occlusion

Bone marrow-derived monocyte lineage cells recruited by MIP-1β promote physiological revascularization in mouse model of oxygen-induced retinopathy

Contact Info

Product

Resources

About