Objective To observe the levels of vascular endothelial growth factor (VEGF), interleukin-6 (IL-6) and monocyte chemotactic protein-1 (MCP-1) in aqueous humor of patients with macular edema secondary to central retinal vein occlusion (CRVO). Methods Forty eyes of 40 consecutive patients with macular edema secondary to CRVO (CRVO group) were enrolled in this study. The patients included 25 males and 15 females. The patient age ranged from 38 to 76 years. The control group was 20 patients with senile cataract who underwent phacoemulsification, including 10 males and 10 females. The levels of VEGF165, VEGF165b, IL-6 and MCP-1 in aqueous humor were determined by enzymelinked immunosorbent assay. The correlation of VEGF, and IL-6, and MCP-1 were analyzed. Results The median aqueous level of VEGF165, IL-6 and MCP-1 were 1089.0, 165.6, 1253.0 pg/ml respectively in CRVO group, which were higher than the control group's results (168.2, 4.7, 216.4 pg/ml respectively), the differences were statistically significant (Z=-4.549, -6.008, -5.343;P＜0.001). The VEGF165b in CRVO group and control group were 834.0, 915.9 pg/ml respectively, the difference was not statistically significant (Z=-0.207，P＞0.05). The ratio of VEGF165b to VEGF165 in CRVO group and control group were 2.71, 7.28 respectively, the difference was statistically significant (t=-3.007，P＜0.05). There was a highly positive correlation between IL-6 and VEGF in CRVO group (r=0.526,P=0.001) and also mild positive correlation in control group (r=0.425，P=0.070). No correlation between MCP-1 and VEGF was observed in both groups (CRVO group: r=0.211,P＞0.05. Control group: r=-0.019,P＞0.05). Conclusions VEGF165, IL-6 and MCP-1 levels were increased in CRVO patients while the VEGF165b was normal. The ratio between VEGF165b and VEGF165 in aqueous humor of patients with macular edema secondary to CRVO was decreased.
ObjectiveTo investigate the relationship between the pathological and functional changes of the retina and the expression of monocyte chemoattractant protein (MCP)-1 after retinal laser injury in mice. MethodsA total of 116 C57BL/6 mice were randomly divided into the normal group (58 mice) and the injured group (58 mice). Retinal laser injuries were induced by Argon ion laser. At 1, 3, 7 days after laser injury, electroretinogram (ERG) responses were recorded to detect the function of the retina. Hematoxylin and eosin (HE) staining was performed to observe pathological changes. Quantitative real-time polymerase chain reaction (PCR) was performed to detect gene expression of MCP-1. Western blot was used to measure the protein expression of MCP-1. ResultsHE staining showed a progressive damage of the retinal structure. The results of ERG showed that the differences of dark-adaptive a wave (t=6.998, 9.594, 13.778) and b wave (t=12.089, 13.310, 21.989) amplitudes of 1, 3 and 7 day post-injury between normal group and injured group were statistically significant (P=0.000). At 1 day post-injury, the differences of light adaptive b wave amplitudes between the two groups were statistically significant (t=8.844, P=0.000). While the differences of light-adaptive a wave amplitudes were not (t=2.659,P=0.200). At 3, 7 days post-injury, the differences of a (t=3.076, 7.544) and b wave amplitudes (t=10.418, 8.485) between the two groups were statistically significant (P=0.000). In dark-adaptive ERG, the differences of a wave amplitudes between 1 day and 3 days (t=3.773), 1 day and 7 days (t=5.070) and b wave amplitudes between 1 day and 7 days (t=4.762) were statistically significant (P<0.01), while the differences of a wave amplitudes between the 3 days and 7 days (t=1.297) and b wave amplitudes between 1 day and 3 days (t=2.236), 3 day and 7 days (t=2.526) were not significant (P=0.660, 0.120, 0.060). In light-adaptive ERG, the differences of a wave amplitudes between 1 day and 7 days (t=2.992) and b wave amplitudes between 1 day and 3 days (t=3.570), 1day and 7 days (t=4.989) were statistically significant (P<0.05), while the differences of a wave amplitudes between 1 day and 3 days (t=0.516), the 3 days and 7 days (t=2.475) and b wave amplitudes between 3 days and 7 days (t=1.419) were not significant (P=1.000, 0.710, 0.070). Quantitative real-time PCR showed that the differences of MCP-1 gene expression at 1, 3 and 7 day post-injury between normal group and injured group were statistically significant (t=14.329, 16.861, 5.743; P<0.05). Western blot showed that the differences of MCP-1 protein expression at 1, 3 and 7 day post-injury between normal group and injured group were statistically significant (t=75.068, 54.145, 14.653; P<0.05). ConclusionIn the first 7 days after mice retinal laser injury, there are progressive pathological and functional damage of the retina, which might be correlated with MCP-1 expression.
Monocyte chemoattractant protein-1(MCP-1) is a cytokine which belongs to the CC chemokine family. Retinal pigment epithelium (RPE) cells, photoreceptors and microglial cells in the retina can secrete MCP-1. Physiological level of MCP-1 is important for preserving morphology of RPE and glial cells, as well as retinal function and gross morphology. MCP-1 is likely released from Müller glia and the RPE cells when retina under stress, and attracts microglia/macrophages to the sites of retinal damage, activates the microglia to ingest cell debris. MCP-1 has been found upregulated in the intraocular fluid of retina in patients and animal models with retinal detachment, posterior uveitis and age-related macular degeneration. The expression of MCP-1 may be response to retinal inflammation. Therefore, it is tempting to speculate that pharmacological targeting of MCP-1 may be a safe and viable strategy in treatment of retinal disease.
Diabetic retinopathy (DR) is one of the most common and serious diabetic complications, which is the main cause of vision loss in adults. The specific vascular and neuropathology mechanism of DR is not clear. It has been demonstrated that Inflammatory reaction might be take effects in the development and progression of DR. Monocyte chemoattractant protein-1 (MCP-1), as an important chemokine in the inflammatory response process, promotes chemotactic and activating factors, destroys the blood-retinal barrier, causes retinal vascular disease, and activates microglia, which is related to the severity of the disease. With further research on MCP-1, it is possible to use chemokines and their receptors as target cells to control or slow down the progression of DR by reducing or inhibiting the production of MCP-1 in diabetic patients in the early stages of the disease. This study can provide new ideas and new methods about preventing and treating DR.