Proliferative vitreoretinopathy (PVR) is a common complication and major cause of blindness of ocular trauma. Many cytokines, including vascular endothelial growth factor (VEGF) and platelet-derived growth factor (PDGF), participate in the process of the pathogenesis of traumatic PVR. VEGF competitively inhibits binding of PDGF to its receptor (PDGFRα), enables indirect activation of PDGFRα by non-PDGF ligands, resulting in reduced p53 expression, cell proliferation and migration, which is a key point in the pathogenesis of traumatic PVR.
ObjectiveTo assess the association of vascular endothelial growth factor (VEGF) gene-460C/T and-634C/G polymorphism with diabetic retinopathy (DR) among patients in Asia and European by meta-analysis. MethodsA systematic search of electronic databases (PubMed, Cochrane Library, EMBASE, VIP, Wanfang technological, CNKI, etc.) was carried out until Jun, 2014. Case-control studies on the relationship between genetic polymorphism of VEGF-460C/T and VEGF-634C/G with diabetic retinopathy were included in this analysis. The data were quantitatively analyzed by RevMan 5.0 software after assessing the quality of included studies. The pooled odds ratios (OR) and their corresponding 95% confidence intervals (CI) were used to assess the strength of the association. ResultsVEGF-460C/T (7 studies:899 cases and 786 controls) and VEGF-634C/G (10 studies:1615 cases and 1861 controls) were inclued in this meta-analysis. Significant association was found for-460C/T polymorphism in Aisa (C versus T:OR=1.52, 95%CI was, Z=3.72, P=0.0002; CC versus CT+TT:OR=1.61, 95%CI was[1.22, 1.90], Z=3.05, P=0.002; TT versus CT+CC:OR=0.64, 95%CI was[1.19, 2.19], Z=2.07, P=0.04), and VEGF-634CC gene type was associated with DR in European (OR=1.56, 95%CI[1.08, 2.25], Z=2.37, P=0.02). No significant publication bias was found. ConclusionsThe meta-analysis demonstrated that DR was associated with VEGF-460C/T polymorphism in Asia, and C alleles and CC gene type was the risk polymorphism; VEGF-634C/G polymorphism was not associated with DR, but its CC genotype maybe the risk factor in European. Further case-control studies based on larger sample size are still needed, especially for-634C/G polymorphism.
ObjectiveTo observe the expression of vascular endothelial growth inhibitor (VEGI, TL1A), vascular endothelial growth factor (VEGF), tumor necrosis factor-α (TNF-α) and interleukin-1β (IL-1β) in diabetes rats' serum, vitreous and retina, and discuss the role of VEGI in the pathogenesis of diabetic retinopathy (DR). MethodsA total of p70 adult male Wistar rats were randomly divided into 4 groups, the control group (10 rats), the diabetes mellitus (DM) 1 month group (20 rats), the DM 3 month group (20 rats) and the DM 6 month group (20 rats). Cytokines of serum and vitreous were determined by enzyme-linked immunosorbent assay (ELISA), and the concentrations of the cytokines in the retina were determined by immunohistochemistry on paraffin retinal sections. Hematoxylin-eosin (HE) staining of retina was used to estimate the pathological change of DR. The results were analyzed by one-way analysis of variances, independent samples t-test and LSD test. ResultsThe serum TL1A levels of the control group, the DM 1 month group, the DM 3 month group and the DM 6 month group rats were (92.09±2.05), (118.36±8.30), (85.90±7.51) and (78.90±4.88) ng/L respectively, the level of TL1A in serum of the DM 1 month group, the DM 3 month group and the DM 6 month group were significantly lower than that of the control group (F=77.405, P < 0.05). The concentration of serum TNF-α and IL-1β increased after DM model was established (F=3.508, 15.416; P < 0.05); the VEGF level in serum showed no difference between the groups (F=1.242, P > 0.05). The vitreous TL1A levels of the control group, the DM 1 month group, the DM 3 month group and the DM 6 month group were (91.50±8.18), (67.03±6.74), (47.44±4.92) and (46.01±4.62) ng/L respectively, every DM groups showed significant difference with the control group (F=114.777, P < 0.05); VEGF level in vitreous increased from 1 month after DM model was established (F=8.816, P < 0.05); TNF-α and IL-1β level in vitreous also showed an upward tendency (F=4.392, 3.635; P < 0.05). Paraffin section immunohistochemistry showed that the absorbance (also called optical density) of TL1A of the DM 1 month group and the DM 3 month group were significantly lower than that of the control group (t=6.851, 6.066; P < 0.05), but the DM 6 month group showed no difference with the control group (t=1.401, P > 0.05); the level of VEGF and TNF-α in DM groups were higher than that of the control group (tVEGF=-4.709, -16.406, -9.228; tTNF-α=-4.703, -6.583, -17.762; P < 0.05); the level of IL-1β were significantly higher in the DM 1 month group and the DM 6 month group (t=-4.108, -3.495; P > 0.05); but the DM 3 month showed no difference with the control group (t=-0.997, P > 0.05). HE staining of retina showed that the retina of the control group and the DM 1 month group had normal retinal structures, the DM 3 month group had retinal edema and disorganization, the DM 6 month group had severe retinal edema, deep stain of ganglion cells, and more neovascularization in inner plexiform layer. ConclusionVEGI is involved in the pathogenesis of DR, and it might interacts with VEGF, TNF-α and IL-1β to affect the development of DR.
Objective To investigate if lactic acid can promote the expression of vascular endothelial growth factor (VEGF) in the rat retinal explants.Methods The retinas of two-week neonatal SD rats were placed onto the culture plate inserts and incubated with Dulbeccoprime;s modified Eagleprime;s medium （DMEM） plus 2% fetal bovine serum (FBS) containing 10,20,30 mmol/L of lactic acid, respectively. Each group had 24 retinas. At 24 hours after incubation, the retinas were sectioned for light microscopy and the expression of VEGF was measured by real time PCR and Western blot. Results The cultured retinas maintained intact construction, and no cytolysis and apoptosis were observed under light microscope. RT-PCR showed the levels of VEGF mRNA were 0.74plusmn;0.06 for 10 mmol/L lactic acid group, 0.99plusmn;0.12 for 20 mmol/L group, and 1.45plusmn;0.17 for 30 mmol/L group respectively. VEGF expression was 0.34plusmn;0.15 for 10 mmol/L, 0.54plusmn;0.16 for 20 mmol/L, and 0.93plusmn;0.23 for 30 mmol/L group respectively by Western blot. Both PCR and Western blot showed 30 mmol/L of lactic acid significantly increased the levels of VEGF mRNA and VEGF expression. Conclusion The induction of retinal VEGF by lactic acid is concentration-dependent.
Objective：To investigate the role of 17beta; estradiol on th e expressi on of vascular endothelial growth factor (VEGF) and on the releasing rate of lac tate dehydrogenase (LDH) in cultured anoxiainjured human retinal pigment epit h eliual (RPE) cells. Methods:Established the anoxiainjuried m odel of human RPE c ells with Cobalt Chloride (CoCl2) after RPE cells were pretreated with 17beta;E 2 and tamoxife, 17beta;E2 antagonist. The expression of VEGF mRNA was detecte d by re v erse transcriptionpolymerase chain reaction technique (RTPCR). The cultured RP E cells were divided into four groups: normal control group, anoxiainjured gro u p, 17beta;E2 pretreatment group and 17beta;E2 with tamoxifen pretreatment grou p. The releasing rate of LDH was detected by chromatometry. The expression of VEGF pro tein were detected by cellular immunohistochemistry. Results:T he expression of VEGF and LDH releasing rate were higher in anoxiainjured grou p than that in nor m al control group (P＜0.05), and were lower in 17beta;E2 pretreatment group than th at in anoxiainjured group （P＜0.05）. When the effect of 17beta;E2 was o bstructe d by tamoxifen, the expression of VEGF and LDH releasing rate increased but didn prime;t differ much from which in anoxiainjured group (P＞0.05). Conc lusion:The ex pression of VEGF increases in anoxiainjured human RPE cells. 17beta;E2 can do wnr egulate the expression of VEGF and decrease the releasing rate of LDH, which can be blocked by tamoxifen.
Objective To observe the effect of panretinal photocoagulation (PRP) on the expression of cyclooxygenase-2 (COX-2), vascular endothelial cell growth factor (VEGF) in epiretinal membrane of proliferative diabetic retinopathy (PDR). Methods Atotal of 35 patients (35 eyes) with PDR and underwent plana vitrectomy were enrolled in this study. The patients were divided into non-PRP group (19 patients, 19 eyes) and PRP group (16 patients, 16 eyes) depends on if they had received PRP before surgery. The epiretinal membranes stripped during operation were collected for pathological examination. The histopathological features was observed by haematoxylin and eosin stain. The expression of CD34, COX-2 and VEGF, and microvessel density (MVD) were measured by immunohistochemistry method. Results Many new dispersed capillary blood vessels were found in the thick epiretinal membranes of non-PRP group, while scattered small blood vessels were found in the relatively thin epiretinal membranes of PRP group. MVD value was (7.42±1.39) in the non-PRP group and (4.56±1.22) in the PRP group, which was lower than the non-PRP group (t=6.41, P<0.01). The expression of CD34, COX-2 and VEGF in the tissues of epiretinal membrane in PRP group were obviously lower than the non-PRP group (t=6.147, 5.944, 7.445; P<0.01). Conclusion PRP can effectively inhibit the expression of COX-2 and VEGF in epiretinal membrane of PRP patients.
Objective To observe the expression of matrix metalloproteinase（MMP-2, MMP-9 and vascular endothelial growth factor (VEGF) in retinoblastoma (RB) and its relationship with the differentiation and optic nerve infiltration of RB.Methods Forty paraffin specimens of pathological confirmed RB were studied. They were divided into differentiated group (15 cases) and undifferentiated group (25 cases) , optic nerve infiltration group（13 cases） and without optic nerve infiltration group（27 cases）. The expression of MMP-2, MMP-9 and VEGF were detected by immunohistochemistry, their relationships with the differentiation and optic nerve infiltration were also analyzed.Results The positive rate of MMP-2, MMP-9 and VEGF expression in 40 RB cases were 52.5％，57.5％ and 72.5% respectively．The expression of MMP-2, MMP-9 and VEGF in the undifferentiated group were significantly higher than those in the differentiated group (chi;2=9.037, 9.253, 8.095; P＜0.05). The expression of MMP-2, MMP-9 and VEGF in RB with optic nerve infiltration group were significantly higher than those in RB without optic nerve infiltration group (chi;2=11.045,10.243, 8.956；P＜0.05). The expression of MMP-2，MMP-9 had a positive correlation with the expression of VEGF in RB (r=0.126,0.314；P＜0.05). Conclusions MMP-2, MMP-9 and VEGF expressed in RB tumor tissues. The expression of MMP-2, MMP-9 has a positive correlation with the expression of VEGF. The levels of MMP-2, MMP-9 and VEGF expression are related to optic nerve infiltration of RB cells.