ObjectiveTo observe the expression of vascular endothelial growth factor (VEGF), fibrogenic mediators and inflammatory mediators in the retinal pigment epithelium (RPE)-choroid complex of mice with experimental subretinal fibrosis. MethodsBy subretinal injection of inflammatory macrophages after retinal photocoagulation, experimental subretinal fibrosis was induced in 64 adult C57BL/6(B6) female mice (7-8 weeks). Masson staining and glial fibrillary acidic protein (GFAP) staining of choroidal wholemont were performed to verify that the subretinal fibrosis at day 7 after subretinal injection. Before subretinal injection and at day 1, 2, 3, 5 and 7 after subretinal injection, the mRNA expression level of VEGF, transforming growth factor (TGF)-β1, TGF-β2, TGF-β3, interleukin (IL)-6, IL-10 and IL-13 in RPE-choroid complex were evaluated by quantitative reverse transcription-polymerase chain reaction. Enzyme-linked immune sorbent assay was next used to detect protein expression of these factors. ResultsAt seven days after subretinal injection of inflammatory macrophages, experimental subretinal fibrosis was detected by Masson staining and GFAP staining. The mRNA level of VEGF, TGF-β1 and TGF-β2 reached the peak at day 5 after modeling, while the mRNA expression of IL-6, IL-10, IL-13 reached the peak at day 2 after modeling. TGF-β3 mRNA was not detected either in naive mice or during the development of experimental subretinal fibrosis. At day 2, 3, 5 and 7 after modeling, compared with the pre-modeling, the mRNA expression of VEGF (t=2.38, 3.65, 4.03, 2.26), TGF-β1 (t=2.58, 2.30, 3.89, 4.15) and TGF-β2 (t=4.37, 4.20, 3.77, 3.98) were significantly increased (P < 0.05). At day 1, 2 and 3 after modeling, compared with the pre-modeling, the mRNA expression of IL-6 were significantly increased (t=2.36, 4.54, 4.01; P < 0.05). At day 2 and 3 after modeling, compared with the pre-modeling, the mRNA expression of IL-10 and IL-13 were significantly increased (t=3.87, 4.20, 2.44, 2.58; P < 0.05). At day 5 after modeling, compared with the pre-modeling, the protein expression of VEGF, total TGF-β1, active TGF-β1, total TGF-β2 and active TGF-β2 were significantly increased (t=2.57, 3.37, 2.45, 3.83, 2.74; P < 0.05). IL-6, IL-10 and IL-13 protein were not detected at pre-modeling eyeballs, but were found at day 2 after modeling. ConclusionThe expression of VEGF, fibrogenic mediators and inflammatory mediators in RPE-choroid complex in mice with experimental subretinal fibrosis are increase significantly.
Objective To investigate the correlation between the vitreomacular adhesion (VMA) and exudative age-related macular degeneration (AMD). Methods A literature research was performed in PubMed, EMbase, Cochrane Library, CNKI and Wanfang database from January 2000 to December 2016. Case-control studies on the relationship between VMA or posterior vitreous detachment and exudative AMD were included in this analysis. Literature screening and data extraction were performed according to inclusion and exclusion criteria. The qualities of the literatures were evaluated according to the Newcastle-Ottawa Scale (NOS). Seven literatures were selected into meta-analysis. The NOS score was 9 points in 1 article, 8 scores in 4 articles, 7 points in 2 articles. A total of 947 eyes with exudative AMD, 638 eyes with dry AMD, and 618 eyes with controls were included. The correlation between exudative AMD and VMA were analyzed using the software Review manager 5.3. Results The prevalence of VMA in exudative AMD eyes was higher than that in controls [odds ratio (OR)=2.14, 95% confidence interval (CI)=1.19 - 3.84, P=0.010] and dry AMD eyes (OR=2.24, 95%CI=1.24 - 4.03, P=0.007). There was no difference in PVD prevalence among exudative AMD eyes, dry AMD eyes (OR=0.44, 95%CI=0.16 - 1.20, P=0.110) and controls (OR=0.70, 95%CI=0.41 - 1.18, P=0.180). Conclusion There is correlation between VMA and exudative AMD.
Choroidal neovascularization is the leading causes of central vision loss in wet age-related macular degeneration (wAMD) patients. Smoking not only aggravates the incidence and severity of the choroidal neovascularization of wAMD, but also affects the clinical treatment, making the prognosis worse. Nicotine, as an important harmful substance in tobacco, is an easily addictive and highly toxic alkaloid. Animal experiments and clinical studies have confirmed that nicotine can aggravate wAMD by mediating angiogenesis through nicotinic acetylcholine receptor, bone marrow blasts, inflammation, complement system, etc. Therefore, in order to early take appropriate intervention measures to prevent and delay the development, we should actively explore the exact pathogenesis by which nicotine aggravates the choroidal neovascularization.