ArticleInternational journal of ophthalmology2016
In vivo bioluminescence imaging of hyperglycemia exacerbating stem cells on choroidal neovascularization in mice.
Article in International journal of ophthalmology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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Who cites it
2 citing papers in PubMed, 3 citations in OpenAlex.
- Molecular and cellular imaging of the eye.Biomedical optics express · 2024Review
- Effect of integrin α5β1 inhibition on SDF-l/CXCR4-mediated choroidal neovascularization.International journal of ophthalmology · 2018Article
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
aimTo investigate the influence of hyperglycemia on the severity of choroidal neovascularization (CNV), especially the involvement of bone marrow-derived cells (BMCs) and underlying mechanisms.
methodsBMCs from firefly luciferase (Fluc)/green fluorescent protein (GFP) double transgenic mice were transplanted into C57BL/6J wide-type mice. The recipient mice were injected intraperitoneally with streptozotocin (STZ) daily for 5 consecutive days to induce diabetes mellitus (DM), followed by CNV laser photocoagulation. The BMCs recruitment in CNV exposed to hyperglycemia was firstly examined in Fluc/GFP chimeric mice by in vivo optical bioluminescence imaging (BLI) and in vitro Fluc assays. The CNV severity was evaluated by H&E staining and choroidal flatmount. The expression of vascular endothelial growth factor (VEGF) and stromal cell derived factor-1 (SDF-1) was detected by Western Blot.
resultsBLI showed that the BMCs exerted dynamic effects in CNV model in Fluc/GFP chimeric mice exposed to hyperglycemia. The signal intensity of transplanted Fluc(+)GFP(+) BMCs in the DM chimeric mice was significantly higher than that in the control chimeric mice with CNV induction at days 5, 7, 14 and 21 (121861.67±9948.81 vs 144998.33±13787.13 photons/second/cm(2)/sr for control and DM mice, P 5d<0.05; 178791.67±30350.8 vs 240166.67±22605.3, P 7d<0.05; 124176.67±16253.52 vs 196376.67±18556.79, P 14d<0.05; 97951.60±10343.09 vs 119510.00±14383.76, P 21d<0.05), which was consistent with in vitro Fluc assay at day 7 [relative light units of Fluc (RLU1)], 215.00±52.05 vs 707.33±88.65, P<0.05; RLU1/ relative light units of renilla luciferase (RLU2), 0.90±0.17 vs 1.83±0.17, P<0.05]. The CNVs in the DM mice were wider than those in the control group at days 5, 7, 14 and 21 (147.83±17.36 vs 220.33±20.17 µm, P 5d<0.05; 212.17±24.63 vs 326.83±19.49, P 7d<0.05; 163.17±18.24 vs 265.17±20.55, P 14d<0.05; 132.00±10.88 vs 205.33±12.98, P 21d<0.05). The average area of CNV in the DM group was larger at 7d (20688.67±3644.96 vs 32218.00±4132.69 µm(2), P<0.05). The expression of VEGF and SDF-1 was enhanced in the DM mice.
conclusionHyperglycemia promots the vasculogenesis of CNV, especially the contribution of BMCs, which might be triggered by VEGF and SDF-1 production.
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