Impact of fenofibrate on choroidal neovascularization formation and VEGF-C plus VEGFR-3 in Brown Norway rats

Zhao, Jianfeng; Hua, Hairong; Chen, Qian-Bo; Guan, Meng; Yang, Jinhui; Xi, Xiaoting; Li, Yan; Geng, Yu

doi:10.1016/j.exer.2018.05.030

Cited by 6 publications

(5 citation statements)

References 13 publications

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“…VEGF‐C is a soluble member of the VEGF family, and the role of VEGF‐C in neovascularization is supported by the fact that exogenous VEGF‐C could recover lymphatic vascularization through stimulating neolymphangiogenesis 8 . Furthermore, VEGF‐C also participates in the laser‐induced choroidal neovascularization formation in Brown Norway rats 9 . High expression of VEGF‐C has been shown in proliferative DR 10 .…”

Section: Introductionmentioning

confidence: 99%

Long non‐coding ribonucleic acid urothelial carcinoma‐associated 1 promotes high glucose‐induced human retinal endothelial cells angiogenesis through regulating micro‐ribonucleic acid‐624‐3p/vascular endothelial growth factor C

Huang

Yao

et al. 2021

J of Diabetes Invest

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Aims/Introduction Emerging evidence has indicated that long non‐coding ribonucleic acids play important roles in the development and progression of diabetic retinopathy (DR). It is reported that urothelial carcinoma‐associated 1 (UCA1) is highly expressed in diabetic lymphoendothelial cells and influences glucose metabolism in rats with DR. The aim of the present study was to explore the role of UCA1 in the mechanism of DR. Materials and Methods Gene expression analyses in fibrovascular membranes excised from patients with DR using public microarray datasets (GSE60436). Reverse transcription polymerase chain reaction was carried out to detect UCA1, micro‐ribonucleic acid (miR)‐624‐3p and vascular endothelial growth factor C (VEGF‐C) expressions in the blood of patients and human retinal endothelial cells (HRECs). Furthermore, Cell Counting kit‐8, Transwell assay, and tube formation assay were used to identify biological effects of UCA1 on HRECs proliferation, migration ability and angiogenesis in vitro. Results UCA1 and VEGF‐C were elevated in DR patients and high glucose‐induced HRECs cell lines, whereas miR‐624‐3p was decreased. UCA1 inhibition inhibited proliferation, angiogenesis and migration of HRECs cells under high‐glucose condition. Luciferase reporter assay showed that UCA1 could sponge with miR‐624‐3p, which could directly target VEGF‐C. Finally, we proved a pathway that UCA1 promoted cell proliferation, migration and angiogenesis through sponging with miR‐624‐3p, thereby upregulating VEGF‐C in high‐glucose‐induced HRECs. Conclusions We identified UCA1 as an important factor associated with DR, which could regulate the expression of VEGF‐C by sponging miR‐624‐3p in human retinal endothelial cells. Our results pave the way for further studies on diagnostic and therapeutic studies related to UCA1 in DR patients.

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Section: Introductionmentioning

confidence: 99%

Long non‐coding ribonucleic acid urothelial carcinoma‐associated 1 promotes high glucose‐induced human retinal endothelial cells angiogenesis through regulating micro‐ribonucleic acid‐624‐3p/vascular endothelial growth factor C

Huang

Yao

et al. 2021

J of Diabetes Invest

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“…If fibrate and statin can benefit DR patients independent of their lipids-lowering activity, ocular delivery may be the next step for these drugs to reduce toxic systemic side effects. This idea has been evaluated in vivo using animal models of ocular diseases; for instance, intravitreal injection of Fenofibrate reduced retinal vascular permeability and white blood cell migration in diabetic rodent models [ 107 ] and inhibited laser-induced CNV model in BN rats [ 108 ]. An atorvastatin-solid lipid nanoparticle eye drop has been tested in rat eyes and ARPE-19 cells [ 109 ].…”

Section: Discussionmentioning

confidence: 99%

Hyperlipidemia and lipid-lowering therapy in diabetic retinopathy (DR): A bibliometric study and visualization analysis in 1993–2023

Tan,

Fu,

Chen

et al. 2023

Heliyon

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“…Samples were measured with the Luminex xMAP suspension array. A Milliplex Kit was used for the detection of epidermal growth factor (EGF) [11], angiopoietin-2 [12], granulocyte colony-stimulating factor (G-CSF) [13], endoglin [14], endothelin-1 [15], broblast growth factor (FGF)-1 [16], FGF-2 [17], interleukin-8 (IL-8) [18], hepatocyte growth factor (HGF) [19], heparin-binding epidermal growth factor (HB-EGF) [20], placental growth factor (PLGF) [21], vascular endothelial growth factor (VEGF)-C [22], VEGF-D [23], and VEGF-A [24]. It is necessary to conduct intensive studies, as many previous investigations have demonstrated that these cytokines may take part in the formation and development of myopic CNV.…”

Section: Methodsmentioning

confidence: 99%

The clinical effects and mechanism of action of ranibizumab in treating myopic choroidal neovascularization

Gu,

Wang,

Peng

et al. 2024

Preprint

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Objective To investigate the clinical effects and factors influencing repeated intravitreal injections of ranibizumab among patients with choroidal neovascularization (CNV) secondary to pathologic myopia. Methods There were 39 patients with myopic CNV and a control group of 10 cataract patients. Logarithm of the minimum angle of resolution units (logMAR) was adopted to evaluate best-corrected visual acuity (BCVA), while the measurement of central macular thickness was made via optical coherence tomography. Luminex xMAP suspension array was adopted to collect and analyze plasma and aqueous humor samples to compare cytokine concentrations between the two groups and assess changes after intravitreal ranibizumab injections. Additionally, BCVA values and CMT were monitored. Results A great diversity in the BCVA values and CMT was found after intravitreal ranibizumab injections (p<0.05 for both). The study group showed greatly higher plasma concentration of vascular endothelial growth factor-A than the cataractgroup (p<0.05). The research group (p<0.05 for both) showed greatly lower epidermal growth factor (EGF) and angiopoietin-2 concentrations. In the aqueous humor, the study group showed greatly higher concentration of fibroblast growth factor (FGF)-2 than the cataract group (p<0.05), and the research group (p<0.05 for both) displayed greatly lower concentrations of EGF and VEGF-A. The decrease in average VEGF-A contents was significant by comparing with baseline at both 1 month (p<0.05) and 2 months (p<0.05), and the reduction in mean VEGF-D and endoglin contents compared to baseline at 2 months were significant (p<0.05 for both), and were significant when compared at 1 month to 2 months (p<0.05 for both). The average EGF contents were significantly higher at 2 months than at baseline (p<0.05). Conclusion Ranibizumab had obvious effects on myopic CNV. For different individuals, different treatment projects should be chosen.

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Impact of fenofibrate on choroidal neovascularization formation and VEGF-C plus VEGFR-3 in Brown Norway rats

Cited by 6 publications

References 13 publications

Long non‐coding ribonucleic acid urothelial carcinoma‐associated 1 promotes high glucose‐induced human retinal endothelial cells angiogenesis through regulating micro‐ribonucleic acid‐624‐3p/vascular endothelial growth factor C

Long non‐coding ribonucleic acid urothelial carcinoma‐associated 1 promotes high glucose‐induced human retinal endothelial cells angiogenesis through regulating micro‐ribonucleic acid‐624‐3p/vascular endothelial growth factor C

Hyperlipidemia and lipid-lowering therapy in diabetic retinopathy (DR): A bibliometric study and visualization analysis in 1993–2023

The clinical effects and mechanism of action of ranibizumab in treating myopic choroidal neovascularization

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