Open Access

Soluble Tei2 fusion protein inhibits retinopathy of prematurity occurrence via regulation of the Ang/Tie2 pathway

  • Authors:
    • Weijing Li
    • Weihua Zhang
    • Cuiying Zhang
    • Chunfang Zhu
    • Xiangling Yi
    • Yan Zhou
    • Yan Lv
  • View Affiliations

  • Published online on: May 24, 2019     https://doi.org/10.3892/etm.2019.7608
  • Pages: 614-620
  • Copyright: © Li et al. This is an open access article distributed under the terms of Creative Commons Attribution License.

Metrics: Total Views: 0 (Spandidos Publications: | PMC Statistics: )
Total PDF Downloads: 0 (Spandidos Publications: | PMC Statistics: )


Abstract

The aim of the present study was to investigate the potential mechanism of retinopathy of prematurity (ROP) using an oxygen‑induced retinopathy (OIR) mouse model. For experiments, mice were divided into either the OIR group or control group. Fluorescein isothiocyanate‑dextran cardiac perfusion and stretched retina preparation were performed. The total retina area, area of instillation, density of microvascular network, area of new blood vessels, vein width and the tortuosity of arteries were measured. Next, mice were randomly assigned into the PBS, soluble TEK receptor tyrosine kinase (sTie2)‑fusion protein (Fc), angiopoietin 1 (Ang1), ranibizumab, ranibizumab + sTie2‑Fc and ranibizumab + Ang1 treatment groups. Following housing for 5 days, the body weight of each mouse was recorded. Mice in the OIR group presented smaller total retina area and larger area of instillation, larger area of new blood vessels, and higher microvascular network density compared with the control PBS group. Obvious retinal vein dilatation and arterial tortuosity were identified in the OIR group. The amount of endotheliocyte nuclei of new vessels beyond the inner limiting membrane was larger in the OIR group compared with the control group. Furthermore in the next set of experiments, a larger area of instillation, smaller area of new blood vessels and decreased amount of endotheliocyte nuclei of new vessels were observed in the sTie2‑Fc group, Ang1 group, ranibizumab group, ranibizumab + sTie2‑Fc group and ranibizumab + Ang1 group compared with the PBS group. Specifically, the ranibizumab + sTie2‑Fc group and ranibizumab + Ang1 group demonstrated markedly reduced retina instillation area and microvascular network density in the instillation area. Total retina area and body weight following 10 days of the experiment for the ranibizumab group were significantly lower compared with other groups. In conclusion, the combined regulation of the Ang/Tie2 and the vascular endothelial growth factor (VEGF)/VEGF receptor pathways markedly increased the efficacy of treatment with retinal neovascularization (RNV). Regulation of these pathways has a potential for treating RNV, in particular ROP.
View Figures
View References

Related Articles

Journal Cover

July-2019
Volume 18 Issue 1

Print ISSN: 1792-0981
Online ISSN:1792-1015

Sign up for eToc alerts

Recommend to Library

Copy and paste a formatted citation
x
Spandidos Publications style
Li W, Zhang W, Zhang C, Zhu C, Yi X, Zhou Y and Lv Y: Soluble Tei2 fusion protein inhibits retinopathy of prematurity occurrence via regulation of the Ang/Tie2 pathway. Exp Ther Med 18: 614-620, 2019
APA
Li, W., Zhang, W., Zhang, C., Zhu, C., Yi, X., Zhou, Y., & Lv, Y. (2019). Soluble Tei2 fusion protein inhibits retinopathy of prematurity occurrence via regulation of the Ang/Tie2 pathway. Experimental and Therapeutic Medicine, 18, 614-620. https://doi.org/10.3892/etm.2019.7608
MLA
Li, W., Zhang, W., Zhang, C., Zhu, C., Yi, X., Zhou, Y., Lv, Y."Soluble Tei2 fusion protein inhibits retinopathy of prematurity occurrence via regulation of the Ang/Tie2 pathway". Experimental and Therapeutic Medicine 18.1 (2019): 614-620.
Chicago
Li, W., Zhang, W., Zhang, C., Zhu, C., Yi, X., Zhou, Y., Lv, Y."Soluble Tei2 fusion protein inhibits retinopathy of prematurity occurrence via regulation of the Ang/Tie2 pathway". Experimental and Therapeutic Medicine 18, no. 1 (2019): 614-620. https://doi.org/10.3892/etm.2019.7608