Anti-angiogenic effect of Interleukin-26 in oxygen-induced retinopathy mice via inhibiting NFATc1-VEGF pathway

• Published in: Biochemical and biophysical research communications 2018-05, Vol.499 (4), p.849
• Main Authors: Bao, Jing, Lv, Zhigang, Wang, Saibin
• Format: Article
• Language: English
• Subjects: Angiogenesis Inhibitors - pharmacology; Angiogenesis Inhibitors - therapeutic use; Animals; Disease Models, Animal; Interleukins - pharmacology; Interleukins - therapeutic use; Mice, Inbred C57BL; NFATC Transcription Factors - metabolism; Oxygen; Retina - metabolism; Retina - pathology; Retinal Neovascularization - drug therapy; Retinal Neovascularization - metabolism; Retinal Neovascularization - pathology; Signal Transduction; Vascular Endothelial Growth Factor A - metabolism
• ISSN: 1090-2104
• DOI: 10.1016/j.bbrc.2018.04.004

Retinal neovascularization (RNV) is a devastating pathological feature of numerous ocular diseases and is a major cause of blindness. In this study, we examined the effect and potential mechanism of interleukin-26 (IL-26) in the pathogenesis of RNV in an oxygen-induced retinopathy (OIR) model. OIR model was induced by exposure of hypoxia (75% oxygen) to C57BL/6J mice from postnatal day 7 (P7) to P12 and then returned to room air. A significant up-regulation of IL-26 was detected in the retina at P17 after OIR, and the expression of IL-26 was observed to be localized mainly in the retinal endothelial cells (RECs). Furthermore, recombinant (r) IL-26 could effectively prevented RNV by reduction the areas of RNV, and IL-26 deficiency markedly increased RNV formation. In addition, the increased expressions of nuclear factor of activated T-cell (NFATc) 1 and vascular endothelial growth factor (VEGF) in the retina at P17 after OIR were increased in IL-26 -/- mice, and were down-regulated following rIL-26 treatment. Collectively, these data suggested a possibility that IL-26 suppressed RNV via NFATc1-VEGF pathway.