| First Author | Lu P | Year | 2009 |
| Journal | Invest Ophthalmol Vis Sci | Volume | 50 |
| Issue | 10 | Pages | 4761-8 |
| PubMed ID | 19458323 | Mgi Jnum | J:154541 |
| Mgi Id | MGI:4397524 | Doi | 10.1167/iovs.08-2732 |
| Citation | Lu P, et al. (2009) Enhanced experimental corneal neovascularization along with aberrant angiogenic factor expression in the absence of IL-1 receptor antagonist. Invest Ophthalmol Vis Sci 50(10):4761-8 |
| abstractText | PURPOSE: To address the roles of the endogenously produced IL-1ra in the course of corneal neovascularization (CNV). METHODS: CNV was induced by alkali injury and compared in wild-type (WT), IL-1 receptor antagonist (ra) knockout (KO) mice and anti-IL-1ra antibody-treated WT mice 2 weeks after injury. Angiogenic factor expression and leukocyte accumulation in the early phase after injury were quantified by RT-PCR and immunohistochemical analysis, respectively. RESULTS: The mRNA expression of IL-1ra, IL-1 alpha, and IL-1beta was augmented, together with infiltration of F4/80(+) macrophages and Gr-1(+) neutrophils, in corneas after alkali injury. Intracorneally infiltrating macrophages, but not neutrophils, expressed IL-1ra. Compared with WT mice, either IL-1ra KO mice or anti-IL-1ra antibody-treated WT mice exhibited enhanced CNV 2 weeks after injury, as evidenced by enlarged CD31(+) areas. Concomitantly, the infiltration of F4/80(+) macrophages was more significantly enhanced in IL-1ra KO mice than in WT mice. Intraocular mRNA expression enhancement of vascular endothelial growth factor (VEGF) and inducible nitric oxide synthase (iNOS) was greater in IL-1ra KO mice than in WT mice after injury. Moreover, IL-1 alpha and IL-1 beta enhanced VEGF and iNOS expression by murine peritoneal macrophages. CONCLUSIONS: IL-1ra KO exhibited enhanced alkali-induced CNV through enhanced intracorneal macrophage infiltration and increased expression of VEGF and iNOS. |
