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Delayed neovascularization in inflammation‐induced corneal neovascularization in interleukin‐10‐deficient mice
Author(s) -
Samolov Branka,
Kvanta Anders,
Van Der Ploeg Ingeborg
Publication year - 2010
Publication title -
acta ophthalmologica
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.534
H-Index - 87
eISSN - 1755-3768
pISSN - 1755-375X
DOI - 10.1111/j.1755-3768.2008.01393.x
Subject(s) - corneal neovascularization , neovascularization , cornea , vascular endothelial growth factor , angiogenesis , inflammation , interleukin 8 , interleukin , medicine , immunohistochemistry , matrix metalloproteinase , fibrous joint , corneal inflammation , immunology , cancer research , vegf receptors , ophthalmology , cytokine , anatomy
. Purpose: To investigate the potential modulatory role of interleukin‐10 (IL‐10) in the suture model for corneal neovascularization. Methods: Neovascularized areas were measured on corneal flat‐mounts in IL‐10 −/− and wild‐type C57BL6 mice. The inflammatory cellular response was characterized with immunohistochemistry. Gene expression was measured by real‐time polymerase chain reaction. Results: IL‐10 −/− mice showed a delayed neovascular response compared to wild‐type animals at day 6 after suture, when approximately half of the cornea was neovascularized. No apparent differences in inflammatory responses or in messenger RNA (mRNA) expression for proangiogenic factors were detected in IL‐10 −/− versus wild‐type mice. Conclusion: IL‐10 appears to have a proangiogenic effect in the suture model for corneal neovascularization that cannot be explained by either IL‐10’s anti‐inflammatory effect or apparent cross‐talk with the angiogenic factors vascular endothelial growth factor (VEGF)‐A, metalloproteinase (MMP)‐2 and MMP‐9, angiopoietin (Ang)‐1 and Ang‐2.