PURPOSE: Corneal avascularity is tightly regulated by a balance between angiogenic and antiangiogenic factors (angiogenic privilege). In the current study, we tested the hypothesis that the CD36+/+ antiangiogenic receptor contributes toward the maintenance of corneal avascularity. METHODS: Corneas of CD36 wild-type (CD36) and knockout (CD36) mice aged 4, 16, 52, and 78 weeks were histologically evaluated for corneal haze and neovascularization (NV). Quantitative real-time polymerase chain reaction was performed on corneal tissue from CD36+/+ and CD36-/- mice aged 4 and 52 weeks to examine the effect of CD36 deficiency on expression of relevant angiogenic factors. RESULTS: Corneal haze and NV were absent in CD36+/+ mice at all ages. Conversely, corneal haze and NV were evident at 52 and 78 weeks in CD36-/- mice, and the latter demonstrated a significant increase in vessel density at 52 and 78 weeks. Interestingly, compared with CD36+/+ mice, in the corneas of 52-week-old CD36-/- mice, thrombospondin-1 messenger RNA was repressed, and vascular endothelial growth factor A, c-Jun N-terminal kinase-1, and c-Jun levels were robustly upregulated. CONCLUSIONS: CD36-/- mice develop corneal NV that increases in severity with age, thus accentuating the role of CD36 in preserving corneal avascularity.
PURPOSE:Corneal avascularity is tightly regulated by a balance between angiogenic and antiangiogenic factors (angiogenic privilege). In the current study, we tested the hypothesis that the CD36+/+ antiangiogenic receptor contributes toward the maintenance of corneal avascularity. METHODS: Corneas of CD36 wild-type (CD36) and knockout (CD36) mice aged 4, 16, 52, and 78 weeks were histologically evaluated for corneal haze and neovascularization (NV). Quantitative real-time polymerase chain reaction was performed on corneal tissue from CD36+/+ and CD36-/- mice aged 4 and 52 weeks to examine the effect of CD36 deficiency on expression of relevant angiogenic factors. RESULTS: Corneal haze and NV were absent in CD36+/+ mice at all ages. Conversely, corneal haze and NV were evident at 52 and 78 weeks in CD36-/- mice, and the latter demonstrated a significant increase in vessel density at 52 and 78 weeks. Interestingly, compared with CD36+/+ mice, in the corneas of 52-week-old CD36-/- mice, thrombospondin-1 messenger RNA was repressed, and vascular endothelial growth factor A, c-Jun N-terminal kinase-1, and c-Jun levels were robustly upregulated. CONCLUSIONS:CD36-/- mice develop corneal NV that increases in severity with age, thus accentuating the role of CD36 in preserving corneal avascularity.
Authors: Julia Klocke; Rita N Barcia; Susan Heimer; Elke Cario; James Zieske; Michael S Gilmore; Bruce R Ksander; Meredith S Gregory Journal: Invest Ophthalmol Vis Sci Date: 2011-01-05 Impact factor: 4.799
Authors: Yijuan Sun; Marina Scavini; Robert A Orlando; Glen H Murata; Karen S Servilla; Antonios H Tzamaloukas; Ronald Schrader; Edward J Bedrick; Mark R Burge; Nada A Abumrad; Philip G Zager Journal: Diabetes Care Date: 2010-06-14 Impact factor: 19.112