Targeted expression of a lumican transgene rescues corneal deficiencies in lumican-null mice

-/- mice. At the EM level, the pronounced disarray of the posterior fibrillar matrix seen in Lum -/- mice was not observed in Lum -/- /Kera-Lum mice. Moreover, analyses of collagen fibril diameter distributions showed a significant reduction in the number of large-diameter (>40 nm) fibrils in Lum -/- /Kera-Lum mice as compared to Lum -/- mice. No significant differ- ences in keratocan expression were found at the mRNA level, but western blot analysis detected an approximately two fold increase in keratocan protein levels in Lum -/- /Kera-Lum over Lum -/- mice. Conclusions: Together these data suggest that despite the low keratocan promoter activity driving the transgene in Lum - /- cornea, transgenic lumican expression was sufficient to partially rescue corneal phenotypic deficiencies.