Development of cataractous macrophthalmia in mice expressing an active MEK1 in the lens

摘要: PURPOSE. To characterize the extracellular signal-regulated kinase (ERK) pathway in lens and to try understand how this contributes function cataractogenesis. METHODS. The members of ERK were examined by Western blotting, immunohistochemical staining, assay. A gain-of-function approach was used perturb lenses transgenic mice via expression a constitutively active mutant mitogenactivated protein 1 (MEK1(E)), direct upstream ERK1 ERK2 kinases, under aAcrystallin promoter. RESULTS. presence an found epithelial cells differentiating fibers. Transgenic that expressed MEK1(E) developed postnatal cataracts as well macrophthalmia. Distinct morphologic alterations, such enlargement, swelling fiber cells, enlarged space, vacuole formation, observed these mice. significant increase glucose transporter (GLUT1) level, detected lens. CONCLUSIONS. MAP is involved regulation metabolism balance mouse Moreover, alteration activity sufficient cause cataract formation with space vacuoles This may provide useful model for understanding mechanism(s) some aspects human cataracts. (Invest Ophthalmol Vis Sci. 2001;42:539 ‐548)