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Shukti Chakravarti, W. Matthew Petroll, John R. Hassell, James V. Jester, Jonathan H. Lass, Jennifer Paul, David E. Birk; Corneal Opacity in Lumican-Null Mice: Defects in Collagen Fibril Structure and Packing in the Posterior Stroma. Invest. Ophthalmol. Vis. Sci. 2000;41(11):3365-3373. doi: https://doi.org/.
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© ARVO (1962-2015); The Authors (2016-present)
purpose. Gene targeted lumican-null mutants
(lum tm1sc /lum tm1sc )
have cloudy corneas with abnormally thick collagen fibrils. The purpose
of the present study was to analyze the loss of transparency
quantitatively and to define the associated corneal collagen fibril and
methods. Backscattering of light, a function of corneal haze and opacification,
was determined regionally using in vivo confocal microscopy in
lumican-deficient and wild-type control mice. Fibril organization and
structure were analyzed using transmission electron microscopy.
Biochemical approaches were used to quantify glycosaminoglycan
contents. Lumican distribution in the cornea was elucidated
results. Compared with control stromas, lumican-deficient stromas displayed a
threefold increase in backscattered light with maximal increase
confined to the posterior stroma. Confocal microscopy through-focusing
(CMTF) measurement profiles also indicated a 40% reduction in stromal
thickness in the lumican-null mice. Transmission electron microscopy
indicated significant collagen fibril abnormalities in the posterior
stroma, with the anterior stroma remaining relatively unremarkable. The
lumican-deficient posterior stroma displayed a pronounced increase in
fibril diameter, large fibril aggregates, altered fibril packing, and
poor lamellar organization. Immunostaining of wild-type corneas
demonstrated high concentrations of lumican in the posterior stroma.
Biochemical assessment of keratan sulfate (KS) content of whole eyes
revealed a 25% reduction in KS content in the lumican-deficient mice.
conclusions. The structural defects and maximum backscattering of light clearly
localized to the posterior stroma of lumican-deficient mice. In normal
mice, an enrichment of lumican was observed in the posterior stroma
compared with that in the anterior stroma. Taken together, these
observations indicate a key role for lumican in the posterior stroma in
maintaining normal fibril architecture, most likely by regulating
fibril assembly and maintaining optimal KS content required for
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