Send to

Choose Destination
See comment in PubMed Commons below
J Proteomics. 2011 Sep 6;74(10):1895-905. doi: 10.1016/j.jprot.2011.04.032. Epub 2011 May 17.

Proteome profiling of wild type and lumican-deficient mouse corneas.

Author information

Department of Medicine, The Johns Hopkins University School of Medicine, USA.


To elucidate how the deficiency of a major corneal proteoglycan, lumican, affects corneal homeostasis, we used mass spectrometry to derive the proteome profile of the lumican-deficient and the heterozygous mouse corneas and compared these to the wild type corneal proteome. 2108 proteins were quantified in the mouse cornea. Selected proteins and transcripts were investigated by Western blot and quantitative RT-PCR, respectively. We observed major changes in the composition of the stromal extracellular matrix (ECM) proteins in the lumican-deficient mice. Lumican deficiency altered cellular proteins in the stroma and the corneal epithelium. The ECM changes included increases in fibril forming collagen type I, Collagen type VI, fibromodulin, perlecan, laminin β₂, collagen type IV, nidogen/entactin and anchoring collagen type VII in the Lum⁺/⁻ and the Lum⁻/⁻ mouse corneas, while the stromal proteoglycans decorin, biglycan and keratocan were decreased in the Lum⁻/⁻( corneas. Cellular protein changes included increases in alcohol dehydrogenase, superoxide dismutase and decreases in epithelial cytokeratins 8 and 14. We also detected proteins that are novel to the cornea. The proteomes will provide an insight into the lumican-deficient corneal phenotype of stromal thinning and loss of transparency and a better understanding of pathogenic changes in corneal and ocular dystrophies.

[Indexed for MEDLINE]
Free PMC Article
PubMed Commons home

PubMed Commons

How to join PubMed Commons

    Supplemental Content

    Full text links

    Icon for Elsevier Science Icon for PubMed Central
    Loading ...
    Support Center