Expression and Localization of Tenomodulin, a Transmembrane Type Chondromodulin-I-Related Angiogenesis Inhibitor, in Mouse Eyes

DOI Web Site PubMed 被引用文献16件 オープンアクセス
  • Yusuke Oshima
    From the Department of Ophthalmology and Visual Science, Osaka University Medical School, Osaka, Japan; the2Department of Molecular Interaction and Tissue Engineering, Institute for Frontier Medical Sciences, Kyoto University, Kyoto, Japan; and the
  • Chisa Shukunami
    Department of Molecular Interaction and Tissue Engineering, Institute for Frontier Medical Sciences, Kyoto University, Kyoto, Japan; and the
  • Junichi Honda
    Department of Molecular Interaction and Tissue Engineering, Institute for Frontier Medical Sciences, Kyoto University, Kyoto, Japan; and the
  • Koji Nishida
    From the Department of Ophthalmology and Visual Science, Osaka University Medical School, Osaka, Japan; the
  • Fumi Tashiro
    Department of Nutrition and Physiological Chemistry, Osaka University Graduate School of Medicine, Osaka, Japan.
  • Jun-ichi Miyazaki
    Department of Nutrition and Physiological Chemistry, Osaka University Graduate School of Medicine, Osaka, Japan.
  • Yuji Hiraki
    Department of Molecular Interaction and Tissue Engineering, Institute for Frontier Medical Sciences, Kyoto University, Kyoto, Japan; and the
  • Yasuo Tano
    From the Department of Ophthalmology and Visual Science, Osaka University Medical School, Osaka, Japan; the

説明

To explore the role in the eye of tenomodulin (TeM), a chondromodulin (ChM)-I-related glycoprotein, the expression, localization, and antiangiogenic potential of TeM were investigated.Gene expression and protein localization of TeM in mouse eyes were examined by Northern blot analysis, in situ hybridization, and immunohistochemical analysis. Antiangiogenic function included in the C terminus of TeM and ChM-I was examined in vascular endothelial cells through adenoviral gene transduction.TeM expression was detectable from day 15 of the embryonic stage and was clearly present in the eye and skin. In situ hybridization of the eye tissues revealed TeM mRNA in the tendon of the extraocular muscle, the sclerocornea, the lens fiber cells, and the ganglion cell layer, inner nuclear layer cells, and pigment epithelium of the retina. Corresponding immunoreactivity of TeM was present in most of these cells. Western blot detected 40- and 45-kDa immunoreactive bands of TeM in the eye as differently glycosylated forms of the transmembrane protein. Production of a secreted form of TeM and ChM-I through adenoviral gene transfer caused effective autocrine suppression of cell proliferation and capillary-like morphogenesis of retina vascular endothelial cells. The condition media from soluble TeM- and ChM-I-overexpressing cells also showed a marked inhibitory effect on in vitro angiogenesis.These results indicate a potential role for TeM in prevention of vascular invasion in the mouse eye and the possibility of both TeM and ChM-I as candidates for use in gene therapy approaches to treatment of ocular angiogenesis.

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