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Publication : Lack of collagen XVIII/endostatin results in eye abnormalities.

First Author  Fukai N Year  2002
Journal  EMBO J Volume  21
Issue  7 Pages  1535-44
PubMed ID  11927538 Mgi Jnum  J:75861
Mgi Id  MGI:2177972 Doi  10.1093/emboj/21.7.1535
Citation  Fukai N, et al. (2002) Lack of collagen XVIII/endostatin results in eye abnormalities. EMBO J 21(7):1535-44
abstractText  Mice lacking collagen XVIII and its proteolytically derived product endostatin show delayed regression of blood vessels in the vitreous along the surface of the retina after birth and lack of or abnormal outgrowth of retinal vessels. This suggests that collagen XVIII/endostatin is critical for normal blood vessel formation in the eye. All basement membranes in wild-type eyes, except Descemet's membrane, showed immunogold labeling with antibodies against collagen XVIII. Labeling at sites where collagen fibrils in the vitreous are connected with the inner limiting membrane and separation of the vitreal matrix from the inner limiting membrane in mutant mice indicate that collagen XVIII is important for anchoring vitreal collagen fibrils to the inner limiting membrane. The findings provide an explanation for high myopia, vitreoretinal degeneration and retinal detachment seen in patients with Knobloch syndrome caused by loss-of-function mutations in collagen XVIII.
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