Lack of collagen XVIII/endostatin results in eye abnormalities
Document Type
Article
Abstract
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 XVHI/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 XVHI 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.
Keywords
Collagen XVIII, Endostatin, Eye abnormalities, Immunogold labeling, Knockout mice
Publication Date
4-2-2002
Publication Title
EMBO Journal
ISSN
02614189
Volume
21
Issue
7
First Page
1535
Last Page
1544
PubMed ID
11927538
Digital Object Identifier (DOI)
10.1093/emboj/21.7.1535
Recommended Citation
Fukai, Naomi; Eklund, Lauri; Marneros, Alexander G.; Oh, Suk Paul; Keene, Douglas R.; Tamarkin, Lawrence; Niemelä, Merja; Ilves, Mika; Li, En; Pihlajaniemi, Taina; and Olsen, Bjorn R., "Lack of collagen XVIII/endostatin results in eye abnormalities" (2002). Translational Neuroscience. 713.
https://scholar.barrowneuro.org/neurobiology/713