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Publication : Metalloproteinase Adamts16 Is Required for Proper Closure of the Optic Fissure.

First Author  Cao M Year  2018
Journal  Invest Ophthalmol Vis Sci Volume  59
Issue  3 Pages  1167-1177
PubMed ID  29625437 Mgi Jnum  J:261618
Mgi Id  MGI:6151212 Doi  10.1167/iovs.17-22827
Citation  Cao M, et al. (2018) Metalloproteinase Adamts16 Is Required for Proper Closure of the Optic Fissure. Invest Ophthalmol Vis Sci 59(3):1167-1177
abstractText  Purpose: Coloboma is a sight-threatening congenital eye disease caused by a failure in optic fissure (OF) closure. The aim of this study was to investigate the role of Adamts16, a metalloproteinase, in OF closure. Methods: RNA in situ hybridization was used to examine the expression of Adamts16 in developing mouse and zebrafish eyes. Morpholino knockdowns were performed to study adamts16 function during zebrafish eye development. Additionally, immunofluorescent staining, RNA in situ hybridization, bromodeoxyuridine (BrdU) labeling, TUNEL assays, and high-throughput sequencing were used to examine altered cellular and molecular events in adamts16-morphant optic cups (OCs). Results: Adamts16 is expressed at the edges of the closing OF in both mice and zebrafish eyes. Zebrafish adamts16 knockdown resulted in coloboma formation. In adamts16-morphant eyes, the basement membrane failed to disassemble at the closing OF edges, OC cells exhibited decreased proliferation and increased apoptosis, and fibroblast growth factor 8 (fgf8) was ectopically upregulated in the OC. Conclusions: adamts16 is required for proper OF closure in zebrafish eyes. adamts16 controls OF closure possibly through the combined functions of degrading the basement membrane at the closing OF edges, promoting cell proliferation and survival, and restricting fgf8 expression. Our study linked a metalloproteinase to OF closure, which may facilitate future etiologic studies on human coloboma cases.
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