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Chelsey McKenna, Peter Lwigale; Sema3a/npn-1 Signaling Is Required To Maintain Corneal Avascularity During Development. Invest. Ophthalmol. Vis. Sci. 2012;53(14):4739.
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To determine the role Semaphorin3A (Sema3A) andNeuropilin-1 (Npn-1) have during the development of corneal avascularity.
We characterized ocular vasculogenesis in wild type mice during the early stages of the developing cornea by immunostaining whole mount and corneal sections with endomucin. Eyes from Npn-1Sema-/- mutant mice that are deficient in Sema3A signaling through the Npn-1 receptor were similarly stained with endomucin and then compared to wild type corneas. Transgenic quail that express YFP in endothelial cells were lens ablated at E3 in one eye, leaving the contralateral lens as a control, and incubated for two additional days and imaged to identify the location of endothelial cells.
In wild type corneas of both quail and mice, angioblasts avoid the developing cornea. In contrast, we observed ectopic migration of angioblasts into the presumptive stroma of Npn-1Sema-/- mutant mice. By E15.5 ectopic blood vessels were visible in Npn-1Sema-/- mutant corneas. Additionally, when the lens is ablated in quail eyes, we observed again the ectopic migration of endothelial cells into the presumptive cornea.
Sema3A signal produced in the lens and acting through the Npn-1 receptor plays a role in the maintenance of corneal avascularity during development, by inhibiting angioblast migration into the developing cornea.
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