Thyroid Hormone Accelerates Pericorneal Nerve Ring Formation and Leads to Precocious Corneal Innervation
Submission Type
Poster
Area of Study or Work
Biology
Faculty Advisor
Tyler Schwend
Expected Graduation Date
2019
Location
Center for Natural Sciences, Illinois Wesleyan University
Start Date
4-13-2019 2:00 PM
End Date
4-13-2019 3:00 PM
Disciplines
Education
Abstract
The cornea, the transparent outermost layer of the eye, protects and hydrates the eye through its dense network of nerves. Inexplicably, damaged corneal nerves can take years to regenerate and regain normal function. Here, we examine the stimulatory potential of thyroid hormone (TH) on the acquisition of nerves by the cornea during development. Normally, presumptive corneal nerves are initially repelled at the corneal margin and instead encircle the periphery of the cornea in a nerve ring prior to their synchronous, circumferential entry. TH exposure accelerated formation of the nerve ring and premature, disorganized nerve entry into the cornea. Commencing TH treatments after nerve ring formation was underway was sufficient to accelerate innervation and increase the density of nerve fibers in the cornea, without altering the radial innervation pattern. Mechanistically, neuronal explants cultured in vitro displayed increased neurite outgrowth in the presence of TH, indicating that the neuro-stimulatory effects of TH are mediated directly on corneal nerves. We conclude that TH treatment may provide a therapeutic strategy to promote corneal re-innervation following injury as it accelerates multiple aspects of cornea innervation.
Thyroid Hormone Accelerates Pericorneal Nerve Ring Formation and Leads to Precocious Corneal Innervation
Center for Natural Sciences, Illinois Wesleyan University
The cornea, the transparent outermost layer of the eye, protects and hydrates the eye through its dense network of nerves. Inexplicably, damaged corneal nerves can take years to regenerate and regain normal function. Here, we examine the stimulatory potential of thyroid hormone (TH) on the acquisition of nerves by the cornea during development. Normally, presumptive corneal nerves are initially repelled at the corneal margin and instead encircle the periphery of the cornea in a nerve ring prior to their synchronous, circumferential entry. TH exposure accelerated formation of the nerve ring and premature, disorganized nerve entry into the cornea. Commencing TH treatments after nerve ring formation was underway was sufficient to accelerate innervation and increase the density of nerve fibers in the cornea, without altering the radial innervation pattern. Mechanistically, neuronal explants cultured in vitro displayed increased neurite outgrowth in the presence of TH, indicating that the neuro-stimulatory effects of TH are mediated directly on corneal nerves. We conclude that TH treatment may provide a therapeutic strategy to promote corneal re-innervation following injury as it accelerates multiple aspects of cornea innervation.