Kip Connor, Ph.D.
|Title||Assistant Professor of Ophthalmology|
|Institution||Massachusetts Eye and Ear Infirmary|
|Address||Massachusetts Eye & Ear Infrm|
243 Charles St
Boston MA 02114
Available: 09/01/13, Expires: 09/07/14
Retinal detachment and subsequent neurodegeneration of the retina continues to be a leading cause of visual impairment resulting from ocular trauma. Photoreceptor apoptosis is a major cause of visual loss in retinal detachment (RD). However, the underlying processes that facilitate this have remained elusive. This project aims to identify the initiating factors involved in photoreceptor cell death (retinal degeneration) in response to traumatic retinal detachment. This study is innovative in that it will begin to define the initiating factors involved in retinal neurodegeneration, a common cause of vision loss. When photoreceptor degeneration occurs it tends to correlate to a rise in immune activity. One possibility is that the immune system is mounting a response against the photoreceptors in the damaged retina to specifically target their removal. This can severely impact visual acuity, understanding the mechanism by which the immune system facilitates photoreceptor apoptosis in retinal detachment remains unresolved and it could be of significant therapeutic value to dampen its effects. The retina is specialized neural tissue and is commonly referred to as the “window into the brain”. Findings in this proposal will likely encompass similar mechanisms found in other neurodegenerations resulting from traumatic brain injury.
The PI and a senior fellow in the laboratory will oversee the student working on this project. They will learn how to effectively employ the mouse model of retinal detachment and utilize key transgenic animals in order to define immune mediators of retinal degeneration. Additionally, if time allows, key pharmaceutical therapeutics will be identified and utilized in vivo in order to temper neurodegeneration.
Available: 09/01/11, Expires: 06/01/14
Pathological neovascularization is a hallmark of numerous vascular diseases. Since the balance between neovessel formation and regression determines severity, modulating neovessel growth is highly desirable. Vascular regression coincides with a spike in immune activity; we therefore hypothesize (and pilot studies suggest) that pathologic vessel regression may be mediated, in part, through the complement system, an integral part of innate immunity. The complement system is an intricate immune surveillance system that is able to discriminate between healthy host tissue, diseased host tissue, apoptotic cells and foreign invaders and is able to modulate the elimination and repair of host tissue accordingly.
Students will work to define the role of the complement system in a mouse model of oxygen induced retinopathy (a model for neovascular disease). Students will have to be comfortable working with animals (previous experience with mice is a plus).
Characterizing the role of the complement system in vascular regression in a mouse model of retinopathy
Summer, 06/17/13 - 08/16/13
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