| Clay Beauregard, Ph.D.
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The overall goal of my project is to examine
the role of apoptosis in corneal inflammation and corneal
allograft rejection in the mouse model. I am measuring apoptosis
and caspase expression in cultured corneal stromal and endothelial
cells, as well as ex vivo from inflamed and grafted mouse
corneas. The hypothesis is that the local cytokine environment
(especially FasL/CD95L and TNF-a) in the cornea during inflammation
and grafting induces apoptosis, leading to "bystander" death
of resident corneal cells. The death of corneal stromal and/or
endothelial cells may be a factor in the rejection of transplanted
corneas. To this end, I am employing anti-apoptotic therapy
to mouse models of corneal inflammation and transplantation.
Publications
Beauregard C, Brandt PC, Chiou GCY. Induction
of nitric oxide synthase and over-production of nitric oxide
by interleukin-1b in cultured lacrimal gland acinar cells.
Exp Eye Res (in press).
Beauregard C, Brandt PC, Chiou GCY. Stimulation
of protein secretion from cultured lacrimal gland acinar cells
by nitric oxide-producing compounds. J Ocular Pharmacol
Ther (in press).
Beauregard C, Liu Q, Chiou GCY. Effects
of nitric oxide donors and nitric oxide synthase substrates
on isolated ciliary muscle contracted with carbachol or endothelin:
possible use in myopia prevention. J Ocular Pharmacol
Ther 2001;17:1-10.
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