The CORnEa Laboratory
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Team Leader -
Assoc. Prof. Trevor Sherwin
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Aims
The work in the CORnEa Laboratory aims to understand disease processes in the cornea
and working towards therapeutic treatments for corneal repair focusing on 3 main
aspects of corneal research:
- Elucidating the pathogenesis of corneal dystrophies. Studies using human tissue
from transplant surgery are elucidating the molecular mechanism that underlie the
pathology of the disease. This work currently focuses on keratoconus, Fuch’s endothelial
dystrophy and bullous keratopathy.
- Modelling the human cornea. These studies are aimed at establishing in vitro laboratory
models for analysing processes in the human cornea.
- Stem cells in corneal wound healing. This project aims to elucidate the role of
corneal stem cells in maintaining homeostasis of the anterior part of the eye.
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Confocal laser scanning micrograph of a cross-section of a keratoconic cornea, labelled
with Celltracker-green (cells), and antibodies to integrin (pink) and fibronectin
(blue-grey).
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Team
Dr Trevor Sherwin - Associate Professor, Jane McGhee - Senior Technician, Nigel
Brookes - Senior Technical Officer, Judy Loh - Technician, PhD students and Honours
students. The work is performed in collaboration with Professor Charles McGhee and
Professor Colin Green.
Keratoconus
The cornea is normally transparent and is the primary optical surface of the human
eye. It collects light and contributes to the focussing of images upon the light-receptive
layer of the eye, the retina. Diseases, which affect corneal transparency, have
significant impact upon vision and quality of life, and constitute a major disability.
Keratoconus is a disease with onset in puberty which results in progressive thinning,
cone-like deformation, and opacification of the cornea. In New Zealand from 1992-1998,
50% of the sight restoration corneal transplants were undertaken for keratoconus,
compared with 30% in Australia and 20% in the United Kingdom.
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A characteristic of keratoconus is "Munson's sign" - a distortion of the
eyelid caused by the abnormal shape of the cornea.
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The front of the cornea, which is the principle region affected by keratoconus,
has four discrete layers: the multi- layered cellular epithelium is separated from
the underlying stroma by its basement membrane and the acellular collagenous Bowman's
layer. The remaining bulk of the cornea is the stroma which consists of interspersed
layers of collagen (tough bands of fibres which support corneal structure) and cells
(keratocytes) which produce and maintain the collagen and other associated matrix
substances. In keratoconus there is progressive, patchy disorganisation and loss
of epithelium, breaks in its basement membrane and Bowman's layer, and loss of stromal
substance (matrix) and cells. Normally, epithelial and keratocyte cells interact
cohesively (via specific mediators such as keratocyte and epithelial growth factors)
to maintain and repair the anterior cornea, but in keratoconus these cells may be
inducing or compounding this patchy structural disorganisation of the cornea.