Regional EuroTimes
Date Posted 13/09/2009
Researchers take 'Scar Wars' approach to modulating corneal healing
Understanding of the cellular and molecular etiologies of corneal haze after refractive corneal surgery is providing new prospects for intervention, said Greg Schultz, PhD, at the XVII Congress of the ESCRS.
Dr Schultz, Institute for Wound Research, departments of obstetrics-gynecology and ophthalmology, University of Florida, Gainesville, presented the keynote lecture during the first clinical research symposium. He described new gene-based approaches to regulating corneal wound healing and scarring and suggested that his talk could be appropriately entitled “Scar Wars.”
“We still face significant challenges in controlling the wound healing response that leads to corneal haze after traumatic injury and refractive procedures. Currently, mitomycin-C can be used effectively, but there are potential risks associated with its nonspecific activity. In the future, we hope new agents will be available that are both highly effective and also safer.”
Dr Schultz explained that following traumatic or iatrogenic injury, the cornea progresses through several phases of healing. Initially there is an apoptotic effect beneath the area of injury. This is followed by transformation of quiescent keratocytes into activated cells that further differentiate into myofibroblasts expressing alpha-smooth muscle actin (a-SMA) and synthesizing a disorganized, nonorthogonal array matrix. Finally, there is another phase of apoptosis and remodeling.
It is now understood that the activated fibroblasts and myofibroblasts repopulating the acellular zone are primarily responsible for light scattering, which is seen clinically as corneal haze, and that the causes for this phenomenon include the loss of corneal crystallin proteins, a-SMA expression, and the presence of the disorganised matrix. In addition, transforming growth factor-beta (TGF-b) and connective tissue growth factor (CTGF), which are produced by epithelial cells and fibroblasts after corneal injury, have been identified as the key regulators of myofibroblast differentiation and expression of corneal crystallin, a-SMA, and collagen genes.
Recognition of the role of these growth factors in the pathologic cascade leading to scarring and haze has suggested the possibility of using specific interventions to block their activity. So far, in both in vitro and in vivo studies conducted in cultured cells and animal models, researchers have used antibodies as well as a number of more advanced nucleotide chemistry technologies with encouraging results, Dr Schultz reported.
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