J Lipid Res. 2009 Nov 3. [Epub ahead of print]
Kenchgowda S, Bazan HE.
Louisiana State University Health Sciences Center, United States.
Corneal injury induces an inflammatory reaction and damages the sensory nerves that exert trophic influences in the corneal epithelium. Alterations in normal healing disrupt the integrity and function of the tissue with undesirable consequences, ranging from dry eye and loss of transparency to ulceration and perforation. Lipids play important roles in this complex process. While lipid mediators such as platelet activating factor (PAF) and cyclooxygenease-2 (COX-2) metabolites contribute to tissue damage and neovascularization, other mediators, such as the lipoxygenase (LOX) derivatives from arachidonic acid (AA), 12- and 15-hydroxy/hydroperoxyeicosatetraenoic acids (12- and 15-HETE) and lipoxin A4 (LxA4), act as second messengers for epidermal growth factor (EGF) to promote proliferation and repair. Stimulation of the cornea with pigment epithelial derived factor (PEDF) in the presence of docosahexaenoic acid (DHA) gives rise to the synthesis of neuroprotectin D1 (NPD1), a derivative of LOX activity, and increases regeneration of corneal nerves. More knowledge about the role that lipids play in corneal wound healing can provide insight into the development of new therapeutic approaches for treating corneal injuries. PAF antagonists, lipoxins and neuroprotectins can be effective therapeutic tools for maintaining the integrity of the cornea.
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