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European Journal of General Medicine, Vol. 7, No. 1, January-March, 2010, pp. 118-119 Brief Report Can hyperbaric oxygen therapy turn off the angiogenic switch in corneal neovascularization? Günalp Uzun1 , Ali Ayata2 , Mesut Mutluoğlu1 , Şenol Yıldız1 , Dilaver Erşanlı 2 Gülhane Military Medical Academy, Haydarpaşa Teaching Hospital, Departments of Underwater and Hyperbaric Medicine1 and Ophthalmology2 , İstanbul, Turkey Code Number: gm10022 To the Editor; Cornea normally does not have blood vessels. Corneal neovascularization may develop secondary to various inflammatory and infectious disorders. In corneal neovascularization, new blood vessels grow from the timbal vascular plexus into the cornea. Corneal neovascularization reduces visual acuity by disturbing corneal transparency and increases the risk of corneal graft rejection. Corneal avascularity is maintained by the equilibrium between the angiogenic and anti-angiogenic factors. A shift towards angiogenic factors in this equilibrium is called as "angiogenic switch" [1] . The role of angiogenic growth factors, such as vascular endothelial growth factor (VEGF) and basic fibroblast growth factor (bFGF), in the pathogenesis of corneal neovascularization has been well defined [2] . Hyperbaric oxygen therapy (HBOT), which involves the inhalation of 100% oxygen at higher atmospheric pressures, increases the amount of oxygen dissolved in the blood and that delivered to the tissues. Besides relieving tissue hypoxia, HBOT exerts various biochemical and physiological effects at cellular level [3],[4] . We think that HBOT may be beneficial to suppress corneal neovascularization by controlling the inflammation and release of angiogenic factors. The main source of the VEGF in corneal neovascularization is inflammatory cells that invade the cornea [5] . Therefore, inhibition of neutrophil adherence to the endothelium has been targeted in recent studies to prevent corneal neovascularization. It is showed that mice deficient for adhesion molecules on neutrophils (CD18) or endothelial cells (intercellular adhesion molecule-1; ICAM-I) developed significantly less corneal neovascularization than controls [6] . The corneal neutrophil counts and VEGF mRNA levels were similarly reduced in CD18- and ICAM-1-deficient mouse compared to controls [6] . HBOT decreases CD18 function on neutrophils [7] as well as the expression of ICAM-1 on endothelial cells [8] . HBOT also decreases inflammation and VEGF levels by down regulation of VEGF/KDR signal axis and facilitates wound healing rate in ischemic wounds [9] . Ersanli et al. demonstrated that HBOT is as effective as corticosterods with respect to anti-inflammatory effectiveness in an experimental uveitis model [10] . Another target for HBOT maybe matrix matalloproteinases (MMPs). This group of protelytic enzymes are involved in angiogenesis and in extracellular matrix remodeling. Corneal infiltrating neutrophils express matrix metalloproteinase-9 (MMP-9) and treatment with specific monoclonal antibody against MMP-9 reduces the extent of angiogenesis [11] . HBOT reduces neuroinflammation and MMP-9 expression in a rat model of traumatic brain injury [12] . Taken together, we hypothesize that HBOT may control corneal neovascularization by relieving corneal hypoxia, attenuating neutrophil infiltration, and reducing VEGF and MMP-9 levels. References
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