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Florian Sennlaub, Yves Courtois, Olivier Goureau; Nitric Oxide Synthase–II Is Expressed in Severe Corneal Alkali Burns and Inhibits Neovascularization. Invest. Ophthalmol. Vis. Sci. 1999;40(12):2773-2779.
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purpose. Inducible nitric oxide synthase (NOS-II) is expressed in many
inflammatory conditions. The implication of nitric oxide (NO) in
angiogenesis remains controversial. The role of NOS-II and its
influence on angiogenesis in corneal neovascularization is unknown and
was investigated in this study.
methods. A mouse model of corneal neovascularization induced by chemical
cauterization was used. NOS-II mRNA expression was analyzed by reverse
transcriptase–polymerase chain reaction, and NOS-II protein was
studied in situ by immunohistochemical analysis of the cornea. The
influence of NOS-II on neovascularization was determined by comparison
of vessel development in “normal” wild-type mice and mice with a
targeted disruption of the NOS-II gene.
results. NOS-II mRNA was induced to very high levels after corneal cauterization
and remained upregulated throughout the disease. Migratory cells in the
center of the cauterization area expressed NOS-II protein. The
neovascular response in mice lacking the NOS-II gene was significantly
stronger than in wild-type mice, and the difference increased over
conclusions. These data are the first evidence that NOS-II is expressed in this
model of sterile corneal inflammation. NOS-II expression
inhibited angiogenesis in severe corneal alkali
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