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Am. J. Respir. Cell Mol. Biol., Volume 20, Number 3, March, 1999 441-447

Endothelial Nitric Oxide Synthase as a Potential Susceptibility Gene in the Pathogenesis of Emphysema in alpha 1-Antitrypsin Deficiency

Alexey Novoradovsky, Mark L. Brantly, Myron A. Waclawiw, Prerna P. Chaudhary, Hideshi Ihara, Lin Qi, N. Tony Eissa, Pauline M. Barnes, Kateri M. Gabriele, Mary E. Ehrmantraut, Paola Rogliani, and Joel Moss

Pulmonary-Critical Care Medicine Branch, and Office of Biostatistics Research, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, Maryland

A role for endothelial nitric oxide synthase (NOS3) in the susceptibility of individuals with alpha 1-antitrypsin (alpha 1AT) deficiency to destructive lung disease was evaluated. Six polymorphic sites were identified within the NOS3 gene (i.e., -924A/G, -788C/T, -691C/T, 774C/T, 894G/T, and 1998C/G). The genotype distribution was determined in 339 patients and 94 control individuals. Frequency of the 774T allele in severely affected individuals was 0.417 versus 0.269 in control subjects (P = 0.018), whereas the 894T allele frequency was 0.427 versus 0.280 in control subjects (P = 0.024). Patients with less severe lung disease had the 774T and 894T allele frequencies of 0.289 and 0.344, respectively, similar to frequencies in a control group (P > 0.3). No direct correlation between pulmonary function and five other NOS3 polymorphisms was observed. Thus, functional allelic variants that are in linkage disequilibrium with the 774C/T and 894G/T may be present in the specified genomic area. These data are consistent with a modulatory role for NOS3 in destructive lung disease associated with alpha 1AT deficiency.




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