Journal
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA
Volume 101, Issue 35, Pages 13014-13019Publisher
NATL ACAD SCIENCES
DOI: 10.1073/pnas.0405389101
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Funding
- NCRR NIH HHS [M01 RR018390] Funding Source: Medline
- NHLBI NIH HHS [HL57506, R01 HL057506, R01 HL073852, P01 HL076491, HL73852, R01 HL077692, R01 HL070621, R37 HL057506, HL077692, HL076491, HL70621] Funding Source: Medline
- NIDDK NIH HHS [DK55875, R01 DK055875] Funding Source: Medline
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Reactive oxygen species (ROS) and reactive nitrogen species (RNS) are produced, in part, from NADPH oxidase in response to host invasion and tissue injury. Defects in NADPH oxidase impair host defense; however, the role of ROS and RNS in the response to tissue injury is not known. We addressed this issue by subjecting leukocyte oxidase (Nox2)-deficient (Nox2(-/-)) mice to arterial injury. Femoral artery injury was associated with increased Nox2 expression, ROS/RNS production, and oxidative protein and lipid modification in wild-type mice. In Nox2(-/-) mice, RNS-mediated protein oxidation, as monitored by protein nitrotyrosine content, was significantly diminished. This was accompanied by reduced neointimal proliferation, as monitored by intimal thickness and intimal/medial ratio, in Nox2(-/-) compared to wild-type mice. In addition, Nox2 deficiency led to reduced cellular proliferation and leukocyte accumulation. These data indicate that Nox2-mediated oxidant production has a requisite role in the response to tissue injury.
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