Cited by 489Atherosclerosis and Cardiovascular DiseasesNitric Oxide and Endothelin EffectsNeutrophil, Myeloperoxidase and Oxidative Mechanisms

p47phox is required for atherosclerotic lesion progression in ApoE–/– mice

Open access
Barry-Lane, Patricia A., Patterson, Cam, van der Merwe, Marié, Hu, Zhaoyong, Holland, Stephen M., Yeh, Edward T.H., Runge, Marschall S.·2001·Journal of Clinical Investigation

Abstract

NADPH oxidase is upregulated in smooth muscle cells (SMCs) in response to growth factor stimulation, concomitant with increased reactive oxygen species (ROS) production. We investigated the role of ROS production by NADPH oxidase in SMC responses to growth factors and in atherosclerotic lesion formation in ApoE(-/-) mice. SMCs from wild-type, p47phox(-/-), and gp91phox(-/-) mice differed markedly with respect to growth factor responsiveness and ROS generation. p47phox(-/-) SMCs had diminished superoxide production and a decreased proliferative response to growth factors compared with wild-type cells, whereas the response of gp91phox(-/-) SMCs was indistinguishable from that of wild-type SMCs. The relevance of these in vitro observations was tested by measuring atherosclerotic lesion formation in genetically modified (wild-type, p47phox(-/-), ApoE(-/-), and ApoE(-/-)/p47phox(-/-)) mice. ApoE(-/-)/p47phox(-/-) mice had less total lesion area than ApoE(-/-) mice, regardless of whether mice were fed standard chow or a high-fat diet. Together, these studies provide convincing support for the hypothesis that superoxide generation in general, and NADPH oxidase in particular, have a requisite role in atherosclerotic lesion formation, and they provide a rationale for further studies to dissect the contributions of ROS to vascular lesion formation.

Integrity signals

Registry

Crossref · 10.1172/jci200111927

Cites

48 of 48 references verified0 citation errors · 0 not checkable

Statistics

Recomputing p-values needs the paper’s full text.

Claims the paper makes

We couldn’t retrieve this paper’s full text, so its claims and self-check weren’t run. The registry and citation checks still apply.

Claims other papers make about this one

Each is checked against this paper’s own text: does it say what the citing paper says it does?

  • Mice combining the mutation of p47phox−/− with ApoE−/− appear to be protected from atherosclerotic lesions compared with ApoE−/− mice.

    “The mice combining the mutation of p47phox−/− with ApoE−/− appear to be protected from atherosclerotic lesions (253) compared with ApoE−/− mice (64, 976), although some reports do not find significant differences in atherosclerosis progression or lesion size (443).”

Cites

Flagged first, then by citations

Cited by

Sorted by citations

Authors
Barry-Lane, P. A., Patterson, C., van der Merwe, M., Hu, Z., Holland, S. M., Yeh, E. T. H., & Runge, M. S.
Affiliations
  • The University of Texas Medical Branch at Galveston (US)
  • National Cancer Institute (US)
  • The University of Texas Health Science Center at Houston (US)
Corresponding author
Runge, Marschall S.
Venue
Journal of Clinical Investigation
Published
2001-11-15
Volume
108
Issue
10
Pages
1513-1522
ISSN
0021-9738 (ISSN-L)
OpenAlex
W2088204476
Cited by
489
References
48
Citations by year
2026: 5 · 2025: 9 · 2024: 6 · 2023: 5 · 2022: 5 · 2021: 14 · 2020: 8 · 2019: 10 · 2018: 16 · 2017: 23 · 2016: 23 · 2015: 23 · 2014: 29 · 2013: 22 · 2012: 27
FWCI
7.73
Type
journal article
Language
en
Open access
Locations
  • Journal of Clinical Investigation (publishedVersion)
  • PubMed Central (publishedVersion)
  • PubMed (publishedVersion)
Funders
  • National Institutes of Health (7r01hl059652-04)
  • National Heart, Lung, and Blood Institute (R01HL057352)
Topics
  • Life Sciences › Immunology and Microbiology › Immunology › Atherosclerosis and Cardiovascular Diseases
  • Health Sciences › Medicine › Physiology › Nitric Oxide and Endothelin Effects
  • Life Sciences › Immunology and Microbiology › Immunology › Neutrophil, Myeloperoxidase and Oxidative Mechanisms
Keywords
p47phox, NADPH oxidase, atherosclerosis, atherosclerosis progression, ApoE-deficient mice, smooth muscle cells, reactive oxygen species, superoxide production, gp91phox, growth factor responsiveness, cell proliferation, high-fat diet
MeSH terms
Animals, Apolipoproteins E, Arteriosclerosis, Base Sequence, Cell Division, Mice, Inbred C57BL, Muscle, Smooth, Vascular, Phosphoproteins, Reactive Oxygen Species, DNA Primers, Disease Progression, NADPH Oxidases, Mice

About these checks

Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.

Statistics and arithmetic are recomputed, not judged.

Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.

What counts as a claim ›How we measure confidence ›How we check this ›

Are you an author, or do you see a problem with this page? Request a review