Evidence map›Paper›PMID 11564648›Full record

ArticleBritish journal of pharmacology2001

Neuronal nitric oxide synthase (NOS) regulates leukocyte-endothelial cell interactions in endothelial NOS deficient mice.

M J Sanz, M J Hickey, B Johnston, D M McCafferty, E Raharjo, P L Huang, P Kubes

Open access · bronzeAbstract read
In one paragraph

Article in British journal of pharmacology, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
1.5field-weighted citation impact, top 19% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

20 citing papers in PubMed, 53 citations in OpenAlex.

  1. Review
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  3. Review
  4. Review
  5. Article
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  7. Article
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  12. Diabetic eNOS-knockout mice develop accelerated retinopathy.Investigative ophthalmology & visual science · 2010
    Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Intercellular communication, NO and the biology of Chinese medicine.Cell communication and signaling : CCS · 2005
    Article
  18. Article
  19. Article
  20. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

7 authors at 1 institution in 1 country.

M J SanzImmunology Research Group, University of Calgary, Calgary, Alberta T2N 4N1, Canada. maria.j.sanz@uv.es
M J Hickey
B Johnston
D M McCafferty
E Raharjo
P L Huang
P Kubes
University of Calgary · CA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

1. The present study was designed to examine the possible role of neuronal nitric oxide synthase (nNOS) in regulation of leukocyte - endothelial cell interactions in the absence of endothelial nitric oxide synthase (eNOS), using intravital microscopy of the cremasteric microcirculation of eNOS(-/-) mice. 2. Baseline leukocyte rolling and adhesion revealed no differences between wild-type and eNOS(-/-) mice in either the cremasteric or intestinal microcirculations. 3. Superfusion with L-NAME (100 microM) caused a progressive and significant increase in leukocyte adhesion in both wild-type and eNOS(-/-) mice, without detecting differences between the two strains of mice. 4. Superfusion with 7-nitroindazole (100 microM), a selective inhibitor of nNOS, had no effect on leukocyte adhesion in wild-type animals. However, it increased leukocyte adhesion significantly in eNOS(-/-) mice, which was reversed by systemic L-arginine pre-administration. 5. Stimulation of the microvasculature with H(2)O(2) (100 microM) induced a transient elevation in leukocyte rolling in wild-type mice. Conversely, the effect persisted during the entire 60 min of experimental protocol in eNOS(-/-) mice either with or without 7-nitroindazole. 6. Semi-quantitative analysis by RT - PCR of the mRNA for nNOS levels in eNOS(-/-) and wild-type animals, showed increased expression of nNOS in both brain and skeletal muscle of eNOS(-/-) mice. 7. In conclusion, we have demonstrated that leukocyte-endothelial cell interactions are predominantly modulated by eNOS isoform in postcapillary venules of normal mice, whereas nNOS appears to assume the same role in eNOS(-/-) mice. Interestingly, unlike eNOS there was insufficient NO produced by nNOS to overcome leukocyte recruitment elicited by oxidative stress, suggesting that nNOS cannot completely compensate for eNOS.

Indexed as

AnimalsArginineCell AdhesionCell CommunicationEndothelium, VascularEnzyme InhibitorsGene Expression Regulation, EnzymologicGenotypeHemodynamicsHydrogen PeroxideIndazolesIntestinal MucosaLeukocytesMaleMiceMice, Inbred C57BL7-nitroindazoleArginineEnzyme InhibitorsHydrogen PeroxideIndazolesNG-Nitroarginine Methyl EsterNitric Oxide SynthaseNitric Oxide Synthase Type INos1 protein, mouseOxidantsRNA, Messenger

Identifiers

PMID11564648
PMCPMC1572945
OpenAlexW1990346928

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.