Evidence map›Paper›PMID 19154781›Full record

ArticleNeuroscience2009

Role of endothelial nitric oxide synthetase in arteriogenesis after stroke in mice.

X Cui, M Chopp, A Zacharek, C Zhang, C Roberts, J Chen

Open access · greenAbstract read
In one paragraph

Article in Neuroscience, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
40citing papers in PubMed, 1 pooled it
2.6field-weighted citation impact, top 10% 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

40 citing papers in PubMed, 1 synthesis or guideline pooled it, 77 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Review
  4. Article
  5. SDMA as a marker and mediator in cerebrovascular disease.Clinical science (London, England : 1979) · 2024
    Review
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  7. Review
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Review
  14. Article
  15. Review
  16. Article
  17. Article
  18. Role of Interleukin-6 in Vascular Health and Disease.Frontiers in molecular biosciences · 2021
    Review
  19. Article
  20. Article
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

6 authors at 1 institution in 1 country.

X CuiDepartment of Neurology, Henry Ford Health System, Detroit, MI 48202, USA.
M Chopp
A Zacharek
C Zhang
C Roberts
J Chen
Henry Ford Health System · US

Funding

PREDICTION OF HUMAN BRAIN INFARCTION BY MRIP01NS023393 · NINDS · HENRY FORD HOSPITAL · PI ZHANG, ZHENG GANG · 1986 to 2011
$11.0M
Neurorestorative therapy of stroke with agents that increase HDLR01AG031811 · NIA · HENRY FORD HEALTH SYSTEM · PI CHEN, JIELI · 2009 to 2013
$1.4M
Neurorestorative Therapy of Stroke with StatinsR01NS047682 · NINDS · HENRY FORD HEALTH SYSTEM · PI CHEN, JIELI · 2004 to 2007
$1.0M
Imaging of Brain Remodeling and Functional RecoveryP50NS023393 · NINDS · HENRY FORD HEALTH SYSTEM · PI CHOPP, MICHAEL · 2007 to 2007
$882k
NIA NIH HHS R01 AG031811NINDS NIH HHS P01 NS023393NINDS NIH HHS P01 NS23393NINDS NIH HHS P50 NS023393NINDS NIH HHS R01 NS047682
6 · The paper itself

Abstract

Arteriogenesis supports restored perfusion in the ischemic brain and improves long-term functional outcome after stroke. We investigate the role of endothelial nitric oxide synthetase (eNOS) and a nitric oxide (NO) donor, (Z)-1-[N-(2-aminoethyl)-N-(2-ammonioethyl) amino] diazen-1-ium-1, 2-diolate (DETA-NONOate), in promoting arteriogenesis after stroke. Adult wild-type (WT, n=18) and eNOS-knockout (eNOS(-/-), n=36) mice were subjected to transient (2.5 h) right middle cerebral artery occlusion (MCAo) and were treated with or without DETA-NONOate (0.4 mg/kg) 24 h after MCAo. Functional evaluation was performed. Animals were sacrificed 3 days after MCAo for arterial cell culture studies, or 14 days for immunohistochemical analysis. Consistent with previous studies, eNOS(-/-) mice exhibited a higher mortality rate (P<0.05, n=18/group) and more severe neurological functional deficit after MCAo than WT mice (P<0.05, n=12/group). Decreased arteriogenesis, was evident in eNOS(-/-) mice compared with WT mice, as demonstrated by reduced vascular smooth muscle cell (VSMC) proliferation, arterial density and diameter in the ischemic brain. eNOS(-/-) mice treated with DETA-NONOate had a significantly decreased mortality rate and improved functional recovery, and exhibited enhanced arteriogenesis identified by increased VSMC proliferation, and upregulated arterial density and diameter compared to eNOS(-/-) mice after stroke (P<0.05, n=12/group). To elucidate the mechanisms underlying eNOS/NO mediated arteriogenesis, VSMC migration was measured in vitro. Arterial cell migration significantly decreased in the cultured common carotid artery (CCA) derived from eNOS(-/-) mice 3 days after MCAo compared to WT arterial cells. DETA-NONOate-treatment significantly attenuated eNOS(-/-)-induced decrease of arterial cell migration compared to eNOS(-/-) control artery (P<0.05; n=6/group). Using VSMC culture, DETA-NONOate significantly increased VSMC migration, while inhibition of NOS significantly decreased VSMC migration (P<0.05; n=6/group). Our data indicated that eNOS not only promotes vascular dilation but also increases VSMC proliferation and migration, and thereby enhances arteriogenesis after stroke. Therefore, increase eNOS may play an important role in regulating of arteriogenesis after stroke.

Indexed as

ActinsAnimalsCarotid Artery, CommonCell MovementCell ProliferationCells, CulturedDisease Models, AnimalEnzyme InhibitorsInfarction, Middle Cerebral ArteryKi-67 AntigenMaleMiceMice, Inbred C57BLMice, KnockoutMyocytes, Smooth MuscleNeovascularization, Physiologic2,2'-(hydroxynitrosohydrazono)bis-ethanamineActinsEnzyme InhibitorsKi-67 AntigenNG-Nitroarginine Methyl EsterNitric Oxide DonorsNitric Oxide Synthase Type IIINitroso Compounds

Identifiers

PMID19154781
PMCPMC2743134
OpenAlexW2079880790

What OpenQuestion holds

Textmetadata
LicenceTDM
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.