Evidence map›Paper›PMID 16293647›Full record

ArticleThe Journal of physiology2006

A differential role for nitric oxide in two forms of physiological angiogenesis in mouse.

James L Williams, David Cartland, Arif Hussain, Stuart Egginton

Open access · greenAbstract read
In one paragraph

Article in The Journal of physiology, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
2.3field-weighted citation impact, top 13% 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

32 citing papers in PubMed, 72 citations in OpenAlex.

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  15. Advances and challenges in skeletal muscle angiogenesis.American journal of physiology. Heart and circulatory physiology · 2016
    Review
  16. Article
  17. Article
  18. Article
  19. Inappropriate heat dissipation ignites brown fat thermogenesis in mice with a mutant thyroid hormone receptor α1.Proceedings of the National Academy of Sciences of the United States of America · 2013
    Article
  20. Microvascular repair: post-angiogenesis vascular dynamics.Microcirculation (New York, N.Y. : 1994) · 2012
    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

4 authors at 1 institution in 1 country.

James L WilliamsAngiogenesis Research Group, Centre for Cardiovascular Sciences, The University of Birmingham, Birmingham B15 2TT, UK.
David Cartland
Arif Hussain
Stuart Egginton
University of Birmingham · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

NO plays a role in a variety of in vitro models of angiogenesis, although confounding effects of NO on non-endothelial tissues make its role during in vivo angiogenesis unclear. We therefore examined the effects of NO on two physiological models of angiogenesis in mouse skeletal muscle: (1) administration of prazosin (50 mg l-1) thereby increasing blood flow; and (2) muscle overload from surgical ablation of a functional synergist. These models induce angiogenesis via longitudinal splitting and capillary sprouting, respectively. Administration of NG-nitro-L-arginine (L-NNA) abolished the increase in capillary to fibre ratio (C:F) in response to prazosin administration, along with the increases in luminal filopodia and large endothelial vacuoles. L-NNA prevented luminal filopodia and vacuolisation in response to extirpation, but had no effect on abluminal sprouting, and little effect on C:F. Comparison of mice lacking endothelial (eNOS-/-) and neuronal NO synthase (nNOS-/-) showed that longitudinal splitting is eNOS-dependent, and Western blotting demonstrated an increase in eNOS but not inducible NOS (iNOS) expression. These data show that there are two pathways of physiological angiogenesis in skeletal muscle characterised by longitudinal splitting and capillary sprouting, respectively. NO generated by eNOS plays an essential role in splitting but not in sprouting angiogenesis, which has important implications for angiogenic therapies that target NO.

Indexed as

AnimalsAntihypertensive AgentsCapillariesEnzyme InhibitorsMaleMiceMice, Inbred C57BLMice, KnockoutMicroscopy, ElectronMitochondriaMuscle, SkeletalNeovascularization, PhysiologicNitric OxideNitric Oxide Synthase Type INitric Oxide Synthase Type IINitric Oxide Synthase Type IIIAntihypertensive AgentsEnzyme InhibitorsNitric OxideNitric Oxide Synthase Type INitric Oxide Synthase Type IINitric Oxide Synthase Type IIINitroarginineNos1 protein, mouseNos2 protein, mouseNos3 protein, mousePrazosin

Identifiers

PMID16293647
PMCPMC1479877
OpenAlexW1576876113

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.