Evidence map›Paper›PMID 20083679›Full record

ArticleCirculation2010

Nitric oxide-dependent bone marrow progenitor mobilization by carbon monoxide enhances endothelial repair after vascular injury.

Barbara Wegiel, David J Gallo, Kathleen G Raman, Jenny M Karlsson, Brett Ozanich, Beek Y Chin, Edith Tzeng, Shakil Ahmad, Asif Ahmed, Catherine J Baty and 1 more

Open access · greenAbstract read
In one paragraph

Article in Circulation, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
42citing papers in PubMed, 1 pooled it
5.0field-weighted citation impact, top 4% 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

42 citing papers in PubMed, 1 synthesis or guideline pooled it, 112 citations in OpenAlex.

  1. Pooled it
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  16. Carbon monoxide in lung cell physiology and disease.American journal of physiology. Cell physiology · 2018
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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

11 authors at 1 institution in 1 country.

Barbara WegielTransplantation Institute, University of Pittsburgh School of Medicine, Pittsburgh, PA, USA.
David J Gallo
Kathleen G Raman
Jenny M Karlsson
Brett Ozanich
Beek Y Chin
Edith Tzeng
Shakil Ahmad
Asif Ahmed
Catherine J Baty
Leo E Otterbein
University of Pittsburgh · US

Funding

Carbon Monoxide to Prevent Circulatory CollapseR01HL076167 · NHLBI · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI OTTERBEIN, LEO E · 2004 to 2007
$1.6M
Endogenous Gas Molecules As Transcription FactorsR01GM088666 · NIGMS · BETH ISRAEL DEACONESS MEDICAL CENTER · PI OTTERBEIN, LEO E · 2009 to 2012
$1.4M
Anti-Inflammatory Effects of Carbon Monoxide in the LungR01HL071797 · NHLBI · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI OTTERBEIN, LEO E · 2003 to 2006
$1.3M
British Heart Foundation RG/09/001/25940Medical Research Council G0600270Medical Research Council G0601295NHLBI NIH HHS HL-071797NHLBI NIH HHS HL-076167NHLBI NIH HHS R01 HL071797NHLBI NIH HHS R01 HL076167NIGMS NIH HHS R01 GM088666
6 · The paper itself

Abstract

backgroundCarbon monoxide (CO) has emerged as a vascular homeostatic molecule that prevents balloon angioplasty-induced stenosis via antiproliferative effects on vascular smooth muscle cells. The effects of CO on reendothelialization have not been evaluated. METHODS AND

resultsExposure to CO has diametrically opposite effects on endothelial cell (EC) and vascular smooth muscle cell proliferation in rodent models of carotid injury. In contrast to its effect of blocking vascular smooth muscle cell growth, CO administered as a gas or as a CO-releasing molecule enhances proliferation and motility of ECs in vitro by >50% versus air controls, and in vivo, it accelerates reendothelialization of the denuded artery by day 4 after injury versus day 6 in air-treated animals. CO enhanced EC proliferation via rapid activation of RhoA (Ras homolog gene family, member A), followed by downstream phosphorylation of Akt, endothelial nitric oxide (NO) synthase phosphorylation, and a 60% increase in NO generation by ECs. CO drives cell cycle progression through phosphorylation of retinoblastoma, which is dependent in part on endothelial NO synthase-generated NO. Similarly, endothelial repair in vivo requires NO-dependent mobilization of bone marrow-derived EC progenitors, and CO yielded a 4-fold increase in the number of mobilized green fluorescent protein-Tie2-positive endothelial progenitor cells versus controls, with a corresponding accelerated deposition of differentiated green fluorescent protein-Tie2-positive ECs at the site of injury. CO was ineffective in augmenting EC repair and the ensuing development of intimal hyperplasia in eNOS(-/-) mice.

conclusionsCollectively, the present data demonstrate that CO accelerates EC proliferation and vessel repair in a manner dependent on NO generation and enhanced recruitment of bone marrow-derived endothelial progenitor cells.

Indexed as

Bone Marrow TransplantationAnimalsAortaCarbon MonoxideCarotid Artery InjuriesCell MovementCell ProliferationCells, CulturedEndothelium, VascularHematopoietic Stem CellsMaleMiceMice, Inbred C57BLMice, KnockoutModels, AnimalNitric OxideCarbon MonoxideNitric OxideNitric Oxide Synthase Type IIIProto-Oncogene Proteins c-aktRetinoblastoma ProteinrhoA GTP-Binding Protein

Identifiers

PMID20083679
PMCPMC2841354
OpenAlexW2038182595

What OpenQuestion holds

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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.