Evidence map›Paper›PMID 19229985›Full record

ArticleAmerican journal of hematology2009

Balancing role of nitric oxide in complement-mediated activation of platelets from mCd59a and mCd59b double-knockout mice.

Xuebin Qin, Weiguo Hu, Wenping Song, Price Blair, Gongxiong Wu, Xuemei Hu, Yanli Song, Selena Bauer, Martin Feelisch, Jane A Leopold and 2 more

Open access · bronzeAbstract read
In one paragraph

Article in American journal of hematology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
1.0field-weighted citation impact, top 24% 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

16 citing papers in PubMed, 31 citations in OpenAlex.

  1. Article
  2. Review
  3. The NO Answer for Autism Spectrum Disorder.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2023
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  5. Review
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  7. Review
  8. Article
  9. Review
  10. Review
  11. Vasculopathy and pulmonary hypertension in sickle cell disease.American journal of physiology. Lung cellular and molecular physiology · 2015
    Review
  12. Article
  13. Updated role of nitric oxide in disorders of erythrocyte function.Cardiovascular & hematological disorders drug targets · 2013
    Review
  14. A novel hemoglobin-binding peptide reduces cell-free hemoglobin in murine hemolytic anemia.American journal of physiology. Heart and circulatory physiology · 2013
    Article
  15. Article
  16. 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

12 authors at 5 institutions in 1 country.

Xuebin QinDepartment of Medicine, Brigham and Women's Hospital, Boston, Massachusetts, USA. xuebin_qin@hms.harvard.edu
Weiguo Hu
Wenping Song
Price Blair
Gongxiong Wu
Xuemei Hu
Yanli Song
Selena Bauer
Martin Feelisch
Jane A Leopold
Joseph Loscalzo
Jose A Halperin
Brigham and Women's Hospital · USBoston University · USCenter for Systems Biology · USHarvard University · USBoston Biomedical Research Institute · US

Funding

Towards a Mouse Model of Complement-Mediated DiseasesR01AI061174 · NIAID · HARVARD UNIVERSITY (MEDICAL SCHOOL) · PI QIN, XUEBIN · 2005 to 2009
$1.8M
Role of Complement in Vascular Diabetic ComplicationsR01DK060979 · NIDDK · HARVARD UNIVERSITY (MEDICAL SCHOOL) · PI HALPERIN, JOSE A · 2002 to 2005
$1.4M
Medical Research Council G0701115NIAID NIH HHS R01 AI061174NIDDK NIH HHS R01 DK060979PHS HHS R01052855
6 · The paper itself

Abstract

CD59 is a membrane protein inhibitor of the membrane attack complex (MAC) of complement. mCd59 knockout mice reportedly exhibit hemolytic anemia and platelet activation. This phenotype is comparable to the human hemolytic anemia known as paroxysmal nocturnal hemoglobinuria (PNH), in which platelet activation and thrombosis play a critical pathogenic role. It has long been suspected but not formally demonstrated that both complement and nitric oxide (NO) contribute to PNH thrombosis. Using mCd59a and mCd59b double knockout mice (mCd59ab(-/-) mice) in complement sufficient (C3(+/+)) and deficient (C3(-/-)) backgrounds, we document that mCd59ab(-/-) platelets are sensitive to complement-mediated activation and provide evidence for possible in vivo platelet activation in mCd59ab(-/-) mice. Using a combination of L-NAME (a NO-synthase inhibitor) and NOC-18 or SNAP (NO-donors), we further demonstrate that NO regulates complement-mediated activation of platelets. These results indicate that the thrombotic diathesis of PNH patients could be due to a combination of increased complement-mediated platelet activation and reduced NO-bioavailability as a consequence of hemolysis.

Indexed as

AnimalsBlood PlateletsCD59 AntigensComplement ActivationComplement C3Complement Membrane Attack ComplexDisease Models, AnimalHemoglobinuria, ParoxysmalMiceMice, KnockoutNG-Nitroarginine Methyl EsterNitric OxideNitric Oxide DonorsNitric Oxide SynthaseNitroso CompoundsPlatelet ActivationCD59 AntigensCD59a protein, mouseCD59b protein, mouseComplement C3Complement Membrane Attack ComplexNG-Nitroarginine Methyl EsterNitric OxideNitric Oxide DonorsNitric Oxide SynthaseNitroso CompoundsNOC 18S-Nitroso-N-Acetylpenicillamine

Identifiers

PMID19229985
PMCPMC4280257
OpenAlexW2079112439

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.