Evidence map›Paper›PMID 19023114›Full record

Trial reportBlood2009

Proteomic identification of altered apolipoprotein patterns in pulmonary hypertension and vasculopathy of sickle cell disease.

Susan Yuditskaya, Ashaunta Tumblin, Gerard T Hoehn, Guanghui Wang, Steven K Drake, Xiuli Xu, Saixia Ying, Amy H Chi, Alan T Remaley, Rong-Fong Shen and 3 more

Open access · greenAbstract readClinical Trial
In one paragraph

Trial report in Blood, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.

0numbers the graph read from it
0cells of the map it votes in
46citing papers in PubMed
3.5field-weighted citation impact, top 7% 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

46 citing papers in PubMed, 78 citations in OpenAlex.

  1. Trial
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Review
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Vascular complications of sickle cell disease.Clinical hemorheology and microcirculation · 2018
    Article
  15. Review
  16. Featured Article: Depletion of HDLExperimental biology and medicine (Maywood, N.J.) · 2017
    Article
  17. Review
  18. Article
  19. Review
  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

13 authors at 4 institutions in 1 country.

Susan YuditskayaPulmonary and Vascular Medicine Branch, National Heart, Lung and Blood Institute, National Institutes of Health, Bethesda, MD 20892-1476, USA.
Ashaunta Tumblin
Gerard T Hoehn
Guanghui Wang
Steven K Drake
Xiuli Xu
Saixia Ying
Amy H Chi
Alan T Remaley
Rong-Fong Shen
Peter J Munson
Anthony F Suffredini
Gregory J Kato
National Heart Lung and Blood Institute · USCenter for Clinical Research (United States) · USCenter for Information Technology · USNational Institutes of Health · US

Funding

Proteomics CoreZICHL005903 · NHLBI · NATIONAL HEART, LUNG, AND BLOOD INSTITUTE · PI GUCEK, MARJAN · 2009 to 2022
$23.3M
Statistical And Computational Methods For Gene Expression and Proteomic AnalysisZIACT000266 · CIT · CENTER FOR INFORMATION TECHNOLOGY · PI MUNSON, PETER J · 2009 to 2016
$4.2M
Prevalence and Prognosis of Pulmonary Hypertension in Adults with Sickle CellZIAHL006012 · NHLBI · NATIONAL HEART, LUNG, AND BLOOD INSTITUTE · PI TAYLOR, JAMES · 2009 to 2016
$3.5M
The NIA Proteomics Core FacilityZICAG000576 · NIA · NATIONAL INSTITUTE ON AGING · PI SHEN, RONG-FONG · 2009 to 2010
$1.9M
Intramural NIH HHS ZIA HL006012
6 · The paper itself

Abstract

Pulmonary arterial hypertension (PAH) is emerging as a major complication and independent risk factor for death among adults with sickle cell disease (SCD). Using surface-enhanced laser desorption/ionization time of flight mass spectrometry (SELDI-TOF MS), we searched for biomarkers of PAH in plasma specimens from 27 homozygous sickle cell anemia (HbSS) patients with PAH and 28 without PAH. In PAH patients, analysis consistently showed lower abundance of a 28.1-kDa peak (P < .001), identified by high-resolution mass spectrometry as the oxidant-scavenging protein apolipoprotein A-I (apoA-I), which correlated with clinical assays of apoA-I (r = .58, P < .001) and high-density lipoprotein (HDL) levels (r = .50, P = .001). Consistent with endothelial dysfunction that may mediate this effect in PAH, HbSS patients with lower apoA-I levels also displayed impaired vasodilatory responses to acetylcholine (mean +/- SEM, 189% +/- 34% [n = 13] vs 339% +/- 51% [n = 13], P < .001). As a group, patients with SCD demonstrated significantly lower apoA-I levels than African-American control subjects. The PAH cohort was further characterized by high levels of apolipoproteins A-II and B and serum amyloid A, and low levels of haptoglobin dimers and plasminogen. These results imply a relationship of apolipoproteins to the development of PAH vasculopathy in SCD, potentially involving an unexpected mechanistic parallel to atherosclerosis, another proliferative vasculopathy.

Indexed as

ProteomicsAdultAnemia, Sickle CellApolipoproteinsBiomarkersBlack or African AmericanCohort StudiesFemaleHumansHypertension, PulmonaryMaleRisk FactorsSerum Amyloid A ProteinApolipoproteinsBiomarkersSerum Amyloid A Protein

Identifiers

PMID19023114
PMCPMC2635077
OpenAlexW1967112180

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.