Evidence map›Paper›PMID 18664622›Full record

ArticleBlood2008

Sickle red cells induce adhesion of lymphocytes and monocytes to endothelium.

Rahima Zennadi, Ai Chien, Ke Xu, Milena Batchvarova, Marilyn J Telen

2 registry-linked trialsOpen access · bronzeAbstract read
In one paragraph

Article in Blood, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to 2 registered trials, which are not on this map. Cited by 47 papers.

0numbers the graph read from it
0cells of the map it votes in
47citing papers in PubMed
2.1field-weighted citation impact, top 14% 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.

NCT01077921 phase2completednot on this mapstarted 2010, after this paper: background citation

Phase II Study of Propranolol as Anti-Adhesive Therapy for Sickle Cell Disease

TypeinterventionalSponsorLaura M. De Castro, MDRan2010 to 2013Enrolled31ConditionsSickle Cell DiseaseArmsPropranolol, Placebo
NCT02824471 recruitingnot on this mapstarted 2014, after this paper: background citation

Sickle Cell Disease (SCD) Biochip': Towards a Simple and Reliable Way to Monitor Sickle Cell Disease

TypeobservationalSponsorUniversity Hospitals Cleveland Medical CenterRan2014 to 2028Enrolled100ConditionsSickle Cell DiseaseArmsSCD Group
3 · Its place in the literature

Who cites it

47 citing papers in PubMed, 79 citations in OpenAlex.

  1. Trial
  2. Trial
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  4. Circulation research · 2025
    Article
  5. Sickle red blood cells directly activate neutrophils.British journal of haematology · 2024
    Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Review
  11. Article
  12. Sickle cell vaso-occlusion: The dialectic between red cells and white cells.Experimental biology and medicine (Maywood, N.J.) · 2021
    Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. Review
  18. Review
  19. Review
  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

5 authors at 1 institution in 1 country.

Rahima ZennadiDivision of Hematology, Department of Medicine, Duke University Medical Center, Durham, NC, USA.
Ai Chien
Ke Xu
Milena Batchvarova
Marilyn J Telen
Duke Medical Center · US

Funding

Pulmonary Hypertension in SCDR01HL079915 · NHLBI · DUKE UNIVERSITY · PI TELEN, MARILYN J · 2005 to 2008
$6.7M
Activation of Sickle Red Cell AdhesionK01DK065040 · NIDDK · DUKE UNIVERSITY · PI ZENNADI, RAHIMA · 2003 to 2006
$464k
NHLBI NIH HHS R01 HL079915NIDDK NIH HHS DK065040NIDDK NIH HHS K01 DK065040
6 · The paper itself

Abstract

Infusion of epinephrine-activated human sickle erythrocytes (SS RBCs) into nude mice promotes both SS RBC and murine leukocyte adhesion to vascular endothelium in vivo. We hypothesized that interaction of epinephrine-stimulated SS RBCs with leukocytes leads to activation of leukocytes, which then adhere to endothelial cells (ECs). In exploring the underlying molecular mechanisms, we have found that coincubation in vitro of epinephrine-treated SS RBCs with human peripheral blood mononuclear cells (PBMCs) results in robust adhesion of PBMCs to ECs. Sham-treated SS RBCs had a similar but less pronounced effect, whereas neither sham- nor epinephrine-treated normal RBCs activated PBMC adhesion. PBMC activation was induced via at least 2 RBC adhesion receptors, LW and CD44. In response to SS RBCs, leukocyte CD44 and beta2 integrins mediated PBMC adhesion to ECs, a process that involved endothelial E-selectin and fibronectin. SS RBCs activated adhesion of both PBMC populations, lymphocytes and monocytes. Thus, our findings reveal a novel mechanism that may contribute to the pathogenesis of vaso-occlusion in sickle cell disease, in which SS RBCs act via LW and CD44 to stimulate leukocyte adhesion to endothelium, and suggest that RBC LW and CD44 may serve as potential targets for antiadhesive therapy designed to prevent vaso-occlusion.

Indexed as

Anemia, Sickle CellAnimalsCD18 AntigensCell AdhesionEndothelium, VascularEpinephrineErythrocytes, AbnormalHumansHyaluronan ReceptorsLeukocytes, MononuclearLymphocytesMiceMice, NudeMonocytesUmbilical VeinsCD18 AntigensEpinephrineHyaluronan Receptors

Identifiers

PMID18664622
PMCPMC2569184
OpenAlexW2019393604

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

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.