Evidence map›Paper›PMID 24616094›Full record

ArticleThe Journal of biological chemistry2014

Hydroxycarbamide decreases sickle reticulocyte adhesion to resting endothelium by inhibiting endothelial lutheran/basal cell adhesion molecule (Lu/BCAM) through phosphodiesterase 4A activation.

Vicky Chaar, Sandrine Laurance, Claudine Lapoumeroulie, Sylvie Cochet, Maria De Grandis, Yves Colin, Jacques Elion, Caroline Le Van Kim, Wassim El Nemer

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
2.2field-weighted citation impact, top 12% 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

23 citing papers in PubMed, 41 citations in OpenAlex.

  1. Trial
  2. Observational
  3. Article
  4. Article
  5. Review
  6. Review
  7. Article
  8. Article
  9. Sickle cell vaso-occlusion: The dialectic between red cells and white cells.Experimental biology and medicine (Maywood, N.J.) · 2021
    Review
  10. Article
  11. Blood rheology biomarkers in sickle cell disease.Experimental biology and medicine (Maywood, N.J.) · 2020
    Review
  12. Article
  13. Article
  14. Review
  15. Review
  16. Red Blood Cells: Chasing Interactions.Frontiers in physiology · 2019
    Review
  17. Article
  18. Inflammation in sickle cell disease.Clinical hemorheology and microcirculation · 2018
    Article
  19. Review
  20. Management of Sickle Cell Disease in Children.Southern medical journal · 2016
    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

9 authors at 5 institutions in 1 country.

Vicky ChaarINSERM, U1134, F-75739 Paris, France,; Université Paris Diderot, Sorbonne Paris Cité, UMR_S 1134, F-75739 Paris, France,; Institut National de la Transfusion Sanguine, F-75739 Paris, France,; Laboratoire d'Excellence GR-Ex, F-75238 Paris, France, and.
Sandrine LauranceINSERM, U1134, F-75739 Paris, France,; Université Paris Diderot, Sorbonne Paris Cité, UMR_S 1134, F-75739 Paris, France.
Claudine LapoumeroulieINSERM, U1134, F-75739 Paris, France,; Université Paris Diderot, Sorbonne Paris Cité, UMR_S 1134, F-75739 Paris, France,; Laboratoire d'Excellence GR-Ex, F-75238 Paris, France, and.
Sylvie CochetINSERM, U1134, F-75739 Paris, France,; Université Paris Diderot, Sorbonne Paris Cité, UMR_S 1134, F-75739 Paris, France,; Institut National de la Transfusion Sanguine, F-75739 Paris, France,; Laboratoire d'Excellence GR-Ex, F-75238 Paris, France, and.
Maria De GrandisINSERM, U1134, F-75739 Paris, France,; Université Paris Diderot, Sorbonne Paris Cité, UMR_S 1134, F-75739 Paris, France,; Institut National de la Transfusion Sanguine, F-75739 Paris, France,; Laboratoire d'Excellence GR-Ex, F-75238 Paris, France, and.
Yves ColinINSERM, U1134, F-75739 Paris, France,; Université Paris Diderot, Sorbonne Paris Cité, UMR_S 1134, F-75739 Paris, France,; Institut National de la Transfusion Sanguine, F-75739 Paris, France,; Laboratoire d'Excellence GR-Ex, F-75238 Paris, France, and.
Jacques ElionINSERM, U1134, F-75739 Paris, France,; Université Paris Diderot, Sorbonne Paris Cité, UMR_S 1134, F-75739 Paris, France,; Laboratoire d'Excellence GR-Ex, F-75238 Paris, France, and; Assistance Publique-Hôpitaux de Paris, Département de Génétique, Hôpital Robert Debré, Paris F-75019, France.
Caroline Le Van KimINSERM, U1134, F-75739 Paris, France,; Université Paris Diderot, Sorbonne Paris Cité, UMR_S 1134, F-75739 Paris, France,; Institut National de la Transfusion Sanguine, F-75739 Paris, France,; Laboratoire d'Excellence GR-Ex, F-75238 Paris, France, and.
Wassim El NemerINSERM, U1134, F-75739 Paris, France,; Université Paris Diderot, Sorbonne Paris Cité, UMR_S 1134, F-75739 Paris, France,; Institut National de la Transfusion Sanguine, F-75739 Paris, France,; Laboratoire d'Excellence GR-Ex, F-75238 Paris, France, and. Electronic address: wassim.el-nemer@inserm.fr.
Laboratory of Excellence GR-Ex · FRSorbonne Paris Cité · FRUniversité Paris Cité · FRDélégation Paris 7 · FRInserm · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Vaso-occlusive crises are the main acute complication in sickle cell disease. They are initiated by abnormal adhesion of circulating blood cells to vascular endothelium of the microcirculation. Several interactions involving an intricate network of adhesion molecules have been described between sickle red blood cells and the endothelial vascular wall. We have shown previously that young sickle reticulocytes adhere to resting endothelial cells through the interaction of α4β1 integrin with endothelial Lutheran/basal cell adhesion molecule (Lu/BCAM). In the present work, we investigated the functional impact of endothelial exposure to hydroxycarbamide (HC) on this interaction using transformed human bone marrow endothelial cells and primary human pulmonary microvascular endothelial cells. Adhesion of sickle reticulocytes to HC-treated endothelial cells was decreased despite the HC-derived increase of Lu/BCAM expression. This was associated with decreased phosphorylation of Lu/BCAM and up-regulation of the cAMP-specific phosphodiesterase 4A expression. Our study reveals a novel mechanism for HC in endothelial cells where it could modulate the function of membrane proteins through the regulation of phosphodiesterase expression and cAMP-dependent signaling pathways.

Indexed as

Anemia, Sickle CellAntisickling AgentsCell AdhesionCell Adhesion MoleculesCyclic AMPCyclic Nucleotide Phosphodiesterases, Type 4Endothelial CellsGene Expression Regulation, EnzymologicHumansHydroxyureaK562 CellsLutheran Blood-Group SystemPhosphorylationReticulocytesSecond Messenger SystemsUp-RegulationAntisickling AgentsBCAM protein, humanCell Adhesion MoleculesCyclic AMPCyclic Nucleotide Phosphodiesterases, Type 4HydroxyureaLutheran Blood-Group SystemPDE4A protein, humanAdhesionBloodCell SignalingEndothelial CellHydroxycarbamideLu/BCAMProtein PhosphorylationSickle Cell Disease

Identifiers

PMID24616094
PMCPMC4036286
OpenAlexW2167271197

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.