Evidence map›Paper›PMID 16624877›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2006

Differential induction of BLT receptor expression on human endothelial cells by lipopolysaccharide, cytokines, and leukotriene B4.

Hong Qiu, Anne-Sofie Johansson, Mattias Sjöström, Min Wan, Oliver Schröder, Jan Palmblad, Jesper Z Haeggström

Open access · greenAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
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

25 citing papers in PubMed, 90 citations in OpenAlex.

  1. Article
  2. Article
  3. Roles of Lipoxygenases in Cardiovascular Diseases.Journal of cardiovascular translational research · 2025
    Review
  4. Review
  5. Article
  6. Elevated cerebrospinal fluid cytokine levels in tuberculous meningitis predict survival in response to dexamethasone.Proceedings of the National Academy of Sciences of the United States of America · 2021
    Article
  7. Article
  8. Review
  9. Article
  10. Article
  11. The yin and yang of leukotriene BSeminars in immunology · 2017
    Review
  12. Review
  13. Systemic leukotriene BThe Journal of physiology · 2016
    Article
  14. Article
  15. Article
  16. Leukotriene Inhibitors in Sinusitis.Current infectious disease reports · 2012
    Article
  17. Review
  18. Article
  19. Article
  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

7 authors at 2 institutions in 2 countries.

Hong QiuDepartment of Medical Biochemistry and Biophysics, Division of Chemistry II, Karolinska Institutet, S-171 77 Stockholm, Sweden.
Anne-Sofie Johansson
Mattias Sjöström
Min Wan
Oliver Schröder
Jan Palmblad
Jesper Z Haeggström
Karolinska Institutet · SEInflammation Research Foundation · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Leukotriene (LT) B4 is a powerful chemotactic and immune modulating agent that signals via two receptors denoted BLT1 and BLT2. Here we report that BLT1 and BLT2 are expressed at low levels in an apparently silent state in human umbilical vein endothelial cells (HUVEC). However, treatment with LPS leads to a >10 fold increase in the levels of BLT1 mRNA without any significant effects on BLT2 mRNA. In parallel, LPS also increases the amounts of BLT1 protein. Tumor necrosis factor-alpha (TNF-alpha) increases the expression of BLT2 mRNA approximately 6 times above basal levels with only a modest increase in BLT1 mRNA. Interleukin-1beta causes variable and parallel increases of both BLT1 and BLT2 mRNA. The natural ligand LTB4 also increases BLT1, but not BLT2, mRNA and protein expression. Along with the induction of BLT1 and/or BLT2, HUVEC acquire the capacity to respond to LTB4 with increased levels of intracellular calcium and these signals can be blocked by isotype selective BLT antagonists, CP-105696 and LY-255283. In addition, treatment of HUVEC with LTB4 causes increased release of both nitrite, presumably reflecting nitric oxide (NO), and monocyte chemoattractant protein-1. Our data indicate that expression of functional BLT receptors may occur at the surface of endothelial cells in response to LPS, cytokines, and ligand, which in turn may have functional consequences during the early vascular responses to inflammation. Moreover, the results point to BLT receptors as potential targets for pharmacological intervention in LT-dependent inflammatory diseases such as asthma, rheumatoid arthritis, and arteriosclerosis.

Indexed as

CalciumCells, CulturedChemokine CCL2Endothelial CellsHumansInterleukin-1Leukotriene AntagonistsLeukotriene B4LipopolysaccharidesNitritesProtein IsoformsReceptors, Leukotriene B4Receptors, Purinergic P2Signal TransductionTetrazolesTumor Necrosis Factor-alphaCalciumCCL2 protein, humanChemokine CCL2Interleukin-1Leukotriene AntagonistsLeukotriene B4LipopolysaccharidesLTB4R2 protein, humanLTB4R protein, humanLY 255283NitritesProtein IsoformsReceptors, Leukotriene B4Receptors, Purinergic P2TetrazolesTumor Necrosis Factor-alpha

Identifiers

PMID16624877
PMCPMC1440767
OpenAlexW2151550078

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.