Evidence map›Paper›PMID 19477492›Full record

ArticleThe Journal of allergy and clinical immunology2009

Expression of functional leukotriene B4 receptors on human airway smooth muscle cells.

Satoko Watanabe, Akira Yamasaki, Kiyoshi Hashimoto, Yasushi Shigeoka, Hiroki Chikumi, Yasuyuki Hasegawa, Takashi Sumikawa, Miyako Takata, Ryota Okazaki, Masanari Watanabe and 6 more

Open access · greenAbstract read
In one paragraph

Article in The Journal of allergy and clinical immunology, 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
3.4field-weighted citation impact, top 8% 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, 43 citations in OpenAlex.

  1. Redox-sensitive GPCR signaling drives Gq-dependent CaAmerican journal of physiology. Cell physiology · 2026
    Article
  2. Article
  3. Neutrophils and Asthma.Diagnostics (Basel, Switzerland) · 2022
    Review
  4. Leukotriene BHeliyon · 2021
    Article
  5. Review
  6. Review
  7. Review
  8. Cigarette smoke-induced lung inflammation in COPD mediated via LTB4/BLT1/SOCS1 pathway.International journal of chronic obstructive pulmonary disease · 2016
    Article
  9. Article
  10. Article
  11. Article
  12. Motility, survival, and proliferation.Comprehensive Physiology · 2012
    Review
  13. Leukotrienes and airway inflammation.Biochimica et biophysica acta · 2011
    Review
  14. Article
  15. Article
  16. An update on the role of leukotrienes in asthma.Current opinion in allergy and clinical immunology · 2010
    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

16 authors at 3 institutions in 3 countries.

Satoko WatanabeDivision of Medical Oncology and Molecular Respirology, Department of Multidisciplinary Internal Medicine, Faculty of Medicine, Tottori University, Tottori, Japan.
Akira Yamasaki
Kiyoshi Hashimoto
Yasushi Shigeoka
Hiroki Chikumi
Yasuyuki Hasegawa
Takashi Sumikawa
Miyako Takata
Ryota Okazaki
Masanari Watanabe
Tsuyoshi Yokogawa
Miki Yamamura
Tatsuya Hayabuchi
William T Gerthoffer
Andrew J Halayko
Eiji Shimizu
Tottori University · JPUniversity of Manitoba · CAUniversity of South Alabama · US

Funding

Small heat shock proteins in smooth muscle plasticityR01HL077726 · NHLBI · UNIVERSITY OF SOUTH ALABAMA · PI GERTHOFFER, WILLIAM T · 2005 to 2013
$2.5M
NHLBI NIH HHS R01 HL077726
6 · The paper itself

Abstract

backgroundLeukotriene B4 (LTB4) increases in induced sputum and exhaled breath condensate in people with asthma. Furthermore, the T(H)2-type immune response and airway hyperresponsiveness induced by ovalbumin sensitization is markedly suppressed in LTB4 receptor (BLT) 1 null mice. These studies suggest that LTB4 may contribute to asthma pathophysiology. However, the direct effects of LTB4 on human airway smooth muscle (ASM) have not been studied.

objectivesWe sought to determine the expression of LTB4 receptors on human ASM and its functional role in mediating responses of human ASM cells, and the effect of LTB4 on these cells.

methodsImmunohistochemistry, RT-PCR, Western blotting, and flow cytometry were used to determine the expression of LTB4 receptors. To determine the effect of LTB4 on human ASM cells, cell proliferation was assessed by counting cells, and chemokinesis was assessed by gold particle phagokinesis assay.

resultsWe confirmed expression of both BLT1 and BLT2 in human ASM cells in bronchial tissue and in cell culture. LTB4 markedly induced cyclin D1 expression, proliferation, and chemokinesis of human ASM cells. LTB4 also induced phosphorylation of both p42/p44 mitogen-activated protein kinase (MAPK) and downstream PI3 kinase effector, Akt1. However, we observed no induction of c-Jun N-terminal kinase or p38 MAPK. Notably, LTB4-induced migration and proliferation of ASM cells were inhibited by the BLT1 specific antagonist, U75302, and by inhibitors of p42/p44 MAPK phosphorylation (U1026), and PI3 kinase (LY294002).

conclusionsThese observations are the first to suggest a role for a LTB4-BLT1 signaling axis in ASM responses that may contribute to the pathogenesis of airway remodeling in asthma.

Indexed as

Gene Expression RegulationBlotting, WesternBronchiCell LineCell MovementCell ProliferationCyclin-Dependent Kinase-Activating KinaseCyclin-Dependent KinasesHumansImmunohistochemistryMitogen-Activated Protein Kinase 3Myocytes, Smooth MusclePhosphorylationReceptors, Leukotriene B4Reverse Transcriptase Polymerase Chain ReactionRNA, MessengerCyclin-Dependent Kinase-Activating KinaseCyclin-Dependent KinasesLTB4R protein, humanMitogen-Activated Protein Kinase 3Receptors, Leukotriene B4RNA, Messenger

Identifiers

PMID19477492
PMCPMC4301732
OpenAlexW2002777932

What OpenQuestion holds

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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.