Evidence map›Paper›PMID 32854115›Full record

ArticleThe Journal of cell biology2020

The LTB4-BLT1 axis regulates actomyosin and β2-integrin dynamics during neutrophil extravasation.

Bhagawat C Subramanian, Nicolas Melis, Desu Chen, Weiye Wang, Devorah Gallardo, Roberto Weigert, Carole A Parent

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of cell biology, 2020. 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
2.8field-weighted citation impact, top 9% 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.

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  6. cPLAScience advances · 2026
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  19. Multiphoton intravital microscopy of rodents.Nature reviews. Methods primers · 2022
    Article
  20. Amoeboid migration in health and disease: Immune responsesFrontiers in cell and developmental biology · 2022
    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

7 authors at 2 institutions in 1 country.

Bhagawat C SubramanianLaboratory of Cellular and Molecular Biology, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD.
Nicolas MelisLaboratory of Cellular and Molecular Biology, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD.
Desu ChenLaboratory of Cellular and Molecular Biology, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD.
Weiye WangLaboratory of Cellular and Molecular Biology, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD.
Devorah GallardoLaboratory Animal Sciences Program, Leidos Biomedical Research, National Cancer Institute, National Institutes of Health, Bethesda, MD.
Roberto WeigertLaboratory of Cellular and Molecular Biology, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD.
Carole A ParentLaboratory of Cellular and Molecular Biology, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD.
National Institutes of Health · USLeidos (United States) · US

Funding

Molecular mechanisms of membrane remodelingZIABC011682 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI WEIGERT, ROBERTO · 2016 to 2025
$17.5M
Intramural NIH HHS ZIA BC011682
6 · The paper itself

Abstract

The eicosanoid leukotriene B4 (LTB4) relays chemotactic signals to direct neutrophil migration to inflamed sites through its receptor BLT1. However, the mechanisms by which the LTB4-BLT1 axis relays chemotactic signals during intravascular neutrophil response to inflammation remain unclear. Here, we report that LTB4 produced by neutrophils acts as an autocrine/paracrine signal to direct the vascular recruitment, arrest, and extravasation of neutrophils in a sterile inflammation model in the mouse footpad. Using intravital subcellular microscopy, we reveal that LTB4 elicits sustained cell polarization and adhesion responses during neutrophil arrest in vivo. Specifically, LTB4 signaling coordinates the dynamic redistribution of non-muscle myosin IIA and β2-integrin, which facilitate neutrophil arrest and extravasation. Notably, we also found that neutrophils shed extracellular vesicles in the vascular lumen and that inhibition of extracellular vesicle release blocks LTB4-mediated autocrine/paracrine signaling required for neutrophil arrest and extravasation. Overall, we uncover a novel complementary mechanism by which LTB4 relays extravasation signals in neutrophils during early inflammation response.

Indexed as

AnimalsAutocrine CommunicationCD18 AntigensCell MovementChemotactic FactorsHumansInflammationLeukotriene B4MiceNeutrophilsNonmuscle Myosin Type IIAParacrine CommunicationReceptors, Leukotriene B4CD18 AntigensChemotactic FactorsLeukotriene B4Ltb4r1 protein, mouseNonmuscle Myosin Type IIAReceptors, Leukotriene B4

Identifiers

PMID32854115
PMCPMC7659729
OpenAlexW3081021025

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.