Evidence map›Paper›PMID 28389621›Full record

ArticleJournal of leukocyte biology2017

Fluid shear-induced cathepsin B release in the control of Mac1-dependent neutrophil adhesion.

Michael L Akenhead, Shunichi Fukuda, Geert W Schmid-Schönbein, Hainsworth Y Shin

Open access · bronzeAbstract read
In one paragraph

Article in Journal of leukocyte biology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
0.6field-weighted citation impact, top 34% 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

9 citing papers in PubMed, 13 citations in OpenAlex.

  1. It's a Trap!-Potential of Cathepsins in NET Formation.International journal of molecular sciences · 2025
    Review
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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

4 authors at 2 institutions in 2 countries.

Michael L AkenheadDepartment of Biomedical Engineering, University of Kentucky, Lexington, Kentucky, USA.
Shunichi FukudaDepartment of Neurosurgery, National Hospital Organization Kyoto Medical Center, Kyoto, Japan; and.
Geert W Schmid-SchönbeinDepartment of Bioengineering, University of California San Diego, La Jolla, California, USA.
Hainsworth Y ShinDepartment of Biomedical Engineering, University of Kentucky, Lexington, Kentucky, USA; hy.shin@uky.edu.
University of California, San Diego · USUniversity of Kentucky · US

Funding

The role of IKKß in linking obesity to adipose tissue inflammation and adipogeneP20GM103527 · NIGMS · UNIVERSITY OF KENTUCKY · PI CASSIS, LISA A · 2012 to 2017
$13.7M
STRUCTURE/FUNCTION OF THE MICROCIRCULATIOMR01HL010881 · NHLBI · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI SCHMID-SCHOENBEIN, GEERT W. · 1985 to 2011
$3.1M
Leukocyte Mechanotransduction of Fluid Shear StressF32HL083740 · NHLBI · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI SHIN, HAINSWORTH Y · 2006 to 2006
$52k
NHLBI NIH HHS F32 HL083740NHLBI NIH HHS R01 HL010881NIGMS NIH HHS P20 GM103527
6 · The paper itself

Abstract

There is compelling evidence that circulatory hemodynamics prevent neutrophil activation, including adhesion to microvessels, in the microcirculation. However, the underlying mechanism or mechanisms by which that mechanoregulation occurs remain unresolved. Here, we report evidence that exposure to fluid shear stress (FSS) promotes neutrophils to release cathepsin B (ctsB) and that this autocrine regulatory event is antiadhesive for neutrophils on endothelial surfaces through Mac1-selective regulation. We used a combined cell-engineering and immunocytochemistry approach to find that ctsB was capable of cleaving Mac1 integrins on neutrophils and demonstrated that this proteolysis alters their adhesive functions. Under no-flow conditions, ctsB enhanced neutrophil migration though a putative effect on pseudopod retraction rates. We also established a flow-based cell detachment assay to verify the role of ctsB in the control of neutrophil adhesion by fluid flow stimulation. Fluid flow promoted neutrophil detachment from platelet and endothelial layers that required ctsB, consistent with its fluid shear stress-induced release. Notably, compared with leukocytes from wild-type mice, those from ctsB-deficient (ctsB

Indexed as

Neutrophil ActivationShear StrengthAnimalsCathepsin BCell AdhesionCell MovementFemaleHL-60 CellsHumansHuman Umbilical Vein Endothelial CellsMacrophage-1 AntigenMaleMiceMice, KnockoutNeutrophilsCathepsin BCTSB protein, humanCtsb protein, mouseMacrophage-1 Antigencell signalingintegrinsleukocytesmechanobiologymechanotransduction

Identifiers

PMID28389621
PMCPMC5470839
OpenAlexW2604417710

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.