Evidence map›Paper›PMID 26333777›Full record

ArticleBlood2015

NOX2 is critical for heterotypic neutrophil-platelet interactions during vascular inflammation.

Kyungho Kim, Jing Li, Alan Tseng, Robert K Andrews, Jaehyung Cho

Open access · bronzeAbstract read
In one paragraph

Article in Blood, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.

0numbers the graph read from it
0cells of the map it votes in
48citing papers in PubMed
2.6field-weighted citation impact, top 10% 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

48 citing papers in PubMed, 79 citations in OpenAlex.

  1. Article
  2. The role of neutrophils in the pathogenesis of abdominal aortic aneurysms.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026
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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

5 authors at 3 institutions in 2 countries.

Kyungho KimDepartment of Pharmacology and.
Jing LiDepartment of Pharmacology and.
Alan TsengDepartment of Pharmacology and Department of Anesthesiology, University of Illinois College of Medicine, Chicago, IL; and.
Robert K AndrewsAustralian Centre for Blood Diseases, Monash University, Melbourne, Australia.
Jaehyung ChoDepartment of Pharmacology and Department of Anesthesiology, University of Illinois College of Medicine, Chicago, IL; and.
Illinois College · USMonash University · AUUniversity of Illinois Chicago · US

Funding

TRAINING PROGRAM IN LUNG BIOLOGY AND PATHOBIOLOGYT32HL007829 · NHLBI · UNIVERSITY OF ILLINOIS AT CHICAGO · PI DOLLY MEHTA · 1995 to 2026
$15.6M
Protein disulfide isomerase in neutrophil recruitment and vascular inflammationR01HL109439 · NHLBI · UNIVERSITY OF ILLINOIS AT CHICAGO · PI CHO, JAEHYUNG · 2011 to 2015
$2.0M
NHLBI NIH HHS R01 HL109439NHLBI NIH HHS T32 HL007829
6 · The paper itself

Abstract

Platelet-leukocyte interactions on activated endothelial cells play an important role during microvascular occlusion under oxidative stress conditions. However, it remains poorly understood how neutrophil-platelet interactions are regulated during vascular inflammation. By using intravital microscopy with mice lacking nicotinamide adenine dinucleotide phosphate (NADPH) oxidase 2 (NOX2) and their bone marrow chimera, we demonstrated that NOX2 from both hematopoietic and endothelial cells is crucial for neutrophil-platelet interactions during tumor necrosis factor alpha-induced venular inflammation. Platelet NOX2-produced reactive oxygen species (ROS) regulated P-selectin exposure upon agonist stimulation and the ligand-binding function of glycoprotein Ibα. Furthermore, neutrophil NOX2-generated ROS enhanced the activation and ligand-binding activity of αMβ2 integrin following N-formyl-methionyl-leucyl phenylalanine stimulation. Studies with isolated cells and a mouse model of hepatic ischemia/reperfusion injury revealed that NOX2 from both platelets and neutrophils is required for cell-cell interactions, which contribute to the pathology of hepatic ischemia/reperfusion injury. Platelet NOX2 modulated intracellular Ca(2+) release but not store-operated Ca(2+) entry (SOCE), whereas neutrophil NOX2 was crucial for SOCE but not intracellular Ca(2+) release. Different regulation of Ca(2+) signaling by platelet and neutrophil NOX2 correlated with differences in the phosphorylation of AKT, ERK, and p38MAPK. Our results indicate that platelet and neutrophil NOX2-produced ROS are critical for the function of surface receptors essential for neutrophil-platelet interactions during vascular inflammation.

Indexed as

Cell CommunicationAnimalsBlood PlateletsCalciumCalcium SignalingFemaleHumansMaleMAP Kinase Signaling SystemMembrane GlycoproteinsMiceMice, KnockoutNADPH Oxidase 2NADPH OxidasesNeutrophilsp38 Mitogen-Activated Protein KinasesCalciumCYBB protein, humanCybb protein, mouseMembrane GlycoproteinsNADPH Oxidase 2NADPH Oxidasesp38 Mitogen-Activated Protein KinasesProto-Oncogene Proteins c-aktReactive Oxygen Species

Identifiers

PMID26333777
PMCPMC4608242
OpenAlexW1905660905

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.