Evidence map›Paper›PMID 26351298›Full record

ArticleBlood2015

Platelet-derived Wnt antagonist Dickkopf-1 is implicated in ICAM-1/VCAM-1-mediated neutrophilic acute lung inflammation.

Yujie Guo, Amarjit Mishra, Emily Howland, Chunling Zhao, Dhananjay Shukla, Tingting Weng, Lin Liu

Open access · greenAbstract 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 52 papers.

0numbers the graph read from it
0cells of the map it votes in
52citing papers in PubMed
7.4field-weighted citation impact, top 2% 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

52 citing papers in PubMed, 87 citations in OpenAlex.

  1. Article
  2. Review
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  6. Wnt signaling - using the bloodstream to send a message.Cellular and molecular life sciences : CMLS · 2025
    Review
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

7 authors at 2 institutions in 2 countries.

Yujie GuoLundberg-Kienlen Lung Biology and Toxicology Laboratory, Department of Physiological Sciences and Oklahoma Center for Respiratory and Infectious Diseases, Oklahoma State University, Stillwater, OK.
Amarjit MishraLundberg-Kienlen Lung Biology and Toxicology Laboratory, Department of Physiological Sciences and.
Emily HowlandLundberg-Kienlen Lung Biology and Toxicology Laboratory, Department of Physiological Sciences and.
Chunling ZhaoLundberg-Kienlen Lung Biology and Toxicology Laboratory, Department of Physiological Sciences and.
Dhananjay ShuklaLundberg-Kienlen Lung Biology and Toxicology Laboratory, Department of Physiological Sciences and.
Tingting WengLundberg-Kienlen Lung Biology and Toxicology Laboratory, Department of Physiological Sciences and.
Lin LiuLundberg-Kienlen Lung Biology and Toxicology Laboratory, Department of Physiological Sciences and Oklahoma Center for Respiratory and Infectious Diseases, Oklahoma State University, Stillwater, OK.ORCID http://orcid.org/0000-0002-4811-4897
Department of Physiological Sciences · RUOklahoma State University · US

Funding

ZFC3H1 Regulation of Host Defense and Influenza A Virus PathogenesisP20GM103648 · NIGMS · OKLAHOMA STATE UNIVERSITY STILLWATER · PI PATRAUCHAN, MARIANNA M. A. · 2013 to 2022
$22.3M
MOLECULAR MECHANISMS OF LUNG SURFACTANT SECRETIONR01HL052146 · NHLBI · OKLAHOMA STATE UNIVERSITY STILLWATER · PI LIU, LIN · 2000 to 2007
$2.3M
Mechanisms of Alveolar Fluid TransportR01HL083188 · NHLBI · OKLAHOMA STATE UNIVERSITY STILLWATER · PI LIU, LIN · 2006 to 2009
$1.4M
miR-101 Control of Pulmonary FibrosisR01HL116876 · NHLBI · OKLAHOMA STATE UNIVERSITY STILLWATER · PI LIU, LIN · 2013 to 2016
$1.4M
Mechanisms of Alveolar Epithelial Cell DifferentiationR01HL071628 · NHLBI · OKLAHOMA STATE UNIVERSITY STILLWATER · PI LIU, LIN · 2003 to 2006
$1.2M
Short Term Research Training for Veterinary StudentsT35OD011186 · OD · OKLAHOMA STATE UNIVERSITY STILLWATER · PI MALAYER, JERRY R · 2012 to 2014
$150k
NHLBI NIH HHS R01 HL052146NHLBI NIH HHS R01 HL071628NHLBI NIH HHS R01 HL083188NHLBI NIH HHS R01 HL116876NIGMS NIH HHS P20 GM103648NIGMS NIH HHS P20GM103648NIH HHS T35 OD011186NIH HHS T35 OD011186-19
6 · The paper itself

Abstract

Neutrophil infiltration represents the early acute inflammatory response in acute lung injury. The recruitment of neutrophils from the peripheral blood across the endothelial-epithelial barrier into the alveolar airspace is highly regulated by the adhesion molecules on alveolar epithelial cells (AECs). Wnt/β-catenin signaling is involved in the progression of inflammatory lung diseases including asthma, emphysema, and pulmonary fibrosis. However, the function of Wnt/β-catenin signaling in acute lung inflammation is unknown. Here, we identified platelet-derived Dickkopf-1 (Dkk1) as the major Wnt antagonist contributing to the suppression of Wnt/β-catenin signaling in AECs during acute lung inflammation. Intratracheal administration of Wnt3a or an antibody capable of neutralizing Dkk1 inhibited neutrophil influx into the alveolar airspace of injured lungs. Activation of Wnt/β-catenin signaling in AECs attenuated intercellular adhesion molecule 1 (ICAM-1)/vascular cell adhesion molecule 1 (VCAM-1)-mediated adhesion of both macrophages and neutrophils to AECs. Our results suggest a role for Wnt/β-catenin signaling in modulating the inflammatory response, and a functional communication between platelets and AECs during acute lung inflammation. Targeting Wnt/β-catenin signaling and the communication between platelets and AECs therefore represents potential therapeutic strategies to limit the damage of acute pulmonary inflammation.

Indexed as

Wnt Signaling PathwayAcute Lung InjuryAnimalsbeta CateninBlood PlateletsIntercellular Adhesion Molecule-1Intercellular Signaling Peptides and ProteinsMaleMiceNeutrophilsRatsVascular Cell Adhesion Molecule-1beta CateninDkk1 protein, mouseDkk1 protein, ratIcam1 protein, mouseIntercellular Adhesion Molecule-1Intercellular Signaling Peptides and ProteinsVascular Cell Adhesion Molecule-1

Identifiers

PMID26351298
PMCPMC4635118
OpenAlexW2274633650

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.