Evidence map›Paper›PMID 23555849›Full record

ArticlePloS one2013

Critical role of non-muscle myosin light chain kinase in thrombin-induced endothelial cell inflammation and lung PMN infiltration.

Fabeha Fazal, Kaiser M Bijli, Matthew Murrill, Antony Leonard, Mohammad Minhajuddin, Khandaker N Anwar, Jacob N Finkelstein, D Martin Watterson, Arshad Rahman

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
1.6field-weighted citation impact, top 17% 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

15 citing papers in PubMed, 21 citations in OpenAlex.

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  9. Autophagy inhibitor 3-methyladenine protects against endothelial cell barrier dysfunction in acute lung injury.American journal of physiology. Lung cellular and molecular physiology · 2018
    Article
  10. Pyk2 phosphorylation of VE-PTP downstream of STIM1-induced CaAmerican journal of physiology. Lung cellular and molecular physiology · 2017
    Article
  11. Phospholipase C-ε signaling mediates endothelial cell inflammation and barrier disruption in acute lung injury.American journal of physiology. Lung cellular and molecular physiology · 2016
    Article
  12. Serpine2 deficiency results in lung lymphocyte accumulation and bronchus-associated lymphoid tissue formation.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2016
    Article
  13. Article
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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

9 authors at 3 institutions in 1 country.

Fabeha FazalDepartment of Pediatrics, University of Rochester School of Medicine and Dentistry, Rochester, New York, United States of America. Fabeha_Fazal@URMC.Rochester.edu
Kaiser M Bijli
Matthew Murrill
Antony Leonard
Mohammad Minhajuddin
Khandaker N Anwar
Jacob N Finkelstein
D Martin Watterson
Arshad Rahman
University of Rochester · USNorthwestern University · USUniversity of Illinois Chicago · US

Funding

VISUAL INDICES OF NEUROTOXICITYP30ES001247 · NIEHS · UNIVERSITY OF ROCHESTER · PI B Paige Lawrence · 1985 to 2026
$42.8M
G-protein-induced Signaling of PMN-mediated Lung InjuryR01HL067424 · NHLBI · UNIVERSITY OF ROCHESTER · PI RAHMAN, ARSHAD · 2002 to 2010
$2.3M
Regulation of Endothelial ICAM-1 and PMN-Mediated Lung Injury by Actin DynamicsR01HL096907 · NHLBI · UNIVERSITY OF ROCHESTER · PI FAZAL, FABEHA · 2010 to 2014
$1.5M
NHLBI NIH HHS HL096907NHLBI NIH HHS HL67424NHLBI NIH HHS R01 HL067424NHLBI NIH HHS R01 HL096907NIEHS NIH HHS ES-01247NIEHS NIH HHS P30 ES001247
6 · The paper itself

Abstract

The pathogenesis of acute lung injury (ALI) involves bidirectional cooperation and close interaction between inflammatory and coagulation pathways. A key molecule linking coagulation and inflammation is the procoagulant thrombin, a serine protease whose concentration is elevated in plasma and lavage fluids of patients with ALI and acute respiratory distress syndrome (ARDS). However, little is known about the mechanism by which thrombin contributes to lung inflammatory response. In this study, we developed a new mouse model that permits investigation of lung inflammation associated with intravascular coagulation. Using this mouse model and in vitro approaches, we addressed the role of non-muscle myosin light chain kinase (nmMLCK) in thrombin-induced endothelial cell (EC) inflammation and lung neutrophil (PMN) infiltration. Our in vitro experiments revealed a key role of nmMLCK in ICAM-1 expression by its ability to control nuclear translocation and transcriptional capacity of RelA/p65 in EC. When subjected to intraperitoneal thrombin challenge, wild type mice showed a marked increase in lung PMN infiltration via expression of ICAM-1. However, these responses were markedly attenuated in mice deficient in nmMLCK. These results provide mechanistic insight into lung inflammatory response associated with intravascular coagulation and identify nmMLCK as a critical target for modulation of lung inflammation.

Indexed as

Gene Expression RegulationAnimalsBlood CoagulationCell NucleusEndothelial CellsFemaleHumansHuman Umbilical Vein Endothelial CellsInflammationIntercellular Adhesion Molecule-1Leukocytes, MononuclearLungMaleMiceMice, Inbred C57BLMice, TransgenicIcam1 protein, mouseIntercellular Adhesion Molecule-1Myosin-Light-Chain KinasePeroxidaseRela protein, mouseThrombinTranscription Factor RelA

Identifiers

PMID23555849
PMCPMC3605402
OpenAlexW2034709854

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.