Evidence map›Paper›PMID 24428690›Full record

ArticleAmerican journal of respiratory cell and molecular biology2014

Nonmuscle myosin light chain kinase regulates murine asthmatic inflammation.

Ting Wang, Liliana Moreno-Vinasco, Shwu-Fan Ma, Tong Zhou, Yuka Shimizu, Saad Sammani, Yulia Epshtein, D Martin Watterson, Steven M Dudek, Joe G N Garcia

Open access · greenAbstract read
In one paragraph

Article in American journal of respiratory cell and molecular biology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
1.1field-weighted citation impact, top 23% 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

16 citing papers in PubMed, 18 citations in OpenAlex.

  1. Review
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  8. Review
  9. Review
  10. Mechanical Stress and Single Nucleotide Variants Regulate Alternative Splicing of the MYLK Gene.American journal of respiratory cell and molecular biology · 2017
    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

10 authors at 4 institutions in 1 country.

Ting Wang1 Arizona Respiratory Center and Department of Medicine, University of Arizona, Tucson, Arizona.
Liliana Moreno-Vinasco
Shwu-Fan Ma
Tong Zhou
Yuka Shimizu
Saad Sammani
Yulia Epshtein
D Martin Watterson
Steven M Dudek
Joe G N Garcia
University of Arizona · USUniversity of Illinois Chicago · USNorthwestern University · USUniversity of Chicago · US

Funding

Tissue Culture Biomechanical CoreP01HL058064 · NHLBI · UNIVERSITY OF ILLINOIS AT CHICAGO · PI LAL, RATNESHWAR · 1998 to 2012
$27.8M
Structure-Function Analysis of nmMLCK in EC Barrier ResponsesP01HL126609 · NHLBI · UNIVERSITY OF FLORIDA · PI STEVEN M DUDEK · 2016 to 2026
$24.4M
Cortactin in Regulation of Pulmonary Vascular PermeabilityR01HL088144 · NHLBI · UNIVERSITY OF ILLINOIS AT CHICAGO · PI DUDEK, STEVEN M · 2007 to 2011
$1.9M
Cortactin in Regulation of Pulmonary Vascular PermeabilityR56HL088144 · NHLBI · UNIVERSITY OF ILLINOIS AT CHICAGO · PI DUDEK, STEVEN M · 2015 to 2015
$422k
NHLBI NIH HHS HL 58064NHLBI NIH HHS HL 88144NHLBI NIH HHS HL 91899NHLBI NIH HHS P01 HL058064NHLBI NIH HHS P01 HL126609NHLBI NIH HHS R01 HL088144NHLBI NIH HHS R56 HL088144
6 · The paper itself

Abstract

Myosin light chain kinase (MLCK; gene code, MYLK) is a multifunctional enzyme involved in isoform-specific nonmuscle (nm) and smooth muscle contraction, inflammation, and vascular permeability, processes directly relevant to asthma pathobiology. In this report, we highlight the contribution of the nm isoform (nmMLCK) to asthma susceptibility and severity, supported by studies in two lines of transgenic mice with knocking out nmMLCK or selectively overexpressing nmMLCK in endothelium. These mice were sensitized to exhibit ovalbumin-mediated allergic inflammation. Genetically engineered mice with targeted nmMLCK deletion (nmMLCK(-/-)) exhibited significant reductions in lung inflammation and airway hyperresponsiveness. Conversely, mice with overexpressed nmMLCK in endothelium (nmMLCK(ec/ec)) exhibited elevated susceptibility and severity in asthmatic inflammation. In addition, reduction of nmMLCK expression in pulmonary endothelium by small interfering RNA results in reduced asthmatic inflammation in wild-type mice. These pathophysiological assessments demonstrate the positive contribution of nmMLCK to asthmatic inflammation, and a clear correlation of the level of nmMLCK with the degree of experimental allergic inflammation. This study confirms MYLK as an asthma candidate gene, and verifies nmMLCK as a novel molecular target in asthmatic pathobiology.

Indexed as

AnimalsAsthmaCytokinesEndothelial CellsEndotheliumLeukocytesLungMiceMice, KnockoutMice, TransgenicMyosin-Light-Chain KinasePneumoniaCytokinesMyosin-Light-Chain Kinase

Identifiers

PMID24428690
PMCPMC4068916
OpenAlexW2001881091

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.