Evidence map›Paper›PMID 23221047›Full record

ArticleAmerican journal of respiratory cell and molecular biology2013

A myristoylated alanine-rich C kinase substrate-related peptide suppresses cytokine mRNA and protein expression in LPS-activated canine neutrophils.

Jingjing Li, Melissa A D'Annibale-Tolhurst, Kenneth B Adler, Shijing Fang, Qui Yin, Adam J Birkenheuer, Michael G Levy, Samuel L Jones, Eui Jae Sung, Eleanor C Hawkins and 2 more

Open access · greenAbstract read
In one paragraph

Article in American journal of respiratory cell and molecular biology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
1.5field-weighted citation impact, top 18% 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

23 citing papers in PubMed, 35 citations in OpenAlex.

  1. Article
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  8. Review
  9. Article
  10. Peptide Inhibitors of MARCKS Suppress Endotoxin Induced Uveitis in Rats.Journal of ocular pharmacology and therapeutics : the official journal of the Association for Ocular Pharmacology and Therapeutics · 2022
    Article
  11. Review
  12. Review
  13. MARCKS and Lung Disease.American journal of respiratory cell and molecular biology · 2019
    Review
  14. Review
  15. Article
  16. Article
  17. 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

12 authors at 2 institutions in 2 countries.

Jingjing LiComparative Biomedical Sciences Graduate Program, North Carolina State University, Raleigh, NC 27606, USA.
Melissa A D'Annibale-Tolhurst
Kenneth B Adler
Shijing Fang
Qui Yin
Adam J Birkenheuer
Michael G Levy
Samuel L Jones
Eui Jae Sung
Eleanor C Hawkins
Jeffrey A Yoder
Shila K Nordone
Center for Translational Molecular Medicine · NLNorth Carolina State University · US

Funding

Mechanism of Oxidant-Induced Respiratory Mucin SecretionR37HL036982 · NHLBI · NORTH CAROLINA STATE UNIVERSITY RALEIGH · PI ADLER, KENNETH BRUCE · 2004 to 2013
$4.0M
Mechanism of HIV latency and viral reactivation in Regulatory T cellsR56AI089313 · NIAID · NORTH CAROLINA STATE UNIVERSITY RALEIGH · PI NORDONE, SHILA K · 2010 to 2010
$384k
NHLBI NIH HHS R37HL36987NIAID NIH HHS 1R56AI089313-01A1NIAID NIH HHS R56 AI089313PHS HHS 550KR21218
6 · The paper itself

Abstract

Myristoylated alanine-rich C kinase substrate (MARCKS) is a ubiquitously expressed protein kinase C substrate that has emerged as a potential therapeutic target for the amelioration of mucin secretion and inflammation in patients with chronic obstructive pulmonary disease. MARCKS also plays a key role in regulating the adhesion, migration, and degranulation of neutrophils. Moreover, given its biological role in epithelial and immune cells, we hypothesized that MARCKS may play an integral role in cytokine secretion by neutrophils. Because the amino terminus of MARCKS is highly conserved across vertebrate species, we successfully applied the well-characterized human MARCKS inhibitory peptide, myristoylated N-terminal sequence (MANS), to attenuate the function of MARCKS in isolated canine neutrophils. Pretreatment of canine neutrophils with MANS peptide significantly reduced both mRNA and protein expression in a broad range of LPS-induced cytokines, including IL-8, a chemokine (C-X-C motif) ligand-1 orthologue, and TNF-α, in comparison with untreated cells or those treated with a control peptide. This reduction in cytokine expression was observed even when neutrophils were treated with MANS 2 hours after LPS exposure. The observed reduction in cytokine secretion was not attributable to protein retention or cell death, but was associated with reduced cytokine transcript synthesis. These observations identify MARCKS protein as a promising therapeutic target in the treatment of inflammatory diseases or syndromes attributed to neutrophil influx and inflammatory cytokine production, such as sepsis, acute lung injury, and acute respiratory distress syndrome.

Indexed as

AnimalsDogsHumansInterleukin-8Intracellular Signaling Peptides and ProteinsLipopolysaccharidesMembrane ProteinsMyristoylated Alanine-Rich C Kinase SubstrateNeutrophilsPeptidesRNA, MessengerTumor Necrosis Factor-alphaInterleukin-8Intracellular Signaling Peptides and ProteinsLipopolysaccharidesMARCKS protein, humanMembrane ProteinsMyristoylated Alanine-Rich C Kinase SubstratePeptidesRNA, MessengerTumor Necrosis Factor-alpha

Identifiers

PMID23221047
PMCPMC3604091
OpenAlexW2152719297

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.