Evidence map›Paper›PMID 24490973›Full record

ArticleAmerican journal of respiratory cell and molecular biology2014

Macrophage migration inhibitory factor is a novel determinant of cigarette smoke-induced lung damage.

Jonathan Fallica, Laurent Boyer, Bo Kim, Leonid Serebreni, Lidenys Varela, Omar Hamdan, Lan Wang, Tiffany Simms, Mahendra Damarla, Todd M Kolb and 4 more

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 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
1.7field-weighted citation impact, top 15% 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

17 citing papers in PubMed, 40 citations in OpenAlex.

  1. Review
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  14. Role of macrophage migration inhibitory factor in age-related lung disease.American journal of physiology. Lung cellular and molecular physiology · 2015
    Review
  15. Endothelial CD74 mediates macrophage migration inhibitory factor protection in hyperoxic lung injury.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2015
    Article
  16. Telomere dysfunction causes alveolar stem cell failure.Proceedings of the National Academy of Sciences of the United States of America · 2015
    Article
  17. Article
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

14 authors at 3 institutions in 2 countries.

Jonathan Fallica1 Division of Pulmonary and Critical Care Medicine, Department of Medicine, Johns Hopkins University, Baltimore, Maryland.
Laurent Boyer
Bo Kim
Leonid Serebreni
Lidenys Varela
Omar Hamdan
Lan Wang
Tiffany Simms
Mahendra Damarla
Todd M Kolb
Richard Bucala
Wayne Mitzner
Paul M Hassoun
Rachel Damico
Johns Hopkins University · USUniversité Paris-Est Créteil · FRYale University · US

Funding

Institute for Clinical and Translational ResearchUL1TR001079 · NCATS · JOHNS HOPKINS UNIVERSITY · PI FORD, DANIEL ERNEST · 2013 to 2017
$60.1M
THE INTEGRATED FUNCTION OF RESPIRATION &CIRCULATIONP01HL010342 · NHLBI · JOHNS HOPKINS UNIVERSITY · PI MITZNER, WAYNE · 1985 to 2015
$24.4M
The Role of Xanthine Oxidoreductase in Ventilator-Associated Lung InjuryR01HL049441 · NHLBI · TUFTS MEDICAL CENTER · PI HASSOUN, PAUL M. · 1999 to 2013
$3.7M
Regulators of Endothelial Cell Apoptosis in LPS-Induced Acute Lung InjuryK08HL088320 · NHLBI · JOHNS HOPKINS UNIVERSITY · PI DAMICO, RACHEL L · 2008 to 2012
$678k
NCATS NIH HHS UL1 TR001079NHLBI NIH HHS K08 HL088320NHLBI NIH HHS K08HL088320NHLBI NIH HHS P01 HL010342NHLBI NIH HHS R01 HL049441NHLBI NIH HHS R01HL049441
6 · The paper itself

Abstract

Cigarette smoke (CS) is the most common cause of chronic obstructive pulmonary diseases (COPD), including emphysema. CS exposure impacts all cell types within the airways and lung parenchyma, causing alveolar tissue destruction through four mechanisms: (1) oxidative stress; (2) inflammation; (3) protease-induced degradation of the extracellular matrix; and (4) enhanced alveolar epithelial and endothelial cell (EC) apoptosis. Studies in human pulmonary ECs demonstrate that macrophage migration inhibitory factor (MIF) antagonizes CS-induced apoptosis. Here, we used human microvascular ECs, an animal model of emphysema (mice challenged with chronic CS), and patient serum samples to address both the capacity of CS to alter MIF expression and the effects of MIF on disease severity. We demonstrate significantly reduced serum MIF levels in patients with COPD. In the murine model, chronic CS exposure resulted in decreased MIF mRNA and protein expression in the intact lung. MIF deficiency (Mif(-/-)) potentiated the toxicity of CS exposure in vivo via increased apoptosis of ECs, resulting in enhanced CS-induced tissue remodeling. This was linked to MIF's capacity to protect against double-stranded DNA damage and suppress p53 expression. Taken together, MIF appears to antagonize CS-induced toxicity in the lung and resultant emphysematous tissue remodeling by suppressing EC DNA damage and controlling p53-mediated apoptosis, highlighting a critical role of MIF in EC homeostasis within the lung.

Indexed as

AnimalsApoptosisBlotting, WesternDNA DamageEndothelial CellsHumansImmunoenzyme TechniquesInflammationIntramolecular OxidoreductasesLungMacrophage Migration-Inhibitory FactorsMiceMice, Inbred C57BLMice, KnockoutOxidative StressPulmonary Disease, Chronic ObstructiveIntramolecular OxidoreductasesMacrophage Migration-Inhibitory FactorsMif protein, mouseSmokeTumor Suppressor Protein p53apoptosiscigaretteemphysemaendothelialmacrophage migration inhibitory factor

Identifiers

PMID24490973
PMCPMC4091857
OpenAlexW2163271706

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.