Evidence map›Paper›PMID 23064953›Full record

ArticleAmerican journal of physiology. Lung cellular and molecular physiology2012

Novel aspects of urokinase function in the injured lung: role of α2-macroglobulin.

Andrey A Komissarov, Dorota Stankowska, Agnieszka Krupa, Rafal Fudala, Galina Florova, Jon Florence, Marek Fol, Timothy C Allen, Steven Idell, Michael A Matthay and 1 more

Abstract read
In one paragraph

Article in American journal of physiology. Lung cellular and molecular physiology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
1.2field-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

10 citing papers in PubMed, 14 citations in OpenAlex.

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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

11 authors at 2 institutions in 2 countries.

Andrey A KomissarovTexas Lung Injury Institute, University of Texas Health Science Center, Tyler, Texas, USA.
Dorota Stankowska
Agnieszka Krupa
Rafal Fudala
Galina Florova
Jon Florence
Marek Fol
Timothy C Allen
Steven Idell
Michael A Matthay
Anna K Kurdowska
The University of Texas Health Science Center at Tyler · USUniversity of California, San Francisco · US

Funding

Urokinase, Defensin and Acute Lung InjuryP01HL076406 · NHLBI · UNIVERSITY OF TEXAS HLTH CTR AT TYLER · PI IDELL, STEVEN · 2005 to 2009
$7.7M
Resolution of Clinical Lung InjuryR37HL051856 · NHLBI · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI MATTHAY, MICHAEL A. · 2006 to 2015
$3.9M
Impact of IL-8 Bound to the Anti-IL-8 AutoantibodyR01HL073245 · NHLBI · UNIVERSITY OF TEXAS HLTH CTR AT TYLER · PI KURDOWSKA, ANNA K · 2004 to 2007
$1.1M
NHLBI NIH HHS HL-073245NHLBI NIH HHS HL-076406NHLBI NIH HHS R37 HL051856
6 · The paper itself

Abstract

The level of active urokinase (uPA) is decreased in lung fluids of patients with acute lung injury/acute respiratory distress syndrome (ALI/ARDS) whereas α(2)-macroglobulin (α(2)-M), a plasma proteinase inhibitor, is a major component of these fluids. Since there have been reports describing the ability of α(2)-M to form complexes with uPA in vitro, we hypothesized that α(2)-M may interact with uPA in the lung to modulate its biological activity. Pulmonary edema fluids and lung tissues from patients with ALI/ARDS were evaluated for the presence of uPA associated with α(2)-M. Complexes between α(2)-M and uPA were detected in alveolar edema fluids as well as in lungs of patients with ALI/ARDS where they were located mainly in close proximity to epithelial cells. While uPA bound to α(2)-M retains its amidolytic activity towards low-molecular-weight substrates, it is not inhibited by its main physiological inhibitor, plasminogen activator inhibitor 1. We also investigated the functional consequences of formation of complexes between uPA and α(2)-M in vitro. We found that when α(2)-M:uPA complexes were added to cultures of human bronchial epithelial cells (BEAS-2B), activation of nuclear factor-κB as well as production of interleukin-6 and -8 was substantially suppressed compared with the addition of uPA alone. Our findings indicate for the first time that the function of uPA in patients with ALI/ARDS may be modulated by α(2)-M and that the effects may include the regulation of the fibrinolytic and signaling activities of uPA.

Indexed as

Acute Lung Injuryalpha-MacroglobulinsCell LineEpithelial CellsHumansInterleukin-6Interleukin-8NF-kappa BPulmonary EdemaRespiratory Distress SyndromeSignal TransductionUrokinase-Type Plasminogen Activatoralpha-MacroglobulinsCXCL8 protein, humanIL6 protein, humanInterleukin-6Interleukin-8NF-kappa BUrokinase-Type Plasminogen Activator

Identifiers

PMID23064953
PMCPMC3532585
OpenAlexW2157969134

What OpenQuestion holds

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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.