Evidence map›Paper›PMID 19029002›Full record

ArticleAmerican journal of respiratory and critical care medicine2009

Post-transcriptional regulation of urokinase-type plasminogen activator receptor expression in lipopolysaccharide-induced acute lung injury.

Yashodhar P Bhandary, Thirunavukkarasu Velusamy, Praveenkumar Shetty, Rashmi S Shetty, Steven Idell, Douglas B Cines, Deepika Jain, Khalil Bdeir, Edward Abraham, Yuko Tsuruta and 1 more

Open access · greenAbstract read
In one paragraph

Article in American journal of respiratory and critical care medicine, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed, 1 pooled it
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

21 citing papers in PubMed, 1 synthesis or guideline pooled it, 34 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Article
  4. The risk of COVID-19 can be predicted by a nomogram based on m6A-related genes.Infection, genetics and evolution : journal of molecular epidemiology and evolutionary genetics in infectious diseases · 2022
    Article
  5. Review
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  8. Review
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  11. Article
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  13. Article
  14. Article
  15. Article
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  17. Article
  18. Article
  19. Induction of tissue factor by urokinase in lung epithelial cells and in the lungs.American journal of respiratory and critical care medicine · 2010
    Article
  20. Update on acute lung injury and critical care medicine 2009.American journal of respiratory and critical care medicine · 2010
    Review
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

11 authors at 3 institutions in 1 country.

Yashodhar P BhandaryThe Texas Lung Injury Institute, The University of Texas Health Center at Tyler, Tyler, TX 75708, USA.
Thirunavukkarasu Velusamy
Praveenkumar Shetty
Rashmi S Shetty
Steven Idell
Douglas B Cines
Deepika Jain
Khalil Bdeir
Edward Abraham
Yuko Tsuruta
Sreerama Shetty
The University of Texas Health Science Center at Tyler · USCalifornia University of Pennsylvania · USUniversity of Alabama · US

Funding

Regulation of Lung Epithelial Fibrinolysis by UrokinaseR01HL071147 · NHLBI · UNIVERSITY OF TEXAS HLTH CTR AT TYLER · PI SHETTY, SREERAMA · 2002 to 2005
$1.0M
CONTROL OF FIBRINOLYTIC PATHWAYS IN LUNG DISEASER01HL062453 · NHLBI · UNIVERSITY OF TEXAS HLTH CTR AT TYLER · PI SHETTY, SREERAMA · 1999 to 2004
$751k
NHLBI NIH HHS P01HL-62453NHLBI NIH HHS R01-HL071147
6 · The paper itself

Abstract

rationaleUrokinase-type plasminogen activator (uPA) receptor (uPAR) is required for the recruitment of neutrophils in response to infection. uPA induces its own expression in lung epithelial cells, which involves its interaction with cell surface uPAR. Regulation of uPAR expression is therefore crucial for uPA-mediated signaling in infectious acute lung injury (ALI).

objectivesTo determine the role of uPA in uPAR expression during ALI caused by sepsis.

methodsWe used Western blot, Northern blot, Northwestern assay, and immunohistochemistry. Phosphate-buffered saline- and lipopolysaccharide (LPS)-treated wild-type and uPA(-/-) mice were used. MEASUREMENTS AND MAIN

resultsBiological activities of uPA, including proteolysis, cell adhesion, migration, proliferation, and differentiation, are dependent on its association with uPAR. Bacterial endotoxin (LPS) is a major cause of pulmonary dysfunction and infection-associated mortality. The present study shows that LPS induces uPAR expression both in vitro and in vivo, and that the mechanism involves post-transcriptional stabilization of uPAR mRNA by reciprocal interaction of phosphoglycerate kinase (PGK) and heterogeneous nuclear ribonucleoprotein C (hnRNPC) with uPAR mRNA coding region and 3' untranslated region determinants, respectively. The process involves tyrosine phosphorylation of PGK and hnRNPC. uPA(-/-) mice failed to induce uPAR expression after LPS treatment. In these mice, LPS treatment failed to alter the binding of PGK and hnRNPC protein with uPAR mRNA due to lack of tyrosine phosphorylation.

conclusionsOur study shows that induction of LPS-mediated uPAR expression is mediated through tyrosine phosphorylation of PGK and hnRNPC. This involves expression of uPA as an obligate intermediary.

Indexed as

LipopolysaccharidesAcute Lung InjuryAnimalsCell Culture TechniquesDisease Models, AnimalGene ExpressionGene Expression RegulationHumansImmunoblottingMiceMice, TransgenicPhosphoglycerate KinaseProtein Processing, Post-TranslationalReceptors, Urokinase Plasminogen ActivatorRespiratory MucosaRNA, MessengerLipopolysaccharidesPhosphoglycerate KinasePlaur protein, mouseReceptors, Urokinase Plasminogen ActivatorRNA, MessengerTyrosine

Identifiers

PMID19029002
PMCPMC2643078
OpenAlexW2039886941

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.