Evidence map›Paper›PMID 25884207›Full record

ArticleAmerican journal of respiratory cell and molecular biology2015

Regulation of alveolar procoagulant activity and permeability in direct acute lung injury by lung epithelial tissue factor.

Ciara M Shaver, Brandon S Grove, Nathan D Putz, Jennifer K Clune, William E Lawson, Robert H Carnahan, Nigel Mackman, Lorraine B Ware, Julie A Bastarache

Open access · greenAbstract read
In one paragraph

Article in American journal of respiratory cell and molecular biology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
3.6field-weighted citation impact, top 7% 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

31 citing papers in PubMed, 50 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Review
  6. Review
  7. Article
  8. Article
  9. Cell-free hemoglobin triggers macrophage cytokine production via TLR4 and MyD88.American journal of physiology. Lung cellular and molecular physiology · 2024
    Article
  10. Review
  11. Article
  12. Article
  13. Article
  14. Lung Epithelial Cell Transcriptional Regulation as a Factor in COVID-19-associated Coagulopathies.American journal of respiratory cell and molecular biology · 2021
    Article
  15. Article
  16. Article
  17. Heparin as a therapy for COVID-19: current evidence and future possibilities.American journal of physiology. Lung cellular and molecular physiology · 2020
    Review
  18. Article
  19. Article
  20. 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

9 authors at 2 institutions in 2 countries.

Ciara M Shaver1 Department of Medicine, Division of Allergy, Pulmonary, and Critical Care Medicine, Vanderbilt University School of Medicine, Nashville, Tennessee.
Brandon S Grove1 Department of Medicine, Division of Allergy, Pulmonary, and Critical Care Medicine, Vanderbilt University School of Medicine, Nashville, Tennessee.
Nathan D Putz1 Department of Medicine, Division of Allergy, Pulmonary, and Critical Care Medicine, Vanderbilt University School of Medicine, Nashville, Tennessee.
Jennifer K Clune1 Department of Medicine, Division of Allergy, Pulmonary, and Critical Care Medicine, Vanderbilt University School of Medicine, Nashville, Tennessee.
William E Lawson1 Department of Medicine, Division of Allergy, Pulmonary, and Critical Care Medicine, Vanderbilt University School of Medicine, Nashville, Tennessee.
Robert H Carnahan3 Department of Cancer Biology, Vanderbilt University School of Medicine, Nashville, Tennessee.
Nigel Mackman4 Thrombosis and Hemostasis Program, Division of Hematology and Oncology, University of North Carolina McAllister Heart Institute, University of North Carolina, Chapel Hill, North Carolina; and.
Lorraine B Ware1 Department of Medicine, Division of Allergy, Pulmonary, and Critical Care Medicine, Vanderbilt University School of Medicine, Nashville, Tennessee.
Julie A Bastarache1 Department of Medicine, Division of Allergy, Pulmonary, and Critical Care Medicine, Vanderbilt University School of Medicine, Nashville, Tennessee.
Vanderbilt University · USUniversity of North Carolina at Chapel Hill · US

Funding

Clinical and Translational Training Program in Pulmonary MedicineT32HL087738 · NHLBI · VANDERBILT UNIVERSITY MEDICAL CENTER · PI Lorraine B Ware · 2007 to 2026
$7.0M
Hemoglobin in ARDS: a novel mediator of aveolar epithelial cell dysfunctionR01HL126671 · NHLBI · VANDERBILT UNIVERSITY MEDICAL CENTER · PI BASTARACHE, JULIE ANNE · 2015 to 2019
$2.0M
Midcareer Investigator Award in Patient-Oriented Research in Acute Lung InjuryK24HL103836 · NHLBI · VANDERBILT UNIVERSITY MEDICAL CENTER · PI WARE, LORRAINE B · 2010 to 2020
$1.6M
Tissue Factor Mediated Fibrin Deposition in Acute Lung InjuryK08HL090785 · NHLBI · VANDERBILT UNIVERSITY · PI BASTARACHE, JULIE ANNE · 2009 to 2013
$629k
Regulation of pulmonary fibrosis by the sonic hedgehog pathwayI01BX001988 · VA · VETERANS HEALTH ADMINISTRATION · PI LAWSON, WILLIAM E · 2013 to 2016
–
BLRD VA I01 BX001988NHLBI NIH HHS HL087738-07NHLBI NIH HHS HL090785NHLBI NIH HHS HL103836NHLBI NIH HHS K08 HL090785NHLBI NIH HHS K24 HL103836NHLBI NIH HHS R01 HL126671NHLBI NIH HHS T32 HL087738
6 · The paper itself

Abstract

Tissue factor (TF) initiates the extrinsic coagulation cascade in response to tissue injury, leading to local fibrin deposition. Low levels of TF in mice are associated with increased severity of acute lung injury (ALI) after intratracheal LPS administration. However, the cellular sources of the TF required for protection from LPS-induced ALI remain unknown. In the current study, transgenic mice with cell-specific deletions of TF in the lung epithelium or myeloid cells were treated with intratracheal LPS to determine the cellular sources of TF important in direct ALI. Cell-specific deletion of TF in the lung epithelium reduced total lung TF expression to 39% of wild-type (WT) levels at baseline and to 29% of WT levels after intratracheal LPS. In contrast, there was no reduction of TF with myeloid cell TF deletion. Mice lacking myeloid cell TF did not differ from WT mice in coagulation, inflammation, permeability, or hemorrhage. However, mice lacking lung epithelial TF had increased tissue injury, impaired activation of coagulation in the airspace, disrupted alveolar permeability, and increased alveolar hemorrhage after intratracheal LPS. Deletion of epithelial TF did not affect alveolar permeability in an indirect model of ALI caused by systemic LPS infusion. These studies demonstrate that the lung epithelium is the primary source of TF in the lung, contributing 60-70% of total lung TF, and that lung epithelial, but not myeloid, TF may be protective in direct ALI.

Indexed as

Acute Lung InjuryAnimalsBlood CoagulationCapillary PermeabilityDisease Models, AnimalEpithelial CellsGene ExpressionHemorrhageLipopolysaccharidesMiceMice, KnockoutMyeloid CellsPulmonary AlveoliRespiratory Distress SyndromeRespiratory MucosaThromboplastinLipopolysaccharidesThromboplastinacute respiratory distress syndromealveolar capillary barrier permeabilitycoagulationfibrinpulmonary

Identifiers

PMID25884207
PMCPMC4742948
OpenAlexW1928766034

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.