Evidence map›Paper›PMID 17099142›Full record

ArticleAmerican journal of respiratory cell and molecular biology2007

Novel role of the human alveolar epithelium in regulating intra-alveolar coagulation.

Ling Wang, Julie A Bastarache, Nancy Wickersham, Xiaohui Fang, Michael A Matthay, Lorraine B Ware

Open access · greenAbstract read
In one paragraph

Article in American journal of respiratory cell and molecular biology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.

0numbers the graph read from it
0cells of the map it votes in
46citing papers in PubMed
3.1field-weighted citation impact, top 8% 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

46 citing papers in PubMed, 85 citations in OpenAlex.

  1. Virulence · 2026
    Article
  2. Review
  3. Review
  4. Review
  5. Review
  6. Article
  7. Review
  8. Article
  9. Antiviral anticoagulation.Research and practice in thrombosis and haemostasis · 2020
    Review
  10. Article
  11. Acute respiratory distress syndrome.Nature reviews. Disease primers · 2019
    Review
  12. Serum thrombomodulin as a metastatic and prognostic marker in soft tissue sarcomas.Cancer biomarkers : section A of Disease markers · 2019
    Article
  13. Review
  14. Article
  15. Article
  16. Article
  17. Article
  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

6 authors at 1 institution in 1 country.

Ling WangDivision of Allergy, Pulmonary, and Critical Care Medicine, Department of Medicine, Vanderbilt University School of Medicine, Nashville, Tennessee, USA.
Julie A Bastarache
Nancy Wickersham
Xiaohui Fang
Michael A Matthay
Lorraine B Ware
University of California, San Francisco · US

Funding

Therapy for Clinical Acute Lung Injury with APCP50HL074005 · NHLBI · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI PITTET, JEAN-FRANCOIS · 2003 to 2007
$9.6M
MECHANISMS OF ALVEOLAR EPITHELIAL FLUID CLEARANCER01HL051854 · NHLBI · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI MATTHAY, MICHAEL A. · 1994 to 2012
$4.4M
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
Alveolar Epithelium in Acute Lung InjuryK08HL070521 · NHLBI · VANDERBILT UNIVERSITY · PI WARE, LORRAINE B · 2001 to 2005
$609k
NHLBI NIH HHS HL51854NHLBI NIH HHS HL70521NHLBI NIH HHS HL81332NHLBI NIH HHS P50HL74005NHLBI NIH HHS R01 HL126671
6 · The paper itself

Abstract

Intra-alveolar fibrin deposition is a common response to localized and diffuse lung infection and acute lung injury (ALI). We hypothesized that the alveolar epithelium modulates intra-alveolar fibrin deposition through activation of protein C. Our objectives [corrected] were to determine whether components of the protein C activation pathway are present in the alveolar compartment in ALI and whether alveolar epithelium is a potential source. In patients with ALI, pulmonary edema fluid levels of endothelial protein C receptor (EPCR) were higher than plasma, suggesting a source in the lung. To determine whether alveolar epithelial cells are a potential source, protein C activation by A549, small airway epithelial, and primary human alveolar epithelial type II cells was measured. All three cell types express thrombomodulin (TM) and EPCR, and activate protein C on the cell surface. Activation of protein C was inhibited by cytomix (TNF-alpha, IL-1beta, and IFN-gamma). Release of EPCR and TM into the conditioned medium was inhibited by the metalloproteinase inhibitors tumor necrosis factor protease inhibitor (TAPI) and GM6001, indicating that the shedding of EPCR and TM from the alveolar epithelium is mediated by a metalloproteinase. These findings provide new evidence that the alveolar epithelium can modulate the protein C pathway and thus could be an important determinant of alveolar fibrin deposition. Local fibrin deposition may be a fundamental mechanism for the lung to localize and confine injury, thus limiting the risk of dissemination of injury or infection to the systemic circulation.

Indexed as

Blood CoagulationAdultAgedAntigensAntigens, CDCase-Control StudiesCells, CulturedCytokinesDose-Response Relationship, DrugEndothelial Protein C ReceptorFemaleHumansMaleMiddle AgedProtein CPulmonary AlveoliAntigensAntigens, CDCytokinesEndothelial Protein C ReceptorPROCR protein, humanProtein CReceptors, Cell SurfaceThrombomodulin

Identifiers

PMID17099142
PMCPMC1899324
OpenAlexW2108664084

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.