Evidence map›Paper›PMID 20172951›Full record

ArticleAmerican journal of physiology. Lung cellular and molecular physiology2010

Chorioamnionitis stimulates angiogenesis in saccular stage fetal lungs via CC chemokines.

J Davin Miller, John T Benjamin, David R Kelly, David B Frank, Lawrence S Prince

Open access · greenAbstract read
In one paragraph

Article in American journal of physiology. Lung cellular and molecular physiology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed
3.8field-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

34 citing papers in PubMed, 57 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Review
  7. Article
  8. Review
  9. Article
  10. Article
  11. Article
  12. Article
  13. Effect of Intranasal Instillation of Lipopolysaccharide on Lung Development and Its Related Mechanism in Newborn Mice.Journal of interferon & cytokine research : the official journal of the International Society for Interferon and Cytokine Research · 2019
    Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Review
  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

5 authors at 3 institutions in 1 country.

J Davin MillerDepartments of Pediatrics, Monroe Carell Jr. Children's Hospital at Vanderbilt, Vanderbilt University School of Medicine, Nashville, Tennessee, USA.
John T Benjamin
David R Kelly
David B Frank
Lawrence S Prince
University of Alabama at Birmingham · USMonroe Carell Jr. Children's Hospital · USVanderbilt University · US

Funding

FGF-10 Expression in a Fetal Mouse Lung Model of Bronchopulmonary DysplasiaR01HL086324 · NHLBI · VANDERBILT UNIVERSITY · PI PRINCE, LAWRENCE S · 2008 to 2017
$3.7M
Role of Fetal Lung Macrophages in Broncopulmonary DysplasiaR01HL097195 · NHLBI · VANDERBILT UNIVERSITY · PI BLACKWELL, TIMOTHY S., PRINCE, LAWRENCE S · 2009 to 2013
$2.6M
NHLBI NIH HHS HL-086324NHLBI NIH HHS HL-097195NHLBI NIH HHS R01 HL086324NHLBI NIH HHS R01 HL097195
6 · The paper itself

Abstract

The fetal lung vasculature forms in tandem with developing airways. Whereas saccular airway morphogenesis is arrested in bronchopulmonary dysplasia (BPD), the potential vascular phenotype in BPD at this stage of development is less well-understood. As inflammation increases the risk of BPD and induces arrest of saccular airway morphogenesis, we tested the effects of Escherichia coli LPS on fetal mouse lung vascular development. Injecting LPS into the amniotic fluid of Tie2-lacZ endothelial reporter mice at embryonic day 15 stimulated angiogenesis in the saccular stage fetal lung mesenchyme. LPS also increased the number of endothelial cells in saccular stage fetal mouse lung explants. Inflammation appeared to directly promote vascular development, as LPS stimulated pulmonary microvascular endothelial cell angiogenesis, cell migration, and proliferation in vitro. Whereas LPS did not increase expression of VEGF, angiopoietin-1 (Ang-1), Tie2, fetal liver kinase-1 (Flk-1), fms-like tyrosine kinase-1 (Flt-1), PDGFA, PDGFB, heparin-binding EGF-like growth factor (HB-EGF), or connective tissue growth factor (CTGF), LPS did stimulate the production of the angiogenic CC chemokines macrophage inflammatory protein-1α (MIP-1α) and monocyte chemoattractant protein-1 (MCP-1). Both MIP-1α and MCP-1 increased angiogenesis in fetal mouse lung explants. In addition, inhibitory antibodies against MIP-1α and MCP-1 blocked the effects of LPS on fetal lung vascular development, suggesting these chemokines are downstream mediators of LPS-induced angiogenesis. We speculate that an inflammation-mediated surge in angiogenesis could lead to formation of aberrant alveolar capillaries in the lungs of patients developing BPD.

Indexed as

Neovascularization, PhysiologicAnimalsBronchopulmonary DysplasiaCase-Control StudiesChemokine CCL2Chemokine CCL3Chemokines, CCChorioamnionitisDisease Models, AnimalEndothelial CellsFemaleHumansImmunity, InnateInfantInfant, NewbornLipopolysaccharidesCcl2 protein, mouseCcl3 protein, mouseChemokine CCL2Chemokine CCL3Chemokines, CCLipopolysaccharides

Identifiers

PMID20172951
PMCPMC2867403
OpenAlexW2108877221

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.