Evidence map›Paper›PMID 28336813›Full record

ArticleAmerican journal of physiology. Lung cellular and molecular physiology2017

The innate immune response in fetal lung mesenchymal cells targets VEGFR2 expression and activity.

Rachel M Medal, Amanda M Im, Yasutoshi Yamamoto, Omar Lakhdari, Timothy S Blackwell, Hal M Hoffman, Debashis Sahoo, Lawrence S Prince

Open access · bronzeAbstract read
In one paragraph

Article in American journal of physiology. Lung cellular and molecular physiology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
0.4field-weighted citation impact, top 35% 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

4 citing papers in PubMed, 5 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. 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

8 authors at 3 institutions in 1 country.

Rachel M MedalDepartment of Pediatrics, University of California, San Diego, and Rady Children's Hospital, San Diego, California; and.
Amanda M ImDepartments of Pediatrics, Medicine, Developmental and Cell Biology, and Cancer Biology, Vanderbilt University School of Medicine, Nashville, Tennessee.
Yasutoshi YamamotoDepartments of Pediatrics, Medicine, Developmental and Cell Biology, and Cancer Biology, Vanderbilt University School of Medicine, Nashville, Tennessee.
Omar LakhdariDepartment of Pediatrics, University of California, San Diego, and Rady Children's Hospital, San Diego, California; and.
Timothy S BlackwellDepartments of Pediatrics, Medicine, Developmental and Cell Biology, and Cancer Biology, Vanderbilt University School of Medicine, Nashville, Tennessee.
Hal M HoffmanDepartment of Pediatrics, University of California, San Diego, and Rady Children's Hospital, San Diego, California; and.
Debashis SahooDepartment of Pediatrics, University of California, San Diego, and Rady Children's Hospital, San Diego, California; and.
Lawrence S PrinceDepartment of Pediatrics, University of California, San Diego, and Rady Children's Hospital, San Diego, California; and lprinceucsd@gmail.com.
University of California, San Diego · USVanderbilt University · USRady Children's Hospital-San Diego · 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
Transcriptional Control of Lung Macrophage DevelopmentR01HL126703 · NHLBI · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI HOFFMAN, HAROLD M, PRINCE, LAWRENCE S · 2015 to 2018
$1.6M
Imaging Activated Macrophages in the LungsR01HL116358 · NHLBI · VANDERBILT UNIVERSITY · PI BLACKWELL, TIMOTHY S., PRINCE, LAWRENCE S · 2012 to 2014
$1.1M
Application of Boolean Networks to discover stem and progenitor cellsR00CA151673 · NCI · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI SAHOO, DEBASHIS · 2014 to 2016
$717k
NCI NIH HHS R00 CA151673NHLBI NIH HHS R01 HL086324NHLBI NIH HHS R01 HL116358NHLBI NIH HHS R01 HL126703
6 · The paper itself

Abstract

In preterm infants, soluble inflammatory mediators target lung mesenchymal cells, disrupting airway and alveolar morphogenesis. However, how mesenchymal cells respond directly to microbial stimuli remains poorly characterized. Our objective was to measure the genome-wide innate immune response in fetal lung mesenchymal cells exposed to the bacterial endotoxin lipopolysaccharide (LPS). With the use of Affymetrix MoGene 1.0st arrays, we showed that LPS induced expression of unique innate immune transcripts heavily weighted toward CC and CXC family chemokines. The transcriptional response was different between cells from E11, E15, and E18 mouse lungs. In all cells tested, LPS inhibited expression of a small core group of genes including the VEGF receptor

Indexed as

Immunity, InnateAnimalsCell CommunicationCell MovementEpithelial CellsFetusGene Expression Regulation, DevelopmentalLipopolysaccharidesLungMesodermMice, Inbred C57BLSignal TransductionVascular Endothelial Growth Factor Receptor-2LipopolysaccharidesVascular Endothelial Growth Factor Receptor-2cell migrationchemokinesepithelial-mesenchymal interactionsinnate immunitylung development

Identifiers

PMID28336813
PMCPMC5495951
OpenAlexW2597574875

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.