Evidence map›Paper›PMID 18535181›Full record

ArticleThe American journal of pathology2008

Fas-ligand-induced apoptosis of respiratory epithelial cells causes disruption of postcanalicular alveolar development.

Monique E De Paepe, Sravanthi Gundavarapu, Umadevi Tantravahi, John R Pepperell, Sheila A Haley, Francois I Luks, Quanfu Mao

Open access · bronzeAbstract read
In one paragraph

Article in The American journal of pathology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
3.0field-weighted citation impact, top 9% 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

16 citing papers in PubMed, 33 citations in OpenAlex.

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  15. Fate and effects of adult bone marrow cells in lungs of normoxic and hyperoxic newborn mice.American journal of respiratory cell and molecular biology · 2009
    Article
  16. The Fas system confers protection against alveolar disruption in hyperoxia-exposed newborn mice.American journal of respiratory cell and molecular biology · 2008
    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

7 authors at 4 institutions in 1 country.

Monique E De PaepeWomen and Infants Hospital, Dept. of Pathology, 101 Dudley St., Providence, RI 02905, USA. mdepaepe@wihri.org
Sravanthi Gundavarapu
Umadevi Tantravahi
John R Pepperell
Sheila A Haley
Francois I Luks
Quanfu Mao
Providence College · USBrown University · USRhode Island Hospital · USWomen & Infants Hospital of Rhode Island · US

Funding

UTERINE NK CELL HOMING FROM THE PERIPHERAL CIRCULATIONP20RR018728 · NCRR · WOMEN AND INFANTS HOSPITAL-RHODE ISLAND · PI BLISS, JOSEPH MARK · 2003 to 2011
$16.7M
NCRR NIH HHS P20 RR018728NCRR NIH HHS P20-RR18728
6 · The paper itself

Abstract

Premature infants are at risk for bronchopulmonary dysplasia, a complex condition characterized by impaired alveolar development and increased alveolar epithelial apoptosis. The functional involvement of pulmonary apoptosis in bronchopulmonary dysplasia- associated alveolar disruption remains undetermined. The aims of this study were to generate conditional lung-specific Fas-ligand (FasL) transgenic mice and to determine the effects of FasL-induced respiratory epithelial apoptosis on alveolar remodeling in postcanalicular lungs. Transgenic (TetOp)(7)-FasL responder mice, generated by pronuclear microinjection, were bred with Clara cell secretory protein (CCSP)-rtTA activator mice. Doxycycline (Dox) was administered from embryonal day 14 to postnatal day 7, and lungs were studied between embryonal day 19 and postnatal day 21. Dox administration induced marked respiratory epithelium-specific FasL mRNA and protein up-regulation in double-transgenic CCSP-rtTA(+)/(TetOp)(7)-FasL(+) mice compared with single-transgenic CCSP-rtTA(+) littermates. The Dox-induced FasL up-regulation was associated with dramatically increased apoptosis of alveolar type II cells and Clara cells, disrupted alveolar development, decreased vascular density, and increased postnatal lethality. These data demonstrate that FasL-induced alveolar epithelial apoptosis during postcanalicular lung remodeling is sufficient to disrupt alveolar development after birth. The availability of inducible lung-specific FasL transgenic mice will facilitate studies of the role of apoptosis in normal and disrupted alveologenesis and may lead to novel therapeutic approaches for perinatal and adult pulmonary diseases characterized by dysregulated apoptosis.

Indexed as

AnimalsApoptosisBase SequenceBlotting, WesternDisease Models, AnimalEpithelial CellsFas Ligand ProteinFemaleImmunohistochemistryIn Situ Nick-End LabelingLung DiseasesMaleMiceMice, TransgenicMicroscopy, Electron, TransmissionMolecular Sequence DataFas Ligand Protein

Identifiers

PMID18535181
PMCPMC2438284
OpenAlexW2135045543

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.