Evidence map›Paper›PMID 26773153›Full record

ArticleJournal of immunology (Baltimore, Md. : 1950)2016

p52 Overexpression Increases Epithelial Apoptosis, Enhances Lung Injury, and Reduces Survival after Lipopolysaccharide Treatment.

Jamie A Saxon, Dong-Sheng Cheng, Wei Han, Vasiliy V Polosukhin, Allyson G McLoed, Bradley W Richmond, Linda A Gleaves, Harikrishna Tanjore, Taylor P Sherrill, Whitney Barham and 2 more

Open access · greenAbstract read
In one paragraph

Article in Journal of immunology (Baltimore, Md. : 1950), 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed, 2 pooled it
3.3field-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

15 citing papers in PubMed, 2 syntheses or guidelines pooled it, 22 citations in OpenAlex.

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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

12 authors at 1 institution in 1 country.

Jamie A SaxonDepartment of Cancer Biology, Vanderbilt University, Nashville, TN 37232;
Dong-Sheng ChengDivision of Allergy, Pulmonary, and Critical Care Medicine, Department of Medicine, Vanderbilt University, Nashville, TN 37232;
Wei HanDivision of Allergy, Pulmonary, and Critical Care Medicine, Department of Medicine, Vanderbilt University, Nashville, TN 37232;
Vasiliy V PolosukhinDivision of Allergy, Pulmonary, and Critical Care Medicine, Department of Medicine, Vanderbilt University, Nashville, TN 37232;
Allyson G McLoedDepartment of Cancer Biology, Vanderbilt University, Nashville, TN 37232;
Bradley W RichmondDivision of Allergy, Pulmonary, and Critical Care Medicine, Department of Medicine, Vanderbilt University, Nashville, TN 37232; Department of Cell and Developmental Biology, Vanderbilt University, Nashville, TN 37232; and.ORCID http://orcid.org/0000-0001-6200-5235
Linda A GleavesDivision of Allergy, Pulmonary, and Critical Care Medicine, Department of Medicine, Vanderbilt University, Nashville, TN 37232;
Harikrishna TanjoreDivision of Allergy, Pulmonary, and Critical Care Medicine, Department of Medicine, Vanderbilt University, Nashville, TN 37232;
Taylor P SherrillDivision of Allergy, Pulmonary, and Critical Care Medicine, Department of Medicine, Vanderbilt University, Nashville, TN 37232;
Whitney BarhamDepartment of Cancer Biology, Vanderbilt University, Nashville, TN 37232;
Fiona E YullDepartment of Cancer Biology, Vanderbilt University, Nashville, TN 37232;ORCID http://orcid.org/0000-0003-1636-7942
Timothy S BlackwellDepartment of Cancer Biology, Vanderbilt University, Nashville, TN 37232; Division of Allergy, Pulmonary, and Critical Care Medicine, Department of Medicine, Vanderbilt University, Nashville, TN 37232; Department of Cell and Developmental Biology, Vanderbilt University, Nashville, TN 37232; and Department of Veterans Affairs Medical Center, Nashville, TN 37232 timothy.blackwell@vanderbilt.edu.
Vanderbilt University · US

Funding

Tumor Immunology and Microenvironment Research ProgramP30CA068485 · NCI · VANDERBILT UNIVERSITY MEDICAL CENTER · PI MATTHEW J TYSKA · 1995 to 2026
$172.8M
Vanderbilt Diabetes Research CenterP30DK020593 · NIDDK · VANDERBILT UNIVERSITY MEDICAL CENTER · PI OWEN P MCGUINNESS · 2012 to 2026
$29.3M
TRANSGENIC MOUSE/ ES CELL SHARES RESOURCESP60DK020593 · NIDDK · VANDERBILT UNIVERSITY · PI MCGUINNESS, OWEN P · 1986 to 2011
$28.1M
Mechanisms of Familial Pulmonary FibrosisP01HL092870 · NHLBI · VANDERBILT UNIVERSITY MEDICAL CENTER · PI SCHWARTZ, DAVID ALBERT · 2010 to 2020
$21.6M
Vanderbilt Mouse Metabolic Physiology CenterU24DK059637 · NIDDK · VANDERBILT UNIVERSITY · PI WASSERMAN, DAVID H · 2001 to 2015
$14.9M
Epithelial-Fibroblast Interactions in Lung FibrosisR01HL085317 · NHLBI · VANDERBILT UNIVERSITY · PI BLACKWELL, TIMOTHY S. · 2007 to 2015
$3.5M
MOLECULAR REGULATION OF LUNG INFLAMMATION BY NF-KBR01HL061419 · NHLBI · VANDERBILT UNIVERSITY · PI BLACKWELL, TIMOTHY S · 1999 to 2006
$1.5M
Mechanisms driving airway inflammation in chronic lung diseaseI01BX002378 · VA · VETERANS HEALTH ADMINISTRATION · PI Timothy S. Blackwell · 2014 to 2026
–
BLRD VA I01 BX002378NCI NIH HHS P30 CA068485NHLBI NIH HHS HL085317NHLBI NIH HHS HL092870NHLBI NIH HHS P01 HL092870NHLBI NIH HHS R01 HL061419NHLBI NIH HHS R01 HL085317NIDDK NIH HHS P30 DK020593NIDDK NIH HHS U24 DK059637
6 · The paper itself

Abstract

Although numerous studies have demonstrated a critical role for canonical NF-κB signaling in inflammation and disease, the function of the noncanonical NF-κB pathway remains ill-defined. In lung tissue from patients with acute respiratory distress syndrome, we identified increased expression of the noncanonical pathway component p100/p52. To investigate the effects of p52 expression in vivo, we generated a novel transgenic mouse model with inducible expression of p52 in Clara cell secretory protein-expressing airway epithelial cells. Although p52 overexpression alone did not cause significant inflammation, p52 overexpression caused increased lung inflammation, injury, and mortality following intratracheal delivery of Escherichia coli LPS. No differences in cytokine/chemokine expression were measured between p52-overexpressing mice and controls, but increased apoptosis of Clara cell secretory protein-positive airway epithelial cells was observed in transgenic mice after LPS stimulation. In vitro studies in lung epithelial cells showed that p52 overexpression reduced cell survival and increased the expression of several proapoptotic genes during cellular stress. Collectively, these studies demonstrate a novel role for p52 in cell survival/apoptosis of airway epithelial cells and implicate noncanonical NF-κB signaling in the pathogenesis of acute respiratory distress syndrome.

Indexed as

AnimalsApoptosisBlotting, WesternDisease Models, AnimalEnzyme-Linked Immunosorbent AssayHumansImmunohistochemistryLipopolysaccharidesMiceMice, TransgenicNF-kappa B p52 SubunitPneumoniaReal-Time Polymerase Chain ReactionRespiratory Distress SyndromeRespiratory MucosaSignal TransductionLipopolysaccharidesNF-kappa B p52 Subunit

Identifiers

PMID26773153
PMCPMC4744539
OpenAlexW2271220861

What OpenQuestion holds

Textmetadata
LicenceTDM
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.