Evidence map›Paper›PMID 23418625›Full record

ArticleJournal of immunology (Baltimore, Md. : 1950)2013

The NF-κB inhibitory proteins IκBα and IκBβ mediate disparate responses to inflammation in fetal pulmonary endothelial cells.

Jen-Ruey Tang, Katherine A Michaelis, Eva Nozik-Grayck, Gregory J Seedorf, Marlena Hartman-Filson, Steven H Abman, Clyde J Wright

Open access · bronzeAbstract readComparative Study
In one paragraph

Article in Journal of immunology (Baltimore, Md. : 1950), 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
1.2field-weighted citation impact, top 22% 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

14 citing papers in PubMed, 23 citations in OpenAlex.

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  14. Pulmonary Hypertension in Preterm Infants with Bronchopulmonary Dysplasia.Pediatric allergy, immunology, and pulmonology · 2014
    Review
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 1 institution in 1 country.

Jen-Ruey TangDepartment of Pediatrics, Pediatric Heart Lung Center, University of Colorado School of Medicine, Aurora, CO 80045, USA.
Katherine A Michaelis
Eva Nozik-Grayck
Gregory J Seedorf
Marlena Hartman-Filson
Steven H Abman
Clyde J Wright
University of Colorado Denver · US

Funding

Role of VEGF in Perinatal Pulmonary HypertensionR01HL068702 · NHLBI · UNIVERSITY OF COLORADO DENVER · PI ABMAN, STEVEN HERBERT, SHEPHERD, DOUGLAS · 2001 to 2021
$6.7M
ACADEMIC TRAINING PROGRAM IN PEDIATRIC PULMONARY DISEASET32HL007670 · NHLBI · UNIVERSITY OF COLORADO DENVER · PI ABMAN, STEVEN HERBERT · 1988 to 2019
$5.9M
Impact of Insufficient Vascular EC-SOD in Pulmonary HypertensionR01HL086680 · NHLBI · UNIVERSITY OF COLORADO DENVER · PI NOZIK, EVA S. · 2008 to 2017
$4.7M
Role of VEGF in Perinatal HypertensionR56HL068702 · NHLBI · UNIVERSITY OF COLORADO DENVER · PI ABMAN, STEVEN HERBERT, SHEPHERD, DOUGLAS · 2018 to 2018
$765k
The unique role of IkBa in modulating NF-kB activity in the newborn lung.K08HL098562 · NHLBI · UNIVERSITY OF COLORADO DENVER · PI WRIGHT, CLYDE JASON · 2010 to 2014
$670k
NHLBI NIH HHS K08 HL098562NHLBI NIH HHS K08HL098562NHLBI NIH HHS R01 HL068702NHLBI NIH HHS R01 HL086680NHLBI NIH HHS R01 HL68702NHLBI NIH HHS R56 HL068702NHLBI NIH HHS T32 HL007670NHLBI NIH HHS T32 HL07670
6 · The paper itself

Abstract

Exposure to intrauterine inflammation impairs lung growth but paradoxically protects the neonatal pulmonary vasculature from hyperoxic injury. The mechanisms mediating these contradictory effects are unknown. The objective is to identify the role of NF-κB in mediating cytoprotective and proinflammatory responses to inflammation in the fetal pulmonary endothelium. In newborn rats exposed to intra-amniotic LPS, we found increased expression of the NF-κB target gene manganese superoxide dismutase (MnSOD) in the pulmonary endothelium. Supporting these in vivo findings, LPS induced NF-κB activation and MnSOD expression in isolated fetal pulmonary arterial endothelial cells. In addition, LPS exposure caused apoptosis and suppressed cellular growth and induced P-selectin expression. LPS-induced NF-κB activation that proceeded through specific isoforms of the inhibitory protein IκB mediated these diverse responses; NF-κB signaling through IκBα degradation resulted in MnSOD upregulation and preserved cell growth, whereas NF-κB signaling through IκBβ degradation mediated apoptosis and P-selectin expression. These findings suggest that selective inhibition of NF-κB activation that results from IκBβ degradation preserves the enhanced antioxidant defense and protects the developing pulmonary vascular endothelium from ongoing inflammatory injury.

Indexed as

AnimalsAnimals, NewbornAntioxidantsApoptosisCells, CulturedEndothelium, VascularFetusI-kappa B KinaseI-kappa B ProteinsInflammation MediatorsLungNF-kappa BNF-KappaB Inhibitor alphaRatsRats, Sprague-DawleySuperoxide DismutaseAntioxidantsI kappa B beta proteinI-kappa B KinaseI-kappa B ProteinsInflammation MediatorsNF-kappa BNF-KappaB Inhibitor alphaNfkbia protein, ratSuperoxide Dismutase

Identifiers

PMID23418625
PMCPMC3594141
OpenAlexW2096302297

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.