Evidence map›Paper›PMID 21985298›Full record

ArticleRespiratory research2011

Conditional deletion of epithelial IKKβ impairs alveolar formation through apoptosis and decreased VEGF expression during early mouse lung morphogenesis.

Vedang A Londhe, Tiffany M Maisonet, Benjamin Lopez, Jade-Ming Jeng, Jing Xiao, Changgong Li, Parviz Minoo

Open access · goldAbstract readComparative Study
In one paragraph

Article in Respiratory research, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
2.0field-weighted citation impact, top 13% 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

17 citing papers in PubMed, 25 citations in OpenAlex.

  1. Observational
  2. Article
  3. Review
  4. Article
  5. Review
  6. Article
  7. Review
  8. Article
  9. Article
  10. Oxidative stress diseases unique to the perinatal period: A window into the developing innate immune response.American journal of reproductive immunology (New York, N.Y. : 1989) · 2018
    Review
  11. Review
  12. Sustained hyperoxia-induced NF-κB activation improves survival and preserves lung development in neonatal mice.American journal of physiology. Lung cellular and molecular physiology · 2014
    Article
  13. Nuclear factor-kappa-B signaling in lung development and disease: one pathway, numerous functions.Birth defects research. Part A, Clinical and molecular teratology · 2014
    Review
  14. Postnatal inflammation in the pathogenesis of bronchopulmonary dysplasia.Birth defects research. Part A, Clinical and molecular teratology · 2014
    Review
  15. Article
  16. Article
  17. Retinoic acid rescues alveolar hypoplasia in the calorie-restricted developing rat lung.American journal of respiratory cell and molecular biology · 2013
    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 3 institutions in 2 countries.

Vedang A LondheDepartment of Pediatrics, Division of Neonatology and Developmental Biology, David Geffen School of Medicine at UCLA, 10833 Le Conte Ave, Mailcode 175217, Los Angeles, CA, USA. vlondhe@mednet.ucla.edu
Tiffany M Maisonet
Benjamin Lopez
Jade-Ming Jeng
Jing Xiao
Changgong Li
Parviz Minoo
University of California, Los Angeles · USKeck Hospital of USC · USDalian Medical University · CN

Funding

Inflammatory and Chemotactic Cytokines in Bronchopulmonary DysplasiaK08HL076538 · NHLBI · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI LONDHE, VEDANG A · 2007 to 2011
$609k
NHLBI NIH HHS K08 HL076538NHLBI NIH HHS R01 HL60231
6 · The paper itself

Abstract

backgroundAlveolar septation marks the beginning of the transition from the saccular to alveolar stage of lung development. Inflammation can disrupt this process and permanently impair alveolar formation resulting in alveolar hypoplasia as seen in bronchopulmonary dysplasia in preterm newborns. NF-κB is a transcription factor central to multiple inflammatory and developmental pathways including dorsal-ventral patterning in fruit flies; limb, mammary and submandibular gland development in mice; and branching morphogenesis in chick lungs. We have previously shown that epithelial overexpression of NF-κB accelerates lung maturity using transgenic mice. The purpose of this study was to test our hypothesis that targeted deletion of NF-κB signaling in lung epithelium would impair alveolar formation.

methodsWe generated double transgenic mice with lung epithelium-specific deletion of IKKβ, a known activating kinase upstream of NF-κB, using a cre-loxP transgenic recombination strategy. Lungs of resulting progeny were analyzed at embryonic and early postnatal stages to determine specific effects on lung histology, and mRNA and protein expression of relevant lung morphoreulatory genes. Lastly, results measuring expression of the angiogenic factor, VEGF, were confirmed in vitro using a siRNA-knockdown strategy in cultured mouse lung epithelial cells.

resultsOur results showed that IKKβ deletion in the lung epithelium transiently decreased alveolar type I and type II cells and myofibroblasts and delayed alveolar formation. These effects were mediated through increased alveolar type II cell apoptosis and decreased epithelial VEGF expression.

conclusionsThese results suggest that epithelial NF-κB plays a critical role in early alveolar development possibly through regulation of VEGF.

Indexed as

Gene DeletionGene Expression Regulation, DevelopmentalAnimalsApoptosis Regulatory ProteinsI-kappa B KinaseLungMiceMice, Inbred C57BLMice, TransgenicMyofibroblastsPulmonary AlveoliRespiratory MucosaVascular Endothelial Growth Factor AApoptosis Regulatory ProteinsI-kappa B KinaseIkbkb protein, mouseVascular Endothelial Growth Factor Avascular endothelial growth factor A, mouse

Identifiers

PMID21985298
PMCPMC3202236
OpenAlexW2108069890

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.