Evidence map›Paper›PMID 29993183›Full record

ArticleJournal of cellular and molecular medicine2018

Distinct roles for IκB kinases alpha and beta in regulating pulmonary endothelial angiogenic function during late lung development.

Cristiana Iosef, Min Liu, Lihua Ying, Shailaja P Rao, Katherine R Concepcion, Westin K Chan, Andrew Oman, Cristina M Alvira

Open access · goldAbstract read
In one paragraph

Article in Journal of cellular and molecular medicine, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
1.3field-weighted citation impact, top 19% 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

8 citing papers in PubMed, 15 citations in OpenAlex.

  1. Endothelial-specific loss of IKKβ disrupts pulmonary endothelial angiogenesis and impairs postnatal lung growth.American journal of physiology. Lung cellular and molecular physiology · 2023
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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

8 authors at 2 institutions in 1 country.

Cristiana IosefDepartment of Pharmacology, Faculty of Medicine, University of Nevada Reno, Reno, NV, USA.ORCID 0000-0002-0535-8605
Min LiuDepartment of Pediatrics, Center for Excellence in Pulmonary Biology, Stanford University School of Medicine, Stanford, CA, USA.
Lihua YingDepartment of Pediatrics, Center for Excellence in Pulmonary Biology, Stanford University School of Medicine, Stanford, CA, USA.
Shailaja P RaoDepartment of Pediatrics, Center for Excellence in Pulmonary Biology, Stanford University School of Medicine, Stanford, CA, USA.
Katherine R ConcepcionDepartment of Pediatrics, Center for Excellence in Pulmonary Biology, Stanford University School of Medicine, Stanford, CA, USA.
Westin K ChanDepartment of Pharmacology, Faculty of Medicine, University of Nevada Reno, Reno, NV, USA.
Andrew OmanDepartment of Pharmacology, Faculty of Medicine, University of Nevada Reno, Reno, NV, USA.
Cristina M AlviraDepartment of Pediatrics, Center for Excellence in Pulmonary Biology, Stanford University School of Medicine, Stanford, CA, USA.
Stanford Medicine · USUniversity of Nevada, Reno · US

Funding

Novel Molecular Mechanisms Regulating Postnatal Pulmonary AngiogenesisR01HL122918 · NHLBI · STANFORD UNIVERSITY · PI ALVIRA, CRISTINA MARIA · 2014 to 2018
$2.3M
NHLBI NIH HHS R01 HL122918
6 · The paper itself

Abstract

Pulmonary angiogenesis is essential for alveolarization, the final stage of lung development that markedly increases gas exchange surface area. We recently demonstrated that activation of the nuclear factor kappa-B (NFκB) pathway promotes pulmonary angiogenesis during alveolarization. However, the mechanisms activating NFκB in the pulmonary endothelium, and its downstream targets are not known. In this study, we sought to delineate the specific roles for the NFκB activating kinases, IKKα and IKKβ, in promoting developmental pulmonary angiogenesis. Microarray analysis of primary pulmonary endothelial cells (PECs) after silencing IKKα or IKKβ demonstrated that the 2 kinases regulate unique panels of genes, with few shared targets. Although silencing IKKα induced mild impairments in angiogenic function, silencing IKKβ induced more severe angiogenic defects and decreased vascular cell adhesion molecule expression, an IKKβ regulated target essential for both PEC adhesion and migration. Taken together, these data show that IKKα and IKKβ regulate unique genes in PEC, resulting in differential effects on angiogenesis upon inhibition, and identify IKKβ as the predominant regulator of pulmonary angiogenesis during alveolarization. These data suggest that therapeutic strategies to specifically enhance IKKβ activity in the pulmonary endothelium may hold promise to enhance lung growth in diseases marked by altered alveolarization.

Indexed as

Gene Expression Regulation, DevelopmentalAnimalsAnimals, NewbornApoptosisCell AdhesionCell MovementCell ProliferationEndothelial CellsI-kappa B KinaseLungMiceMice, Inbred C57BLNeovascularization, PhysiologicNF-kappa BOrganogenesisPrimary Cell CultureChuk protein, mouseI-kappa B KinaseNF-kappa BRNA, Small InterferingVascular Cell Adhesion Molecule-1alveolarizationangiogenesisendothelial cellslung developmentnuclear factor kappa-B

Identifiers

PMID29993183
PMCPMC6111877
OpenAlexW2880911558

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.