Evidence map›Paper›PMID 35217866›Full record

ArticleDevelopment (Cambridge, England)2022

The β8 integrin cytoplasmic domain activates extracellular matrix adhesion to promote brain neurovascular development.

Arpan De, John E Morales, Zhihua Chen, Sumod Sebastian, Joseph H McCarty

Open access · bronzeAbstract read
In one paragraph

Article in Development (Cambridge, England), 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
2.2field-weighted citation impact, top 12% 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

11 citing papers in PubMed, 19 citations in OpenAlex.

  1. Cell-to-Cell Signaling Networks at the Blood-Brain Barrier in Health and Disease.Arteriosclerosis, thrombosis, and vascular biology · 2026
    Review
  2. Development of the blood-brain barrier.Development (Cambridge, England) · 2026
    Review
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Glial Cell Adhesion Molecule (GlialCAM) Determines Proliferative versus Invasive Cell States in Glioblastoma.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2023
    Article
  9. Article
  10. Article
  11. 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

5 authors at 1 institution in 1 country.

Arpan DeDepartment of Neurosurgery and Brain Tumor Center, Unit 1004, University of Texas MD Anderson Cancer Center, 1515 Holcombe Boulevard, Houston, Texas 77030, USA.
John E MoralesDepartment of Neurosurgery and Brain Tumor Center, Unit 1004, University of Texas MD Anderson Cancer Center, 1515 Holcombe Boulevard, Houston, Texas 77030, USA.
Zhihua ChenDepartment of Neurosurgery and Brain Tumor Center, Unit 1004, University of Texas MD Anderson Cancer Center, 1515 Holcombe Boulevard, Houston, Texas 77030, USA.
Sumod SebastianDepartment of Neurosurgery and Brain Tumor Center, Unit 1004, University of Texas MD Anderson Cancer Center, 1515 Holcombe Boulevard, Houston, Texas 77030, USA.
Joseph H McCartyDepartment of Neurosurgery and Brain Tumor Center, Unit 1004, University of Texas MD Anderson Cancer Center, 1515 Holcombe Boulevard, Houston, Texas 77030, USA.ORCID 0000-0002-8345-5478
The University of Texas MD Anderson Cancer Center · US

Funding

Tumor Evolution and Metastasis ProgramP30CA016672 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI Fabien Delerue · 1985 to 2026
$290.8M
Tropism Enhanced Oncolytic Adenovirus for the Treatment of Brain TumorsP50CA127001 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI Juan Fueyo · 2008 to 2026
$41.2M
Signal Transduction by alphaVbeta8 IntegrinR01NS087635 · NINDS · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI MCCARTY, JOSEPH H · 2014 to 2024
$3.7M
Analyzing Cell-Cell Fusion in Glioblastoma Growth and ProgressionR21NS103841 · NINDS · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI MCCARTY, JOSEPH H · 2019 to 2020
$440k
NCI NIH HHS P30 CA016672NCI NIH HHS P50 CA127001NINDS NIH HHS R01 NS087635NINDS NIH HHS R21 NS103841
6 · The paper itself

Abstract

In the developing mammalian brain, neuroepithelial cells interact with blood vessels to regulate angiogenesis, blood-brain barrier maturation and other key neurovascular functions. Genetic studies in mice have shown that neurovascular development is controlled, in part, by Itgb8, which encodes the neuroepithelial cell-expressed integrin β8 subunit. However, these studies have involved complete loss-of-function Itgb8 mutations, and have not discerned the relative roles for the β8 integrin extracellular matrix (ECM) binding region versus the intracellular signaling tail. Here, Cre/lox strategies have been employed to selectively delete the cytoplasmic tail of murine Itgb8 without perturbing its transmembrane and extracellular domains. We report that the β8 integrin cytoplasmic domain is essential for inside-out modulation of adhesion, including activation of latent-TGFβs in the ECM. Quantitative sequencing of the brain endothelial cell transcriptome identifies TGFβ-regulated genes with putative links to blood vessel morphogenesis, including several genes linked to Wnt/β-catenin signaling. These results reveal that the β8 integrin cytoplasmic domain is essential for the regulation of TGFβ-dependent gene expression in endothelial cells and suggest that cross-talk between TGFβs and Wnt pathways is crucial for neurovascular development.

Indexed as

Endothelial CellsIntegrin beta ChainsAnimalsBrainExtracellular MatrixIntegrinsMammalsMiceTransforming Growth Factor betaintegrin beta8Integrin beta ChainsIntegrinsTransforming Growth Factor betaAngiogenesisEndothelial cellLatent-TGFβMouseNeuroepithelialPerivascular astrocyteWnt

Identifiers

PMID35217866
PMCPMC8977100
OpenAlexW4214494994

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.