Evidence map›Paper›PMID 24425872›Full record

ArticleThe Journal of biological chemistry2014

CD44 regulation of endothelial cell proliferation and apoptosis via modulation of CD31 and VE-cadherin expression.

Masayuki Tsuneki, Joseph A Madri

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers.

0numbers the graph read from it
0cells of the map it votes in
49citing papers in PubMed
3.8field-weighted citation impact, top 6% 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

49 citing papers in PubMed, 75 citations in OpenAlex.

  1. Review
  2. Schisandrin B targets CD44 to inhibit glioblastoma multiforme.Naunyn-Schmiedeberg's archives of pharmacology · 2026
    Article
  3. Article
  4. The Yin and Yang of copper in cardiovascular health and disease.Molecular and cellular biochemistry · 2026
    Review
  5. Observational
  6. Article
  7. Article
  8. Article
  9. CD31 as a probable responding and gate-keeping protein of the blood-brain barrier and the risk of Alzheimer's disease.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2023
    Review
  10. Article
  11. Article
  12. Review
  13. Article
  14. Article
  15. Article
  16. Angiogenesis in Chronic Inflammatory Skin Disorders.International journal of molecular sciences · 2021
    Review
  17. Article
  18. Article
  19. Article
  20. 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

2 authors at 1 institution in 1 country.

Masayuki TsunekiFrom the Department of Pathology, Yale University School of Medicine, New Haven, Connecticut 06520.
Joseph A Madri
Yale University · US

Funding

NINDS NIH HHS P01-NS00344738
6 · The paper itself

Abstract

CD44 has been implicated in a diverse array of cell behaviors and in a diverse range of signaling pathway activations under physiological and pathophysiological conditions. We have documented a role for CD44 in mediating vascular barrier integrity via regulation of PECAM-1 (CD31) expression. We now report our findings on the roles of CD44 in modulating proliferation and apoptosis of microvascular endothelial cells via its modulation of CD31 and VE-cadherin expression and the Hippo pathway. In this report, we demonstrate persistent increased proliferation and reduced activations of both effector and initiator caspases in high cell density, postconfluent CD44 knock-out (CD44KO), and CD31KO cultures. We found that reconstitution with murine CD44 or CD31 restored the proliferative and caspase activation rates to WT levels. Moreover, we have confirmed that the CD31 ecto-domain plays a key role in specific caspase cascades as well as cell adhesion-mediated cell growth and found that CD31 deficiency results in a reduction in VE-cadherin expression. Last, we have shown that both CD44KO and CD31KO endothelial cells exhibit a reduced VE-cadherin expression correlating with increased survivin expression and YAP nuclear localization, consistent with inactivation of the Hippo pathway, resulting in increased proliferation and decreased apoptosis. These findings support the concept that CD44 mediates several of its effects on endothelia through modulation of adhesion protein expression, which, in addition to its known modulation of junctional integrity, matrix metalloproteinase levels and activation, interactions with cortical membrane proteins, and selected signaling pathways, plays a key role as a critical regulator of vascular function.

Indexed as

Cell ProliferationAnimalsAntigens, CDApoptosisCadherin 5CadherinsCell AdhesionCells, CulturedEndothelial CellsGene Expression RegulationHippo Signaling PathwayHyaluronan ReceptorsInhibitor of Apoptosis ProteinsMiceMice, KnockoutPlatelet Endothelial Cell Adhesion Molecule-1Antigens, CDBirc5 protein, mouseCadherin 5CadherinsCd44 protein, mouseHyaluronan ReceptorsInhibitor of Apoptosis ProteinsPlatelet Endothelial Cell Adhesion Molecule-1Protein Serine-Threonine KinasesRepressor ProteinsSurvivinApoptosisCaspaseCd31Cd44Cell ProliferationEndothelial CellSurvivinVascular BiologyWestern Blotting

Identifiers

PMID24425872
PMCPMC3937614
OpenAlexW2075060412

What Socratic 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 Socratic graph.