Evidence map›Paper›PMID 20810911›Full record

ArticleAmerican journal of physiology. Cell physiology2010

PECAM-1 regulates proangiogenic properties of endothelial cells through modulation of cell-cell and cell-matrix interactions.

SunYoung Park, Terri A DiMaio, Elizabeth A Scheef, Christine M Sorenson, Nader Sheibani

Open access · greenAbstract read
In one paragraph

Article in American journal of physiology. Cell physiology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
42citing papers in PubMed, 1 pooled it
1.3field-weighted citation impact, top 24% 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

42 citing papers in PubMed, 1 synthesis or guideline pooled it, 90 citations in OpenAlex.

  1. Endotheliopathy in Acute COVID-19 and Long COVID.International journal of molecular sciences · 2023
    Pooled it
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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

5 authors at 2 institutions in 1 country.

SunYoung ParkDepartment of Ophthalmology and Visual Sciences, University of Wisconsin School of Medicine and Public Health, Madison, Wisconsin 53792-4673, USA.
Terri A DiMaio
Elizabeth A Scheef
Christine M Sorenson
Nader Sheibani
Pediatrics and Genetics · USUniversity of Wisconsin–Madison · US

Funding

UW COMPREHENSIVE CANCER CENTER SUPPORTP30CA014520 · NCI · UNIVERSITY OF WISCONSIN-MADISON · PI Christian Capitini · 1985 to 2026
$142.6M
VISION RESEARCHP30EY003790 · NEI · SCHEPENS EYE RESEARCH INSTITUTE · PI Patricia Ann D'Amore · 1985 to 2026
$25.5M
UW Vision Research Core - Administrative CoreP30EY016665 · NEI · UNIVERSITY OF WISCONSIN-MADISON · PI Donna M Peters · 2005 to 2026
$12.6M
PECAM-1 and Retinopathy of PrematurityR01EY016695 · NEI · UNIVERSITY OF WISCONSIN-MADISON · PI SHEIBANI, NADER · 2007 to 2011
$1.6M
CYP1B1 and Retinopathy of PrematurityR01EY018179 · NEI · UNIVERSITY OF WISCONSIN-MADISON · PI SHEIBANI, NADER · 2009 to 2010
$713k
NCI NIH HHS P30 CA014520NCI NIH HHS P30-CA-014520NEI NIH HHS EY-16995NEI NIH HHS EY-18179NEI NIH HHS P30 EY003790NEI NIH HHS P30 EY016665NEI NIH HHS P30-EY-16665NEI NIH HHS R01 EY016695NEI NIH HHS R01 EY018179
6 · The paper itself

Abstract

Platelet endothelial cell adhesion molecule-1 (PECAM-1/CD31) is a member of the immunoglobulin superfamily of cell adhesion molecules with important roles in angiogenesis and inflammation. However, the molecular and cellular mechanisms, and the role that specific PECAM-1 isoforms play in these processes, remain elusive. We recently showed attenuation of retinal vascular development and neovascularization in PECAM-1-deficient (PECAM-1-/-) mice. To gain further insight into the role of PECAM-1 in these processes, we isolated primary retinal endothelial cells (EC) from wild-type (PECAM-1+/+) and PECAM-1-/- mice. Lack of PECAM-1 had a significant impact on endothelial cell-cell and cell-matrix interactions, resulting in attenuation of cell migration and capillary morphogenesis. Mechanistically these changes were associated with a significant decrease in expression of endothelial nitric oxide synthase (eNOS) and nitric oxide (NO) bioavailability in PECAM-1-/- retinal EC. PECAM-1-/- retinal EC also exhibited a lower rate of apoptosis under basal and challenged conditions, consistent with their increased growth rate. Furthermore, reexpression of PECAM-1 was sufficient to restore migration and capillary morphogenesis of null cells in an isoform-specific manner. Thus PECAM-1 expression modulates proangiogenic properties of EC, and these activities are significantly influenced by alternative splicing of its cytoplasmic domain.

Indexed as

Cell CommunicationExtracellular MatrixNeovascularization, PhysiologicAlternative SplicingAnimalsApoptosisCapillariesCell MovementCells, CulturedEndothelium, VascularMiceMice, Inbred C57BLMorphogenesisNitric Oxide Synthase Type IIIPlatelet Endothelial Cell Adhesion Molecule-1Retinal VesselsNitric Oxide Synthase Type IIIPlatelet Endothelial Cell Adhesion Molecule-1

Identifiers

PMID20810911
PMCPMC3006334
OpenAlexW1989361067

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.