Evidence map›Paper›PMID 18206868›Full record

ArticleDevelopmental biology2008

Attenuation of retinal vascular development and neovascularization in PECAM-1-deficient mice.

Terri A Dimaio, Shoujian Wang, Qiong Huang, Elizabeth A Scheef, Christine M Sorenson, Nader Sheibani

Open access · greenAbstract readComparative Study
In one paragraph

Article in Developmental biology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed
1.7field-weighted citation impact, top 17% 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

35 citing papers in PubMed, 59 citations in OpenAlex.

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  12. PECAM-1 isoforms, eNOS and endoglin axis in regulation of angiogenesis.Clinical science (London, England : 1979) · 2015
    Review
  13. PTH receptor signaling in osteoblasts regulates endochondral vascularization in maintenance of postnatal growth plate.Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research · 2015
    Article
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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

6 authors at 1 institution in 1 country.

Terri A DimaioDepartment of Ophthalmology and Visual Sciences, University of Wisconsin School of Medicine and Public Health, Madison, WI 53792-4673, USA.
Shoujian Wang
Qiong Huang
Elizabeth A Scheef
Christine M Sorenson
Nader Sheibani
University of Wisconsin–Madison · US

Funding

UW Vision Research Core - Administrative CoreP30EY016665 · NEI · UNIVERSITY OF WISCONSIN-MADISON · PI ROBERT W NICKELLS · 2005 to 2026
$12.6M
PECAM-1 and Retinopathy of PrematurityR01EY016695 · NEI · UNIVERSITY OF WISCONSIN-MADISON · PI SHEIBANI, NADER · 2007 to 2011
$1.6M
Bcl-2 &Branching MorphogenesisR01DK067120 · NIDDK · UNIVERSITY OF WISCONSIN-MADISON · PI SORENSON, CHRISTINE M · 2005 to 2008
$1.1M
NEI NIH HHS EY16695NEI NIH HHS P30 EY016665NEI NIH HHS R01 EY016695NIDDK NIH HHS DK67120NIDDK NIH HHS R01 DK067120
6 · The paper itself

Abstract

Platelet-endothelial cell adhesion molecule-1 (PECAM-1/CD31) is expressed on the surface of endothelial cells (EC) at high levels with important roles in angiogenesis and inflammation. However, the physiological role PECAM-1 plays during vascular development and angiogenesis remains largely unknown. Here we determined the role of PECAM-1 in the postnatal development of retinal vasculature and retinal neovascularization during oxygen-induced ischemic retinopathy (OIR) using PECAM-1-deficient (PECAM-1-/-) mice. A significant decrease in retinal vascular density was observed in PECAM-1-/- mice compared with PECAM-1+/+ mice. This was attributed to a decreased number of EC in the retinas of PECAM-1-/- mice. An increase in the rate of apoptosis was observed in retinal vessels of PECAM-1-/- mice, which was compensated, in part, by an increase in the rate of proliferation. However, the development and regression of hyaloid vasculature were not affected in the absence of PECAM-1. We did not observe a significant defect in astrocytes, the number of endothelial tip cell filopodias, and the rate of developing retinal vasculature progression in PECAM-1-/- mice. However, we observed aberrant organization of arterioles and venules, decreased secondary branching, and dilated vessels in retinal vasculature of PECAM-1-/- mice. In addition, retinal neovascularization was attenuated in PECAM-1-/- mice during OIR despite an expression of VEGF similar to that of PECAM-1+/+ mice. Mechanistically, these changes were associated with an increase in EphB4 and ephrin B2, and a decrease in eNOS, expression in retinal vasculature of PECAM-1-/- mice. These results suggest that PECAM-1 expression and its potential interactions with EphB4/ephrin B2 and eNOS are important for survival, migration, and functional organization of EC during retinal vascular development and angiogenesis.

Indexed as

AnimalsApoptosisCell ProliferationCollagen Type IVEndothelial CellsHypoxiaImmunohistochemistryIn Situ Nick-End LabelingIschemiaMiceMice, Inbred C57BLMice, KnockoutNeovascularization, PathologicNitric Oxide Synthase Type IIIOxygenPericytesCollagen Type IVEphb4 protein, mouseNitric Oxide Synthase Type IIIOxygenPlatelet Endothelial Cell Adhesion Molecule-1Receptor, EphB2Receptor, EphB4TrypsinVascular Endothelial Growth Factor A

Identifiers

PMID18206868
PMCPMC2275901
OpenAlexW2094957208

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.