Evidence map›Paper›PMID 18029285›Full record

ArticleMicrovascular research2008

PECAM-1 isoform-specific functions in PECAM-1-deficient brain microvascular endothelial cells.

Terri A DiMaio, Nader Sheibani

Open access · greenAbstract read
In one paragraph

Article in Microvascular research, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
0.7field-weighted citation impact, top 32% 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

19 citing papers in PubMed, 26 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Article
  6. Review
  7. Article
  8. Article
  9. Factors controlling permeability of the blood-brain barrier.Cellular and molecular life sciences : CMLS · 2016
    Review
  10. PECAM-1 isoforms, eNOS and endoglin axis in regulation of angiogenesis.Clinical science (London, England : 1979) · 2015
    Review
  11. Article
  12. Review
  13. Lack of Cyp1b1 promotes the proliferative and migratory phenotype of perivascular supporting cells.Laboratory investigation; a journal of technical methods and pathology · 2013
    Article
  14. Article
  15. Article
  16. Opposing effects of bim and bcl-2 on lung endothelial cell migration.American journal of physiology. Lung cellular and molecular physiology · 2010
    Article
  17. Review
  18. Article
  19. Evaluation of lymphangiogenesis in acellular dermal matrix.Indian journal of plastic surgery : official publication of the Association of Plastic Surgeons of India
    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.

Terri A DiMaioDepartment of Ophthalmology and Visual Sciences, University of Wisconsin, Madison, WI 53792-4673, USA.
Nader Sheibani
University of Wisconsin–Madison · US

Funding

PECAM-1 and Retinopathy of PrematurityR01EY016695 · NEI · UNIVERSITY OF WISCONSIN-MADISON · PI SHEIBANI, NADER · 2007 to 2011
$1.6M
Thrombospondin-1 and retininal vascular homeostasisR03EY013700 · NEI · UNIVERSITY OF WISCONSIN MADISON · PI SHEIBANI, NADER · 2003 to 2005
$437k
NEI NIH HHS EY13700NEI NIH HHS EY16695NEI NIH HHS R01 EY016695NEI NIH HHS R03 EY013700
6 · The paper itself

Abstract

Platelet endothelial cell adhesion molecule-1 (PECAM-1) is alternatively spliced generating eight isoforms that only differ in the length of their cytoplasmic domain. Multiple isoforms of PECAM-1 are present in the endothelium and their expression levels are regulated during vascular development and angiogenesis. However, the functional significance of PECAM-1 isoforms during these processes remains largely unknown. We recently showed that mouse brain endothelial (bEND) cells prepared from PECAM-1-deficient (PECAM-1-/-) mice differ in their cell adhesive and migratory properties compared to PECAM-1+/+ bEND cells. Here we demonstrate that the restoration of PECAM-1 expression in these cells affects their adhesive and migratory properties in an isoform-specific manner. Expression of Delta14&15 PECAM-1, the predominant isoform present in the mouse endothelium, in PECAM-1-/- bEND cells activated MAPK/ERKs, disrupted adherens junctions, and enhanced cell migration and capillary morphogenesis in Matrigel. In contrast, expression of Delta15 PECAM-1 in PECAM-1-/- bEND cells had minimal effects on their activation of MAPK/ERKs, migration, and capillary morphogenesis. The effects of PECAM-1 on cell adhesive and migratory properties were mediated in an isoform-specific manner, at least in part, through its interactions with intracellular signaling proteins, including SHP-2 and Src. These results suggest that the impact of PECAM-1 on EC adhesion, migration, and capillary morphogenesis is modulated by alternative splicing of its cytoplasmic domain.

Indexed as

Alternative SplicingNeovascularization, PhysiologicAdherens JunctionsAnimalsAnimals, NewbornAntigens, CDbeta CateninBrainCadherin 5CadherinsCell AdhesionCell MovementCells, CulturedCell ShapeEndothelial CellsEnzyme ActivationAntigens, CDbeta CateninCadherin 5CadherinsCTNNB1 protein, mouseExtracellular Signal-Regulated MAP KinasesMitogen-Activated Protein KinasesPlatelet Endothelial Cell Adhesion Molecule-1Protein IsoformsProtein Tyrosine Phosphatase, Non-Receptor Type 11Ptpn11 protein, mousesrc-Family Kinases

Identifiers

PMID18029285
PMCPMC2271141
OpenAlexW1988874027

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.