Evidence map›Paper›PMID 11549580›Full record

ArticleThe American journal of pathology2001

Members of the Jagged/Notch gene families are expressed in injured arteries and regulate cell phenotype via alterations in cell matrix and cell-cell interaction.

V Lindner, C Booth, I Prudovsky, D Small, T Maciag, L Liaw

Open access · bronzeAbstract read
In one paragraph

Article in The American journal of pathology, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 61 papers.

0numbers the graph read from it
0cells of the map it votes in
61citing papers in PubMed
4.3field-weighted citation impact, top 5% 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

61 citing papers in PubMed, 185 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Notch Signaling in Vascular Endothelial and Mural Cell Communications.Cold Spring Harbor perspectives in medicine · 2022
    Article
  5. Article
  6. Review
  7. Article
  8. Review
  9. Review
  10. Lateral induction limits the impact of cell connectivity on Notch signaling in arterial walls.International journal for numerical methods in biomedical engineering · 2020
    Article
  11. Article
  12. Article
  13. Review
  14. Article
  15. Notch2 and Proteomic Signatures in Mouse Neointimal Lesion Formation.Arteriosclerosis, thrombosis, and vascular biology · 2018
    Article
  16. Article
  17. Article
  18. Selective regulation of Notch ligands during angiogenesis is mediated by vimentin.Proceedings of the National Academy of Sciences of the United States of America · 2017
    Article
  19. Article
  20. Notch Signaling in Vascular Smooth Muscle Cells.Advances in pharmacology (San Diego, Calif.) · 2017
    Review

1 more citing papers are in PubMed but not listed here.

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 3 institutions in 1 country.

V LindnerCenter for Molecular Medicine, Maine Medical Center Research Institute, Scarborough, Maine, USA.
C Booth
I Prudovsky
D Small
T Maciag
L Liaw
Maine Medical Center · USMaine Medical Center Research Institute · USUniversity of Maine · US

Funding

Transcriptional Decisions in Endothelial Cell DifferentiationP20RR015555 · NCRR · MAINE MEDICAL CENTER · PI PRUDOVSKY, IGOR · 2000 to 2009
$21.4M
THE PATHOLOGY OF HUMAN ENDOTHELIAL CELL PHENOTYPESR01HL035627 · NHLBI · MELOY LABORATORIES, INC. · PI PRUDOVSKY, IGOR · 1985 to 2010
$2.3M
NCRR NIH HHS P20 RR015555NHLBI NIH HHS R01 HL035627
6 · The paper itself

Abstract

The Jagged/Notch signaling pathways control cell fate determination and differentiation, and their dysfunction is associated with human pathologies involving cardiovascular abnormalities. To determine the presence of these genes during vascular response to injury, we analyzed expression of Jagged1, Jagged2, and Notch1 through 4 after balloon catheter denudation of the rat carotid artery. Although low levels of Jagged1, Jagged2, and constitutive expression of Notch1 were seen in uninjured endothelium, expression of all was significantly increased in injured vascular cells. High Jagged1 expression was restricted to the regenerating endothelial wound edge, whereas Notch transcripts were abundant in endothelial and smooth muscle cells. To understand the basis for Jagged/Notch control of cellular phenotype, we studied an in vitro model of NIH3T3 cells transfected with a secreted form of the extracellular domain of Jagged1. We report that the soluble Jagged1 protein caused decreased cell-matrix adhesion and cell migration defects. Cadherin-mediated intercellular junctions as well as focal adhesions were modified in soluble Jagged1 transfectants, demonstrating that cell-cell contacts and adhesion plaques may be targets of Jagged/Notch activity. We suggest that Jagged regulation of cell-cell and cell-matrix interactions may contribute to the control of cell migration in situations of tissue remodeling in vivo.

Indexed as

Gene ExpressionMultigene Family3T3 CellsAnimalsCalcium-Binding ProteinsCarotid Artery InjuriesCell CommunicationCell-Matrix JunctionsCell MovementIntercellular Signaling Peptides and ProteinsIn Vitro TechniquesJagged-1 ProteinJagged-2 ProteinMembrane ProteinsMicePhenotypeCalcium-Binding ProteinsIntercellular Signaling Peptides and ProteinsJAG1 protein, humanJag1 protein, mouseJag1 protein, ratJAG2 protein, humanJagged-1 ProteinJagged-2 ProteinMembrane ProteinsProteinsReceptors, NotchSerrate-Jagged Proteins

Identifiers

PMID11549580
PMCPMC1850458
OpenAlexW1968068296

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.