Evidence map›Paper›PMID 10082563›Full record

ArticleMolecular and cellular biology1999

Fisp12/mouse connective tissue growth factor mediates endothelial cell adhesion and migration through integrin alphavbeta3, promotes endothelial cell survival, and induces angiogenesis in vivo.

A M Babic, C C Chen, L F Lau

Open access · greenAbstract read
In one paragraph

Article in Molecular and cellular biology, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 156 papers.

0numbers the graph read from it
0cells of the map it votes in
156citing papers in PubMed
10.0field-weighted citation impact, top 1% 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

156 citing papers in PubMed, 449 citations in OpenAlex.

  1. Article
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  9. Matricellular proteins in atherosclerosis development.Matrix biology : journal of the International Society for Matrix Biology · 2023
    Review
  10. Analysis of Chemotactic Property of CCN2/CTGF in Intramembranous Osteogenesis.Methods in molecular biology (Clifton, N.J.) · 2023
    Article
  11. Article
  12. Review
  13. Review
  14. Article
  15. Matricellular proteins in cutaneous wound healing.Frontiers in cell and developmental biology · 2022
    Review
  16. Review
  17. Article
  18. Article
  19. Review
  20. Article

96 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

3 authors at 1 institution in 1 country.

A M BabicDepartment of Molecular Genetics, University of Illinois at Chicago College of Medicine, Chicago, Illinois 60607-7170, USA.
C C Chen
L F Lau
University of Illinois Chicago · US

Funding

Structure and Function of the Matricellular Protein CCN1R01CA046565 · NCI · UNIVERSITY OF ILLINOIS AT CHICAGO · PI LAU, LESTER F · 1988 to 2008
$3.0M
NCI NIH HHS CA46565NCI NIH HHS CA80080NCI NIH HHS R01 CA046565
6 · The paper itself

Abstract

Fisp12 was first identified as a secreted protein encoded by a growth factor-inducible immediate-early gene in mouse fibroblasts, whereas its human ortholog, CTGF (connective tissue growth factor), was identified as a mitogenic activity in conditioned media of human umbilical vein endothelial cells. Fisp12/CTGF is a member of a family of secreted proteins that includes CYR61, Nov, Elm-1, Cop-1/WISP-2, and WISP-3. Fisp12/CTGF has been shown to promote cell adhesion and mitogenesis in both fibroblasts and endothelial cells and to stimulate cell migration in fibroblasts. These findings, together with the localization of Fisp12/CTGF in angiogenic tissues, as well as in atherosclerotic plaques, suggest a possible role for Fisp12/CTGF in the regulation of vessel growth during development, wound healing, and vascular disease. In this study, we show that purified Fisp12 (mCTGF) protein promotes the adhesion of microvascular endothelial cells through the integrin receptor alphavbeta3. Furthermore, Fisp12 stimulates the migration of microvascular endothelial cells in culture, also through an integrin-alphavbeta3-dependent mechanism. In addition, the presence of Fisp12 promotes endothelial cell survival when cells are plated on laminin and deprived of growth factors, a condition that otherwise induces apoptosis. In vivo, Fisp12 induces neovascularization in rat corneal micropocket implants. These results demonstrate that Fisp12 is a novel angiogenic inducer and suggest a direct role for Fisp12 in the adhesion, migration, and survival of endothelial cells during blood vessel growth. Taken together with the recent finding that the related protein CYR61 also induces angiogenesis, we suggest that Fisp12/mCTGF and CYR61 comprise prototypes of a new family of angiogenic regulators that function, at least in part, through integrin-alphavbeta3-dependent pathways.

Indexed as

Intercellular Signaling Peptides and ProteinsNeovascularization, PhysiologicAnimalsCell AdhesionCell MovementCell SurvivalConnective Tissue Growth FactorCorneaEndothelium, VascularGrowth SubstancesHumansImmediate-Early ProteinsNephroblastoma Overexpressed ProteinRatsReceptors, VitronectinCCN2 protein, humanCCN2 protein, mouseCCN2 protein, ratCCN3 protein, humanCcn3 protein, mouseConnective Tissue Growth FactorGrowth SubstancesImmediate-Early ProteinsIntercellular Signaling Peptides and ProteinsNephroblastoma Overexpressed ProteinReceptors, Vitronectin

Identifiers

PMID10082563
PMCPMC84090
OpenAlexW2142799375

What Socratic holds

Texttitle and abstract
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.