Evidence map›Paper›PMID 12446788›Full record

ArticleMolecular and cellular biology2002

CYR61 (CCN1) is essential for placental development and vascular integrity.

Fan-E Mo, Andrew G Muntean, Chih-Chiun Chen, Donna B Stolz, Simon C Watkins, Lester F Lau

Abstract read
In one paragraph

Article in Molecular and cellular biology, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 194 papers.

0numbers the graph read from it
0cells of the map it votes in
194citing papers in PubMed
–field-weighted citation impact
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

194 citing papers in PubMed.

  1. Trial
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  17. Matricellular Proteins in the Homeostasis, Regeneration, and Aging of Skin.International journal of molecular sciences · 2023
    Review
  18. Why do humans need thrombospondin-1?Journal of cell communication and signaling · 2023
    Review
  19. Structural insights into regulation of CCN protein activities and functions.Journal of cell communication and signaling · 2023
    Review
  20. Significance of CCNs in liver regeneration.Journal of cell communication and signaling · 2023
    Review

134 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.

Fan-E MoDepartment of Molecular Genetics, University of Illinois at Chicago, Chicago, Illinois 60607-7170, USA.
Andrew G Muntean
Chih-Chiun Chen
Donna B Stolz
Simon C Watkins
Lester F Lau

Funding

Structure and Function of the Matricellular Protein CCN1R01CA046565 · NCI · UNIVERSITY OF ILLINOIS AT CHICAGO · PI LAU, LESTER F · 1988 to 2008
$3.0M
Liver Regeneration as a Model for AngiogenesisR01CA076541 · NCI · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI STOLZ, DONNA BEER · 2004 to 2008
$1.1M
LIVER REGENERATION AS A MODEL FOR ANGIOGENESISR29CA076541 · NCI · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI STOLZ, DONNA BEER · 1998 to 2002
$368k
NCI NIH HHS CA46565NCI NIH HHS CA76541NCI NIH HHS R01 CA046565NCI NIH HHS R01 CA076541NCI NIH HHS R29 CA076541
6 · The paper itself

Abstract

CYR61 (CCN1) is a member of the CCN family of secreted matricellular proteins that includes connective tissue growth factor (CCN2), NOV (CCN3), WISP-1 (CCN4), WISP-2 (CCN5), and WISP-3 (CCN6). First identified as the product of a growth factor-inducible immediate-early gene, CYR61 is an extracellular matrix-associated angiogenic inducer that functions as a ligand of integrin receptors to promote cell adhesion, migration, and proliferation. Aberrant expression of Cyr61 is associated with breast cancer, wound healing, and vascular diseases such as atherosclerosis and restenosis. To understand the functions of CYR61 during development, we have disrupted the Cyr61 gene in mice. We show here that Cyr61-null mice suffer embryonic death: approximately 30% succumbed to a failure in chorioallantoic fusion, and the reminder perished due to placental vascular insufficiency and compromised vessel integrity. These findings establish CYR61 as a novel and essential regulator of vascular development. CYR61 deficiency results in a specific defect in vessel bifurcation (nonsprouting angiogenesis) at the chorioallantoic junction, leading to an undervascularization of the placenta without affecting differentiation of the labyrinthine syncytiotrophoblasts. This unique phenotype is correlated with impaired Vegf-C expression in the allantoic mesoderm, suggesting that CYR61-regulated expression of Vegf-C plays a role in vessel bifurcation. The genetic and molecular basis of vessel bifurcation is presently unknown, and these findings provide new insight into this aspect of angiogenesis.

Indexed as

Neovascularization, PathologicNeovascularization, PhysiologicPlacentationAnimalsBlood VesselsCell DifferentiationCysteine-Rich Protein 61Embryo, MammalianEndothelial Growth FactorsGene TargetingGenotypeHumansImmediate-Early ProteinsIn Situ Nick-End LabelingIntercellular Signaling Peptides and ProteinsMiceCCN1 protein, humanCCN1 protein, mouseCysteine-Rich Protein 61Endothelial Growth FactorsImmediate-Early ProteinsIntercellular Signaling Peptides and ProteinsPlatelet Endothelial Cell Adhesion Molecule-1Vascular Endothelial Growth Factor C

Identifiers

PMID12446788
PMCPMC139880

What OpenQuestion holds

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Read underepoch 390

Registered trials

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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.