Evidence map›Paper›PMID 19364818›Full record

ArticleMolecular and cellular biology2009

Fas-mediated apoptosis is regulated by the extracellular matrix protein CCN1 (CYR61) in vitro and in vivo.

Vladislava Juric, Chih-Chiun Chen, Lester F Lau

Open access · greenAbstract read
In one paragraph

Article in Molecular and cellular biology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed
3.1field-weighted citation impact, top 8% 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

38 citing papers in PubMed, 67 citations in OpenAlex.

  1. Article
  2. Review
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  4. Article
  5. Identification of the RecombinantFrontiers in cell and developmental biology · 2021
    Article
  6. Article
  7. Article
  8. Article
  9. Review
  10. Article
  11. Article
  12. Article
  13. CCN2 induces cellular senescence in fibroblasts.Journal of cell communication and signaling · 2017
    Article
  14. Cell surface receptors for CCN proteins.Journal of cell communication and signaling · 2016
    Review
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. 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

3 authors at 1 institution in 1 country.

Vladislava JuricDepartment of Biochemistry and Molecular Genetics, University of Illinois at Chicago College of Medicine, Chicago, IL 60607, USA.
Chih-Chiun Chen
Lester F Lau
University of Illinois Chicago · US

Funding

Regulation of TNF-alpha by Integrin-Mediated Matrix SignalingR01GM078492 · NIGMS · UNIVERSITY OF ILLINOIS AT CHICAGO · PI LAU, LESTER F · 2007 to 2018
$4.3M
Structure and Function of the Matricellular Protein CCN1R01CA046565 · NCI · UNIVERSITY OF ILLINOIS AT CHICAGO · PI LAU, LESTER F · 1988 to 2008
$3.0M
GENE CONTROL BY GROWTH FACTORS--FROM CELLS TO ORR01CA052220 · NCI · UNIVERSITY OF ILLINOIS AT CHICAGO · PI LAU, LESTER F · 1990 to 2000
$317k
NCI NIH HHS CA46565NCI NIH HHS R01 CA046565NCI NIH HHS R01 CA052220NIGMS NIH HHS GM78492NIGMS NIH HHS R01 GM078492
6 · The paper itself

Abstract

Although Fas ligand (FasL) is primarily expressed by lymphoid cells, its receptor Fas (CD95/Apo-1) is broadly expressed in numerous nonlymphoid tissues and can mediate apoptosis of parenchymal cells upon injury and infiltration of inflammatory cells. Here we show that CCN1 (CYR61) and CCN2 (CTGF), matricellular proteins upregulated at sites of inflammation and wound repair, synergize with FasL to induce apoptosis by elevating cellular levels of reactive oxygen species (ROS). CCN1 acts through engagement of integrin alpha(6)beta(1) and cell surface heparan sulfate proteoglycans, leading to ROS-dependent hyperactivation of p38 mitogen-activated protein kinase in the presence of FasL to enhance mitochondrial cytochrome c release. We show that CCN1 activates neutral sphingomyelinase, which functions as a key source of CCN1-induced ROS critical for synergism with FasL. Furthermore, Fas-dependent hepatic apoptosis induced by an agonistic monoclonal anti-Fas antibody or intragastric administration of alcohol is severely blunted in knock-in mice expressing an apoptosis-defective Ccn1 allele. These results demonstrate that CCN1 is a physiologic regulator of Fas-mediated apoptosis and that the extracellular matrix microenvironment can modulate Fas-dependent apoptosis through CCN1 expression.

Indexed as

AnimalsApoptosisBase SequenceCells, CulturedCeramidesConnective Tissue Growth FactorCysteine-Rich Protein 61Cytochromes cDNA PrimersEthanolFas Ligand Proteinfas ReceptorHeparan Sulfate ProteoglycansHepatocytesHumansIntegrin alpha6beta1CCN1 protein, humanCCN1 protein, mouseCCN2 protein, humanCeramidesConnective Tissue Growth FactorCysteine-Rich Protein 61Cytochromes cDNA PrimersEthanolFASLG protein, humanFas Ligand ProteinFasl protein, mouseFAS protein, humanFas protein, mousefas ReceptorHeparan Sulfate ProteoglycansIntegrin alpha6beta1Mitogen-Activated Protein Kinase 14Reactive Oxygen SpeciesRNA, Small InterferingSMPD2 protein, humanSphingomyelin Phosphodiesterase

Identifiers

PMID19364818
PMCPMC2698731
OpenAlexW2160860957

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.