Evidence map›Paper›PMID 20139355›Full record

ArticleArteriosclerosis, thrombosis, and vascular biology2010

CCN3 inhibits neointimal hyperplasia through modulation of smooth muscle cell growth and migration.

Tatsushi Shimoyama, Shûichi Hiraoka, Minoru Takemoto, Masaya Koshizaka, Hirotake Tokuyama, Takahiko Tokuyama, Aki Watanabe, Masaki Fujimoto, Harukiyo Kawamura, Seiya Sato and 5 more

Abstract read
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In one paragraph

Article in Arteriosclerosis, thrombosis, and vascular biology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
56citing papers in PubMed, 1 pooled it
4.2field-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

56 citing papers in PubMed, 1 synthesis or guideline pooled it, 84 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Review
  5. Article
  6. Article
  7. Article
  8. Elevated reactive aggression in forebrain-specificJournal of cell communication and signaling · 2024
    Article
  9. CD4Scientific reports · 2024
    Article
  10. Article
  11. Review
  12. Article
  13. Review
  14. Review
  15. Aneurysm severity is suppressed by deletion of CCN4.Journal of cell communication and signaling · 2021
    Article
  16. [Regulatory effect of CCN3 on proliferation of mouse embryonic fibroblasts and its mechanism].Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2021
    Article
  17. Review
  18. The Roles of CCN1/CYR61 in Pulmonary Diseases.International journal of molecular sciences · 2020
    Review
  19. CCN3 (NOV) Drives Degradative Changes in Aging Articular Cartilage.International journal of molecular sciences · 2020
    Article
  20. Dynamic CCN3 expression in the murine CNS does not confer essential roles in myelination or remyelination.Proceedings of the National Academy of Sciences of the United States of America · 2020
    Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

15 authors at 3 institutions in 1 country.

Tatsushi ShimoyamaDepartment of Clinical Cell Biology and Medicine, Chiba University Graduate School of Medicine, Chiba, Japan.
Shûichi Hiraoka
Minoru Takemoto
Masaya Koshizaka
Hirotake Tokuyama
Takahiko Tokuyama
Aki Watanabe
Masaki Fujimoto
Harukiyo Kawamura
Seiya Sato
Yuya Tsurutani
Yasushi Saito
Bernard Perbal
Haruhiko Koseki
Koutaro Yokote
National Center For Child Health and Development · JPChiba University · JPChiba University Hospital · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectiveCCN3 belongs to the CCN family, which constitutes multifunctional secreted proteins that act as matrix cellular regulators. We investigated the pathophysiological roles of CCN3 in the vessels. METHODS AND

resultsWe examined the effects of CCN3 on the proliferation and migration of rat vascular smooth muscle cells (VSMC). CCN3 knockout mice were created, and vascular phenotypes and neointimal hyperplasia induced by photochemically induced thrombosis were investigated. CCN3 suppressed the VSMC proliferation induced by fetal bovine serum. The neutralizing antibody for transforming growth factor-beta did not affect the growth inhibitory effect of CCN3. Moreover, CCN3 enhanced the mRNA expression of cyclin-dependent kinase inhibitors, p21 and p15. Gamma secretase inhibitor, an inhibitor of Notch signaling, partially inhibited the enhanced expression of p21 induced by CCN3. CCN3 also inhibited the VSMC migration. Finally, the histopathologic evaluation of the arteries 21 days after the endothelial injury revealed a 6-fold enhancement of neointimal thickening in the null mice compared with the wild-type mice.

conclusionsCCN3 suppresses neointimal thickening through the inhibition of VSMC migration and proliferation. Our findings indicate the involvement of CCN3 in vascular homeostasis, especially on injury, and the potential usefulness of this molecule in the modulation of atherosclerotic vascular disease.

Indexed as

Cell MovementCell ProliferationAmyloid Precursor Protein SecretasesAnimalsAortaCell CycleCells, CulturedCyclin-Dependent Kinase Inhibitor p15Cyclin-Dependent Kinase Inhibitor p21Diabetes Mellitus, ExperimentalDiabetic AngiopathiesFemoral ArteryGenotypeHyperplasiaMaleMiceAmyloid Precursor Protein SecretasesCCN3 protein, humanCdkn1a protein, ratCyclin-Dependent Kinase Inhibitor p15Cyclin-Dependent Kinase Inhibitor p21Nephroblastoma Overexpressed ProteinProtease InhibitorsReceptors, NotchRecombinant ProteinsTransforming Growth Factor beta

Identifiers

PMID20139355
OpenAlexW2101168563

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.