Evidence mapPaperPMID 22185776Full record

ArticleCell cycle (Georgetown, Tex.)2012

TNF-α-mediated proliferation of vascular smooth muscle cells involves Raf-1-mediated inactivation of Rb and transcription of E2F1-regulated genes.

Rebecca Davis, Smitha Pillai, Nicholas Lawrence, Said Sebti, Srikumar P Chellappan

Abstract read
In one paragraph

Article in Cell cycle (Georgetown, Tex.), 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing 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

26 citing papers in PubMed.

  1. Article
  2. Article
  3. Review
  4. Review
  5. Review
  6. Inflammatory Mediators in Atherosclerotic Vascular Remodeling.Frontiers in cardiovascular medicine · 2022
    Review
  7. The Effect of TNF-Cardiology research and practice · 2022
    Review
  8. Article
  9. Review
  10. Review
  11. Article
  12. Article
  13. TiOACS biomaterials science & engineering · 2020
    Article
  14. Article
  15. Restoring extracellular matrix synthesis in senescent stem cells.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2019
    Article
  16. Article
  17. Review
  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

5 authors.

Rebecca DavisH. Lee Moffitt Cancer Center and Research Institute, Tampa, FL, USA.
Smitha Pillai
Nicholas Lawrence
Said Sebti
Srikumar P Chellappan

Funding

Tissue CoreP30CA076292 · NCI · UNIVERSITY OF SOUTH FLORIDA · 1998 to 2025
$32.8M
NCI NIH HHS CA118210NCI NIH HHS P01 CA118210NCI NIH HHS P30 CA076292
6 · The paper itself

Abstract

Atherosclerosis is characterized by hyperplastic neointima and an inflammatory response with cytokines such as TNFα. TNFα is a pleiotropic cytokine that mediates inflammatory, proliferative, cytostatic and cytotoxic effects in a variety of cell types, including endothelial cells and vascular smooth muscle cells (VSMCs). Interestingly, TNFα has been shown to play two very opposing roles in these cell types; it inhibits proliferation and induces apoptosis in endothelial cells, while it enhances the proliferation and migration of VSMCs. Here we show that TNFα is capable of stimulating proliferation of rat VSMCs as well as human VSMCs in a Raf-1/MAP K-dependent manner. TNFα could increase the expression of E2F-regulated proliferative cdc6, Thymidylate synthase (TS) and cdc25A genes in Aortic smooth muscle cells (AoSMC), as seen by real time PCR assays. There is an activation of the stress-induced kinase, JNK1, in VSMCs upon TNFα stimulation. TNFα was capable of inducing binding of the Raf-1 kinase to Rb, and treatment with the Rb-Raf-1 inhibitor, RRD-251, could prevent TNFα-induced S-phase entry in AoSMCs. In addition, inhibition of Raf-1 or Src kinases using pharmacologic inhibitors could also prevent S-phase entry, while inhibition of JNK was not as effective. These results suggest that inhibiting the Rb-Raf-1 interaction is a potential avenue to prevent VSMC proliferation associated with atherosclerosis.

Indexed as

Animalscdc25 PhosphatasesCell Cycle ProteinsCell LineCell ProliferationChromosomal Proteins, Non-HistoneE2F1 Transcription FactorGene Expression RegulationHumansMAP Kinase Kinase KinasesMitogen-Activated Protein Kinase 8Muscle, Smooth, VascularProto-Oncogene Proteins c-rafRatsRetinoblastoma ProteinRNA InterferenceCdc25a protein, ratcdc25 PhosphatasesCdc6 protein, ratCell Cycle ProteinsChromosomal Proteins, Non-HistoneE2F1 Transcription FactorMAP Kinase Kinase KinasesMitogen-Activated Protein Kinase 8Proto-Oncogene Proteins c-rafRaf1 protein, ratRetinoblastoma ProteinRNA, Small InterferingRRD 251ThioureaThymidylate SynthaseTumor Necrosis Factor-alpha

Identifiers

PMID22185776
PMCPMC3272234

What Socratic 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 Socratic graph.