Evidence map›Paper›PMID 22024359›Full record

ArticleVascular pharmacology

Inhibition of Mitogen Activated Protein Kinase Activated Protein Kinase II with MMI-0100 reduces intimal hyperplasia ex vivo and in vivo.

Akihito Muto, Alyssa Panitch, Namho Kim, Kinam Park, Padmini Komalavilas, Colleen M Brophy, Alan Dardik

Open access · greenAbstract read
In one paragraph

Article in Vascular pharmacology. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
1.2field-weighted citation impact, top 23% 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

21 citing papers in PubMed, 29 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Excipients for the lyoprotection of MAPKAP kinase 2 inhibitory peptide nano-polyplexes.Journal of controlled release : official journal of the Controlled Release Society · 2018
    Article
  5. Heparin-functionalized polymer graft surface eluting MK2 inhibitory peptide to improve hemocompatibility and anti-neointimal activity.Journal of controlled release : official journal of the Controlled Release Society · 2017
    Article
  6. Article
  7. Review
  8. Article
  9. Review
  10. Article
  11. Article
  12. Review
  13. Article
  14. Review
  15. Article
  16. Article
  17. Article
  18. Article
  19. Characterization of endocytic uptake of MK2-inhibitor peptides.Journal of peptide science : an official publication of the European Peptide Society · 2013
    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

7 authors at 3 institutions in 1 country.

Akihito MutoDepartment of Surgery, Yale University School of Medicine, New Haven, CT, USA.
Alyssa Panitch
Namho Kim
Kinam Park
Padmini Komalavilas
Colleen M Brophy
Alan Dardik
Purdue University West Lafayette · USVA Tennessee Valley Healthcare System · USYale University · US

Funding

PREVENTION OF VEIN GRAFT SPASMR01HL070715 · NHLBI · VANDERBILT UNIVERSITY MEDICAL CENTER · PI BROPHY, COLLEEN M · 2003 to 2021
$7.2M
Molecular Regulation of Vein Graft AdapationR01HL095498 · NHLBI · YALE UNIVERSITY · PI DARDIK, ALAN · 2009 to 2013
$2.4M
NHLBI NIH HHS 2R01HL070715NHLBI NIH HHS R01 HL070715NHLBI NIH HHS R01 HL095498NHLBI NIH HHS R01-HL095498-01
6 · The paper itself

Abstract

Vein graft intimal hyperplasia remains the leading cause of graft failure, despite many pharmacological approaches that have failed to translate to human therapy. We investigated whether local suppression of inflammation and fibrosis with MMI-0100, a novel peptide inhibitor of Mitogen Activated Protein Kinase Activated Protein Kinase II (MK2), would be an alternative strategy to reduce cell proliferation and intimal hyperplasia. The cell permeant peptide MMI-0100 was synthesized using standard Fmoc chemistry. Pharmacological doses of MMI-0100 induced minimal human endothelial and smooth muscle cell proliferation (30% and 12% respectively). MMI-0100 suppressed IL-6 expression to control levels, without effect on IL-8 expression. MMI-0100 caused sodium nitroprusside induced smooth muscle cell relaxation and inhibited intimal thickening in human saphenous vein rings in a dose-dependent fashion. In a murine aortic bypass model, MMI-0100 reduced intimal thickness in vein grafts by 72%, and there were fewer F4/80-reactive cells in vein grafts treated with MMI-0100. MMI-0100 prevents vein graft intimal thickening ex vivo and in vivo. These results suggest that inhibition of MK2 with the cell-permeant peptide MMI-0100 may be a novel strategy to suppress fibrotic processes such as vein graft disease.

Indexed as

Amino Acid SequenceAnimalsAnti-Inflammatory AgentsCell ProliferationCells, CulturedEndothelial CellsFibrosisGraft Occlusion, VascularHumansHyperplasiaInterleukin-6Interleukin-6 InhibitorsInterleukin-8Intracellular Signaling Peptides and ProteinsMAP-Kinase-Activated Kinase 2MiceAnti-Inflammatory AgentsIL6 protein, humanInterleukin-6Interleukin-6 InhibitorsInterleukin-8Intracellular Signaling Peptides and ProteinsMAP-Kinase-Activated Kinase 2NitroprussidePeptidesProtein Kinase InhibitorsProtein Serine-Threonine Kinases

Identifiers

PMID22024359
PMCPMC3268886
OpenAlexW1979383541

What OpenQuestion holds

Textmetadata
LicenceTDM
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.