Evidence map›Paper›PMID 18645058›Full record

ArticleCirculation2008

Requirement for p38 mitogen-activated protein kinase activity in neointima formation after vascular injury.

Brandon M Proctor, Xiaohua Jin, Traian S Lupu, Louis J Muglia, Clay F Semenkovich, Anthony J Muslin

Open access · bronzeAbstract read
In one paragraph

Article in Circulation, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
1.4field-weighted citation impact, top 20% 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

12 citing papers in PubMed, 34 citations in OpenAlex.

  1. Article
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  6. Article
  7. p38 MAPK in cardioprotection - are we there yet?British journal of pharmacology · 2015
    Review
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  9. Article
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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 at 1 institution in 1 country.

Brandon M ProctorCenter for Cardiovascular Research, Department of Medicine, Washington University, St. Louis, School of Medicine, ST. Louis, Mo., USA.
Xiaohua Jin
Traian S Lupu
Louis J Muglia
Clay F Semenkovich
Anthony J Muslin
Washington University in St. Louis · US

Funding

Washington University DDRCC Supplemental Equipment RequestP30DK052574 · NIDDK · WASHINGTON UNIVERSITY · PI Nicholas O. Davidson · 2000 to 2026
$30.8M
Washington University Nutrition Obesity Research CenterP30DK056341 · NIDDK · WASHINGTON UNIVERSITY · PI Brian N Finck · 1999 to 2026
$30.2M
TRANSGENICS COREP60DK020579 · NIDDK · WASHINGTON UNIVERSITY · PI SCHAFFER, JEAN E. · 1986 to 2012
$25.2M
ErbB Activation via a Metalloprotease by Angiotensin IIR01HL076770 · NHLBI · VANDERBILT UNIVERSITY · PI EGUCHI, SATORU · 2004 to 2012
$2.8M
RGS PROTEIN FUNCTION IN CARDIAC PHYSIOLOGYR01HL061567 · NHLBI · WASHINGTON UNIVERSITY · PI MUSLIN, ANTHONY JUSTIN · 2000 to 2008
$2.3M
MAP Kinase and AKT Signaling in Congestive Heart FailureR01HL076670 · NHLBI · WASHINGTON UNIVERSITY · PI MUSLIN, ANTHONY JUSTIN · 2005 to 2009
$1.7M
NHLBI NIH HHS HL061567NHLBI NIH HHS HL076770NHLBI NIH HHS R01 HL061567NHLBI NIH HHS R01 HL076670NHLBI NIH HHS R01 HL076770NIDDK NIH HHS P30 DK052574NIDDK NIH HHS P30 DK056341NIDDK NIH HHS P60 DK020579
6 · The paper itself

Abstract

backgroundAngioplasty and stent delivery are performed to treat atherosclerotic vascular disease but often cause deleterious neointimal lesion formation. Previously, growth factor receptor-bound protein 2 (Grb2), an intracellular linker protein, was shown to be essential for neointima formation and for p38 mitogen-activated protein kinase (MAPK) activation in vascular smooth muscle cells (SMCs). In this study, the role of vascular SMC p38alpha MAPK in neointimal development was examined. METHODS AND

resultsCompound transgenic mice were generated with doxycycline-inducible SMC-specific expression of dominant-negative p38alpha MAPK (DN-p38alpha). Doxycycline treatment resulted in the expression of DN-p38alpha mRNA and protein in transgenic arteries. Doxycycline-treated compound transgenic mice were resistant to neointima formation 21 days after carotid injury and showed reduced arterial p38 MAPK activation. To explore the mechanism by which p38alpha MAPK promotes neointima formation, an in vitro SMC culture system was used. Inhibition of p38alpha MAPK in cultured SMCs by treatment with SB202190 or small interfering RNA blocked platelet-derived growth factor-induced SMC proliferation, DNA replication, phosphorylation of the retinoblastoma protein, and induction of minichromosome maintenance protein 6.

conclusionsSMC p38alpha MAPK activation is required for neointima formation, perhaps because of its ability to promote retinoblastoma protein phosphorylation and minichromosome maintenance protein 6 expression.

Indexed as

AngioplastyAnimalsCarotid Artery InjuriesCell Cycle ProteinsCell DivisionFemaleGene ExpressionMaleMiceMice, Inbred C57BLMice, TransgenicMinichromosome Maintenance Complex Component 6Muscle, Smooth, Vascularp38 Mitogen-Activated Protein KinasesPhosphorylationRetinoblastoma ProteinCell Cycle ProteinsMcm6 protein, mouseMinichromosome Maintenance Complex Component 6p38 Mitogen-Activated Protein KinasesRetinoblastoma ProteinRNA, Small Interfering

Identifiers

PMID18645058
PMCPMC2700025
OpenAlexW2118689570

What OpenQuestion holds

Textmetadata
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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.