Evidence map›Paper›PMID 22328773›Full record

ArticleArteriosclerosis, thrombosis, and vascular biology2012

Protein kinase C-delta mediates adventitial cell migration through regulation of monocyte chemoattractant protein-1 expression in a rat angioplasty model.

Yi Si, Jun Ren, Pu Wang, Debra L Rateri, Alan Daugherty, Xu-Dong Shi, K Craig Kent, Bo Liu

Open access · bronzeAbstract read
In one paragraph

Article in Arteriosclerosis, thrombosis, and vascular biology, 2012. 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
2.6field-weighted citation impact, top 10% 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, 40 citations in OpenAlex.

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  15. A rapamycin-releasing perivascular polymeric sheath produces highly effective inhibition of intimal hyperplasia.Journal of controlled release : official journal of the Controlled Release Society · 2014
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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

8 authors at 1 institution in 1 country.

Yi SiDivision of Vascular Surgery, University of Wisconsin Madison, 53705, USA.
Jun Ren
Pu Wang
Debra L Rateri
Alan Daugherty
Xu-Dong Shi
K Craig Kent
Bo Liu
University of Wisconsin–Madison · US

Funding

TGF-Beta in Intimal Hyperplasia after Vascular BypassR01HL068673 · NHLBI · WEILL MEDICAL COLLEGE OF CORNELL UNIV · PI KENT, K CRAIG · 2002 to 2017
$4.9M
PKC-Delta in Intimal Hyperplasia after Vascular BypassR01HL081424 · NHLBI · WEILL MEDICAL COLL OF CORNELL UNIV · PI LIU, BO · 2005 to 2008
$1.6M
NHLBI NIH HHS R01 HL068673NHLBI NIH HHS R01 HL081424NHLBI NIH HHS R01 HL-81424
6 · The paper itself

Abstract

objectiveThe adventitia is increasingly recognized as an important player during the development of intimal hyperplasia. However, the mechanism of adventitial cell recruitment to the subintimal space remains largely undefined. We have shown previously that gene transfer of protein kinase C-delta (PKCδ) increases apoptosis of smooth muscle cells following balloon injury. In the current study, we investigated a potential role of PKCδ in regulating the recruitment of adventitial cells. METHODS AND

resultsConditioned media from PKCδ-overexpressing smooth muscle cells stimulated migration and CCR2 expression of adventitial fibroblasts through a MCP-1 dependent mechanism. Following balloon injury of rat carotid arteries, overexpression of PKCδ in smooth muscle cells significantly increased MCP-1 and CCR2 expression and the number of adventitia-originated cells detected in the neointima. Administration of an anti-MCP-1 antibody markedly diminished the recruitment of adventitial cells. Combined PKCδ overexpression and anti-MCP-1 inhibited intimal hyperplasia more effectively than either approach alone.

conclusionsOur data suggest that PKCδ regulates recruitment of adventitial cells to the neointima via a mechanism involving upregulation of the MCP-1/CCR2 signaling axis in injured arteries. Blockage of MCP-1 while enhancing apoptosis may serve as a potential therapeutic strategy to attenuate intimal hyperplasia.

Indexed as

Angioplasty, BalloonCell MovementGenetic TherapyAnimalsAntibodiesApoptosisCarotid Artery InjuriesCell ProliferationCells, CulturedChemokine CCL2Connective TissueCulture Media, ConditionedDisease Models, AnimalFibroblastsHyperplasiaMaleAntibodiesCcl2 protein, ratCcr2 protein, ratChemokine CCL2Culture Media, ConditionedProtein Kinase C-deltaReceptors, CCR2

Identifiers

PMID22328773
PMCPMC3311123
OpenAlexW2154891460

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.