Evidence map›Paper›PMID 21540027›Full record

ArticleExperimental and molecular pathology2011

Suppressor of cytokine signaling-3 and intimal hyperplasia in porcine coronary arteries following coronary intervention.

Gaurav K Gupta, Kajari Dhar, Michael G Del Core, William J Hunter, Georgios I Hatzoudis, Devendra K Agrawal

Open access · greenAbstract read
In one paragraph

Article in Experimental and molecular pathology, 2011. 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
1.5field-weighted citation impact, top 17% 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.

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  6. Epigenetics of Mucus Hypersecretion in Chronic Respiratory Diseases.American journal of respiratory cell and molecular biology · 2018
    Review
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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.

Gaurav K GuptaDepartment of Biomedical Sciences and Center for Clinical and Translational Science, Creighton University School of Medicine, Omaha, NE 68178, USA.
Kajari Dhar
Michael G Del Core
William J Hunter
Georgios I Hatzoudis
Devendra K Agrawal
Creighton University · US

Funding

VITAMIN D AND IMMUNOMODULATION IN CORONARY ARTERY DISEASER01HL116042 · NHLBI · CREIGHTON UNIVERSITY · PI AGRAWAL, DEVENDRA K. · 2012 to 2016
$3.3M
GENE THERAPY WITH SOCS-3 IN INTIMAL HYPERPLASIA AND IN-STENT RESTENOSISR01HL104516 · NHLBI · CREIGHTON UNIVERSITY · PI AGRAWAL, DEVENDRA K. · 2011 to 2014
$2.4M
NHLBI NIH HHS R01 HL104516NHLBI NIH HHS R01HL104516NHLBI NIH HHS R01 HL116042
6 · The paper itself

Abstract

aimsThe growth and differentiation of cells is regulated by cytokines by binding to cell-surface receptors and activating intracellular signal transduction cascade. Suppressor of cytokine signaling (SOCS)-3 is a negative regulator of cytokines. In this study we examined the expression of SOCS-3 in porcine coronary artery smooth muscle cells (PCASMCs) in vitro and in proliferating smooth muscle cells of neointimal lesions after coronary artery intervention in a swine model. METHODS AND

resultsPCASMCs were cultured and stimulated with TNF-α and/or IGF-1 individually or in combination. Protein expression of SOCS-3 was examined using Western blot. For in vivo studies, six female Yucatan miniswine were fed with special high cholesterol diet for 8 months. At 4 months of high cholesterol diet, animals underwent coronary balloon angioplasty. At the end of 8 months animals were euthanized, coronary arteries were isolated and morphological and histological studies were performed. Western blot data revealed significantly high SOCS-3 expression in PCASMCs in the presence of either TNF-α or IGF-1 (5-6 fold) alone. However, in the presence of both TNF-α and IGF-1 the SOCS-3 expression was significantly decreased (4-5 fold). Results from morphological studies including, H&E and Masson's trichrome stain showed typical lesions with significant neointimal proliferation. Histological evaluation showed expression of smooth muscle α-actin and significantly increased proliferating cell nuclear antigen (PCNA) in neointimal lesion. Interestingly, there was significantly decreased expression of SOCS-3 in smooth muscle cells of neointima as compared to control.

conclusionsThese data suggest that SOCS-3 expression is decreased in proliferating smooth muscle cells of neointimal lesions. This leads to uncontrolled growth of vascular smooth muscle cells in injured arteries leading to restenosis. Therefore, local delivery of SOCS-3 gene at the site of injury after coronary artery intervention could regulate the proliferation of vascular smooth muscle cells and help in preventing the neointimal hyperplasia and restenosis.

Indexed as

ActinsAngioplasty, Balloon, CoronaryAnimalsCell ProliferationCells, CulturedCholesterol, DietaryCoronary VesselsDisease Models, AnimalFemaleHyperplasiaInsulin-Like Growth Factor IMuscle, Smooth, VascularProliferating Cell Nuclear AntigenSuppressor of Cytokine Signaling ProteinsSwineSwine, MiniatureActinsCholesterol, DietaryInsulin-Like Growth Factor IProliferating Cell Nuclear AntigenSuppressor of Cytokine Signaling ProteinsTumor Necrosis Factor-alpha

Identifiers

PMID21540027
PMCPMC3139760
OpenAlexW2047972161

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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.