ArticlePloS one2012
Local gene silencing of monocyte chemoattractant protein-1 prevents vulnerable plaque disruption in apolipoprotein E-knockout mice.
Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 40 citations in OpenAlex.
- RETRACTION: HSP90 Inhibition Suppresses Inflammatory Response and Reduces Carotid Atherosclerotic Plaque Formation in ApoE Mice.Cardiovascular therapeutics · 2026Article
- Estrogen Receptor Subtypes Elicit a Distinct Gene Expression Profile of Endothelial-Derived Factors Implicated in Atherosclerotic Plaque Vulnerability.International journal of molecular sciences · 2022Article
- Preliminary study on the differentiation of vulnerable carotid plaques via analysis of calcium content and spectral curve slope by using gemstone spectral imaging.Experimental and therapeutic medicine · 2022Article
- A Common Variant at the 3'untranslated Region of the CCL7 Gene (rs17735770) Is Associated With Decreased Susceptibility to Coronary Heart Disease.Frontiers in cardiovascular medicine · 2022Article
- Retro-orbital injection of FITC-dextran combined with isolectin B4 in assessing the retinal neovascularization defect.BMC ophthalmology · 2021Article
- Correlation between monocyte chemoattractant protein-1/chemokine (C-C motif) ligand 2 and coronary plaque characteristics.Experimental biology and medicine (Maywood, N.J.) · 2020Article
- Nucleic Acid-Based Therapies for Atherosclerosis.Current atherosclerosis reports · 2020Review
- Epigenetics and Vascular Senescence-Potential New Therapeutic Targets?Frontiers in pharmacology · 2020Review
- Folic Acid Supplementation Delays Atherosclerotic Lesion Development by Modulating MCP1 and VEGF DNA Methylation Levels In Vivo and In Vitro.International journal of molecular sciences · 2017Article
- Updates on cardiovascular comorbidities associated with psoriatic diseases: epidemiology and mechanisms.Rheumatology international · 2017Review
- Cytokines: roles in atherosclerosis disease progression and potential therapeutic targets.Future medicinal chemistry · 2016Review
- Tongxinluo mitigates atherogenesis by regulating angiogenic factors and inhibiting vasa vasorum neovascularization in apolipoprotein E-deficient mice.Oncotarget · 2016Article
- Monocyte Subsets and Related Chemokines in Carotid Artery Stenosis and Ischemic Stroke.International journal of molecular sciences · 2016Article
- Epigenetic associations in relation to cardiovascular prevention and therapeutics.Clinical epigenetics · 2016Review
- Cytokines in atherosclerosis: Key players in all stages of disease and promising therapeutic targets.Cytokine & growth factor reviews · 2015Review
- Tissue factor pathway inhibitor gene transfer prevents vascular smooth muscle cell proliferation by interfering with the MCP-3/CCR2 pathway.Laboratory investigation; a journal of technical methods and pathology · 2015Article
- Age-associated pro-inflammatory remodeling and functional phenotype in the heart and large arteries.Journal of molecular and cellular cardiology · 2015Review
- Epigenetic reprogramming in atherosclerosis.Current atherosclerosis reports · 2015Review
- Article
- Programmed cell death-4 deficiency prevents diet-induced obesity, adipose tissue inflammation, and insulin resistance.Diabetes · 2013Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Monocyte chemoattractant protein-1 (MCP-1), a CC chemokine (CCL2), has been demonstrated to play important roles in atherosclerosis and becoming an important therapeutic target for atherosclerosis. The present study was undertaken to test the hypothesis that local RNAi of MCP-1 by site-specific delivery of adenovirus-mediated small hairpin RNA (shRNA) may enhance plaque stability and prevent plaque disruption in ApoE-/- mice. We designed an adenovirus-mediated shRNA against mouse MCP-1 (rAd5-MCP-1-shRNA). Male apolipoprotein E-knockout (ApoE-/-) mice (n = 120) were fed a high-fat diet and vulnerable plaques were induced by perivascular placement of constrictive collars around the carotid artery, intraperitoneal injection of lipopolysaccharide and stress stimulation. Mice were randomly divided into RNA interference (Ad-MCP-1i) group receiving local treatment of rAd5-MCP-1-shRNA suspension, Ad-EGFP group receiving treatment of rAd5-mediated negative shRNA and mock group receiving treatment of saline. Two weeks after treatment, plaque disruption rates were significantly lower in the Ad-MCP-1i group than in the Ad-EGFP group (13.3% vs. 60.0%, P = 0.01), and local MCP-1 expression was significantly inhibited in the Ad-MCP-1i group confirmed by immunostaining, qRT-PCR and western blot (P<0.001). Compared with the Ad-EGFP group, carotid plaques in the Ad-MCP-1i group showed increased levels of collagen and smooth muscle cells, and decreased levels of lipid and macrophages. The expression of inflammatory cytokines and activities of matrix metalloproteinases (MMPs) were lower in the Ad-MCP-1i group than in the Ad-EGFP group. In conclusion, site-specific delivery of adenoviral-mediated shRNA targeting mouse MCP-1 downregulated MCP-1 expression, turned a vulnerable plaque into a more stable plaque phenotype and prevented plaque disruption. A marked suppression of the local inflammatory cytokine expression may be the central mechanism involved.
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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.