Cited by 203Atherosclerosis and Cardiovascular DiseasesCerebrovascular and Carotid Artery DiseasesCoronary Interventions and Diagnostics

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Induction of Atherosclerotic Plaque Rupture in Apolipoprotein E −/− Mice After Adenovirus-Mediated Transfer of p53

von der Thüsen, Jan H., van Vlijmen, Bart J.M., Hoeben, Rob C., Kockx, Mark M., Havekes, L.M., van Berkel, Theo J.C., Biessen, Erik A.L.·2002·Circulation

DOI 10.1161/01.cir.0000015502.97828.93

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Abstract

Background — The presence of the tumor-suppressor gene p53 in advanced atherosclerotic plaques and the sensitivity to p53-induced cell death of smooth muscle cells isolated from these plaques have fueled speculation about the role of p53 in lesion destabilization and plaque rupture. In this study, we describe a strategy to promote (thrombotic) rupture of preexisting atherosclerotic lesions using p53-induced lesion remodeling. Methods and Results — Carotid atherogenesis was initiated in apolipoprotein E knockout mice by placement of a perivascular silastic collar. The resulting plaques were incubated transluminally with recombinant adenovirus carrying either a p53 or β-galactosidase ( lacZ ) transgene. p53 transfection was restricted to the smooth muscle cell-rich cap of the plaque and led to an increase in cap cell apoptosis 1 day after transfer. p53 overexpression resulted in a marked decrease in the cellular and extracellular content of the cap, reflected by a markedly reduced cap/intima ratio (0.21±0.04 versus 0.46±0.03, P <0.001). The latter is a characteristic feature of plaque vulnerability to rupture, and whereas spontaneous rupture of p53-treated lesions was rare, it was found in 40% of cases after treatment with the vasopressor compound phenylephrine ( P =0.003). Conclusions — We have demonstrated a potential role of p53-induced remodeling in atherosclerotic plaque destabilization. Being the first example of inducible rupture at a predefined location, this model offers a unique opportunity to delineate the processes that precede rupture and to evaluate plaque-stabilizing therapies.

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Authors: von der Thüsen, J. H., van Vlijmen, B. J. M., Hoeben, R. C., Kockx, M. M., Havekes, L. M., van Berkel, T. J. C., & Biessen, E. A. L.
Affiliations: From the Division of Biopharmaceutics (J.H.v.d.T., T.J.C.v.B., E.A.L.B.), Leiden/Amsterdam Center for Drug Research; Molecular Virology Group, Department of Molecular Cell Biology (R.C.H.) and Department of Cardiology (J.H.v.d.T.), Leiden University Medical Center; and TNO-PG (B.J.M.v.V., L.M.H.), Leiden, the Netherlands; and Department of Pathology (M.M.K.), Middelheim Academic Hospital, Antwerp, Belgium.
Leiden University (NL)
ORCID: Hoeben, Rob C.
Kockx, Mark M.
Biessen, Erik A.L.
Venue: Circulation
Publisher: Ovid Technologies (Wolters Kluwer Health)
Published: 2002-04-30
Volume: 105
Issue: 17
Pages: 2064-2070
ISSN: 0009-7322 (ISSN-L)
1524-4539
DOI: 10.1161/01.cir.0000015502.97828.93
OpenAlex: W2122574397
Cited by: 203
References: 32
Citations by year: 2026: 2 · 2025: 3 · 2024: 2 · 2023: 1 · 2022: 3 · 2021: 6 · 2020: 3 · 2019: 6 · 2018: 5 · 2017: 5 · 2016: 4 · 2015: 7 · 2014: 8 · 2013: 10 · 2012: 8
FWCI: 5.80
Type: journal article
Language: en
Open access: closed
Locations: Circulation (publishedVersion)
PubMed (publishedVersion)
TNO Repository (submittedVersion)
Repository hosted by TU Delft Library (TU Delft) (submittedVersion)
Data Archiving and Networked Services (DANS) (submittedVersion)
Funders: Koninklijke Nederlandse Akademie van Wetenschappen
Topics: Life Sciences › Immunology and Microbiology › Immunology › Atherosclerosis and Cardiovascular Diseases
Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cerebrovascular and Carotid Artery Diseases
Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Coronary Interventions and Diagnostics
Keywords: atherosclerotic plaque rupture, p53, plaque destabilization, plaque remodeling, smooth muscle cell apoptosis, ApoE-deficient mice, adenoviral gene transfer, phenylephrine, plaque vulnerability
MeSH terms: Adenoviridae, Animals, Apolipoproteins E, Arteriosclerosis, beta-Galactosidase, Carotid Artery Diseases, Cell Division, Genetic Vectors, Immunohistochemistry, Muscle, Smooth, Vascular, Transfection, Biomarkers, Tumor Suppressor Protein p53, Apoptosis, Mice, Knockout, Mice

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Induction of Atherosclerotic Plaque Rupture in Apolipoprotein E −/− Mice After Adenovirus-Mediated Transfer of p53

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