Ikk2-mediated inflammatory activation of arterial endothelial cells promotes the development and progression of atherosclerosis.


Journal

Atherosclerosis
ISSN: 1879-1484
Titre abrégé: Atherosclerosis
Pays: Ireland
ID NLM: 0242543

Informations de publication

Date de publication:
08 2020
Historique:
received: 28 08 2019
revised: 14 05 2020
accepted: 05 06 2020
pubmed: 28 7 2020
medline: 24 6 2021
entrez: 26 7 2020
Statut: ppublish

Résumé

Inflammatory activation of endothelial cells is considered to be the first step in the development of atherosclerosis. Here, we determined the consequences of chronic endothelial activation via the NF-κB activator Ikk2 (Inhibitor of nuclear factor kappa-B kinase 2, Ikk-beta) on the development and progression of atherosclerosis. We established a conditional transgenic mouse model, expressing a tamoxifen-inducible, constitutively active form of Ikk2 exclusively in arterial endothelial cells (caIkk2 En face preparations of isolated aortas revealed a significant increase in plaque area in caIkk2 Our results show for the first time that chronic inflammatory activation of arterial endothelial cells accelerates the development and progression of atherosclerosis both at early and late stages of disease development. Thus, pharmacological targeting of endothelial inflammation emerges as a promising treatment approach.

Sections du résumé

BACKGROUND AND AIMS
Inflammatory activation of endothelial cells is considered to be the first step in the development of atherosclerosis. Here, we determined the consequences of chronic endothelial activation via the NF-κB activator Ikk2 (Inhibitor of nuclear factor kappa-B kinase 2, Ikk-beta) on the development and progression of atherosclerosis.
METHODS
We established a conditional transgenic mouse model, expressing a tamoxifen-inducible, constitutively active form of Ikk2 exclusively in arterial endothelial cells (caIkk2
RESULTS
En face preparations of isolated aortas revealed a significant increase in plaque area in caIkk2
CONCLUSIONS
Our results show for the first time that chronic inflammatory activation of arterial endothelial cells accelerates the development and progression of atherosclerosis both at early and late stages of disease development. Thus, pharmacological targeting of endothelial inflammation emerges as a promising treatment approach.

Identifiants

pubmed: 32711212
pii: S0021-9150(20)30301-4
doi: 10.1016/j.atherosclerosis.2020.06.005
pii:
doi:

Substances chimiques

NF-kappa B 0
I-kappa B Kinase EC 2.7.11.10
Ikbkb protein, mouse EC 2.7.11.10

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

21-31

Informations de copyright

Copyright © 2020 Elsevier B.V. All rights reserved.

Auteurs

Marion Mussbacher (M)

Institute of Vascular Biology and Thrombosis Research, Medical University Vienna, Vienna, Austria.

Manuel Salzmann (M)

Institute of Vascular Biology and Thrombosis Research, Medical University Vienna, Vienna, Austria.

Barbara Haigl (B)

Institute of Vascular Biology and Thrombosis Research, Medical University Vienna, Vienna, Austria.

José Basílio (J)

Institute of Vascular Biology and Thrombosis Research, Medical University Vienna, Vienna, Austria.

Bernhard Hochreiter (B)

Institute of Vascular Biology and Thrombosis Research, Medical University Vienna, Vienna, Austria.

Viola Gleitsmann (V)

Institute of Vascular Biology and Thrombosis Research, Medical University Vienna, Vienna, Austria.

Bernhard Moser (B)

Institute of Vascular Biology and Thrombosis Research, Medical University Vienna, Vienna, Austria.

Bastian Hoesel (B)

Institute of Vascular Biology and Thrombosis Research, Medical University Vienna, Vienna, Austria.

Bianca E Suur (BE)

Cardiovascular Medicine Unit, Center of Molecular Medicine, Department of Medicine, Karolinska Institutet, Karolinska University Hospital, Stockholm, Sweden.

Florian Puhm (F)

Department of Laboratory Medicine, Medical University of Vienna, Vienna, Austria; CeMM Research Center for Molecular Medicine of the Austrian Academy of Sciences, Vienna, Austria.

Caroline Ungerböck (C)

Institute of Vascular Biology and Thrombosis Research, Medical University Vienna, Vienna, Austria.

Mario Kuttke (M)

Institute of Vascular Biology and Thrombosis Research, Medical University Vienna, Vienna, Austria.

Maria J Forteza (MJ)

Cardiovascular Medicine Unit, Center of Molecular Medicine, Department of Medicine, Karolinska Institutet, Karolinska University Hospital, Stockholm, Sweden.

Christoph J Binder (CJ)

Department of Laboratory Medicine, Medical University of Vienna, Vienna, Austria; CeMM Research Center for Molecular Medicine of the Austrian Academy of Sciences, Vienna, Austria.

Daniel F J Ketelhuth (DFJ)

Cardiovascular Medicine Unit, Center of Molecular Medicine, Department of Medicine, Karolinska Institutet, Karolinska University Hospital, Stockholm, Sweden.

Alice Assinger (A)

Institute of Vascular Biology and Thrombosis Research, Medical University Vienna, Vienna, Austria.

Johannes A Schmid (JA)

Institute of Vascular Biology and Thrombosis Research, Medical University Vienna, Vienna, Austria. Electronic address: johannes.schmid@meduniwien.ac.at.

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Classifications MeSH