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Cells
Volume 13
Issue 9
10.3390/cells13090773
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Article

Effects of Chronic Inflammatory Activation of Murine and Human Arterial Endothelial Cells at Normal Lipoprotein and Cholesterol Levels In Vivo and In Vitro

by
Marion Mussbacher
1,2,†,
José Basílio
1,3,4,†,
Barbora Belakova
1,
Anita Pirabe
1,
Elisabeth Ableitner
2,
Manuel Campos-Medina
1 and
Johannes A. Schmid
1,*
1
Department of Vascular Biology and Thrombosis Research, Centre for Physiology and Pharmacology, Medical University of Vienna, 1090 Vienna, Austria
2
Department of Pharmacology and Toxicology, Institute of Pharmaceutical Sciences, University of Graz, 8010 Graz, Austria
3
INESC ID, Instituto Superior Técnico, Universidade de Lisboa, 1000-029 Lisboa, Portugal
4
Institute of Pathophysiology and Allergy Research, Medical University of Vienna, 1090 Vienna, Austria
*
Author to whom correspondence should be addressed.
†
These authors contributed equally to this work.
Cells 2024, 13(9), 773; https://doi.org/10.3390/cells13090773
Submission received: 22 December 2023 / Revised: 24 April 2024 / Accepted: 26 April 2024 / Published: 30 April 2024
(This article belongs to the Section Cells of the Cardiovascular System)
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Abstract

The activation of endothelial cells is crucial for immune defense mechanisms but also plays a role in the development of atherosclerosis. We have previously shown that inflammatory stimulation of endothelial cells on top of elevated lipoprotein/cholesterol levels accelerates atherogenesis. The aim of the current study was to investigate how chronic endothelial inflammation changes the aortic transcriptome of mice at normal lipoprotein levels and to compare this to the inflammatory response of isolated endothelial cells in vitro. We applied a mouse model expressing constitutive active IκB kinase 2 (caIKK2)—the key activator of the inflammatory NF-κB pathway—specifically in arterial endothelial cells and analyzed transcriptomic changes in whole aortas, followed by pathway and network analyses. We found an upregulation of cell death and mitochondrial beta-oxidation pathways with a predicted increase in endothelial apoptosis and necrosis and a simultaneous reduction in protein synthesis genes. The highest upregulated gene was ACE2, the SARS-CoV-2 receptor, which is also an important regulator of blood pressure. Analysis of isolated human arterial and venous endothelial cells supported these findings and also revealed a reduction in DNA replication, as well as repair mechanisms, in line with the notion that chronic inflammation contributes to endothelial dysfunction.
Keywords: arteries; endothelial cells; inflammation; NF-kappa B; transcriptomics; pathway analysis arteries; endothelial cells; inflammation; NF-kappa B; transcriptomics; pathway analysis

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MDPI and ACS Style

Mussbacher, M.; Basílio, J.; Belakova, B.; Pirabe, A.; Ableitner, E.; Campos-Medina, M.; Schmid, J.A. Effects of Chronic Inflammatory Activation of Murine and Human Arterial Endothelial Cells at Normal Lipoprotein and Cholesterol Levels In Vivo and In Vitro. Cells 2024, 13, 773. https://doi.org/10.3390/cells13090773

AMA Style

Mussbacher M, Basílio J, Belakova B, Pirabe A, Ableitner E, Campos-Medina M, Schmid JA. Effects of Chronic Inflammatory Activation of Murine and Human Arterial Endothelial Cells at Normal Lipoprotein and Cholesterol Levels In Vivo and In Vitro. Cells. 2024; 13(9):773. https://doi.org/10.3390/cells13090773

Chicago/Turabian Style

Mussbacher, Marion, José Basílio, Barbora Belakova, Anita Pirabe, Elisabeth Ableitner, Manuel Campos-Medina, and Johannes A. Schmid. 2024. "Effects of Chronic Inflammatory Activation of Murine and Human Arterial Endothelial Cells at Normal Lipoprotein and Cholesterol Levels In Vivo and In Vitro" Cells 13, no. 9: 773. https://doi.org/10.3390/cells13090773

APA Style

Mussbacher, M., Basílio, J., Belakova, B., Pirabe, A., Ableitner, E., Campos-Medina, M., & Schmid, J. A. (2024). Effects of Chronic Inflammatory Activation of Murine and Human Arterial Endothelial Cells at Normal Lipoprotein and Cholesterol Levels In Vivo and In Vitro. Cells, 13(9), 773. https://doi.org/10.3390/cells13090773

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