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Cited by 339Atherosclerosis and Cardiovascular DiseasesCholesterol and Lipid MetabolismCell death mechanisms and regulation

The DOI matches its Crossref record; 59 of the 59 references it cites were found in a registry or an index.

Altered Activation of Endothelial Anti- and Proapoptotic Pathways by High-Density Lipoprotein from Patients with Coronary Artery Disease: Role of High-Density Lipoprotein–Proteome Remodeling

Open access
Riwanto, Meliana, Rohrer, Lucia, Roschitzki, Bernd, Besler, Christian, Mocharla, Pavani, Mueller, Maja, Perisa, Damir, Heinrich, Kathrin, Altwegg, Lukas, von Eckardstein, Arnold, Lüscher, Thomas F., Landmesser, Ulf·2013·Circulation
DOI 10.1161/circulationaha.112.108753
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Abstract

Background—: Endothelial dysfunction and injury are thought to play an important role in the progression of coronary artery disease (CAD). High-density lipoprotein from healthy subjects (HDL Healthy ) has been proposed to exert endothelial antiapoptotic effects that may represent an important antiatherogenic property of the lipoprotein. The present study therefore aimed to compare effects of HDL CAD and HDL Healthy on the activation of endothelial anti- and proapoptotic pathways and to determine which changes of the lipoprotein are relevant for these processes. Methods and Results—: HDL was isolated from patients with stable CAD (HDL sCAD ), an acute coronary syndrome (HDL ACS ), and healthy subjects. HDL Healthy induced expression of the endothelial antiapoptotic Bcl-2 protein Bcl-xL and reduced endothelial cell apoptosis in vitro and in apolipoprotein E–deficient mice in vivo. In contrast, HDL sCAD and HDL ACS did not inhibit endothelial apoptosis, failed to activate endothelial Bcl-xL, and stimulated endothelial proapoptotic pathways, in particular, p38-mitogen-activated protein kinase–mediated activation of the proapoptotic Bcl-2 protein tBid. Endothelial antiapoptotic effects of HDL Healthy were observed after inhibition of endothelial nitric oxide synthase and after delipidation, but not completely mimicked by apolipoprotein A-I or reconstituted HDL, suggesting an important role of the HDL proteome. HDL proteomics analyses and subsequent validations and functional characterizations suggested a reduced clusterin and increased apolipoprotein C-III content of HDL sCAD and HDL ACS as mechanisms leading to altered effects on endothelial apoptosis. Conclusions—: The present study demonstrates for the first time that HDL CAD does not activate endothelial antiapoptotic pathways, but rather stimulates potential endothelial proapoptotic pathways. HDL-proteome remodeling plays an important role for these altered functional properties of HDL. These findings provide novel insights into mechanisms leading to altered vascular effects of HDL in coronary disease.

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Crossref · 10.1161/circulationaha.112.108753

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  1. 10.1021/pr070271 · DOI

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Metadata

Authors
Riwanto, M., Rohrer, L., Roschitzki, B., Besler, C., Mocharla, P., Mueller, M., Perisa, D., Heinrich, K., Altwegg, L., von Eckardstein, A., Lüscher, T. F., & Landmesser, U.
Affiliations
  • University of Zurich (CH)
  • From Cardiology, Cardiovascular Center, University Hospital Zurich, Switzerland (M.R., C.B., P.M., M.M., K.H., L.A., T.F.L., U.L.); Cardiovascular Research, Institute of Physiology, University of Zurich, Switzerland (M.R., C.B., P.M., K.H., L.A., T.F.L., U.L.); Center for Integrative Human Physiology, University of Zurich, Switzerland (M.R., L.R., C.B., L.A., A.v.E., T.F.L., U.L.); Institute of Clinical Chemistry, University Hospital Zurich, Switzerland (L.R., A.v.E.); and Functional Genomics Center...
ORCID
Venue
Circulation
Publisher
Ovid Technologies (Wolters Kluwer Health)
Published
2013-02-26
Volume
127
Issue
8
Pages
891-904
ISSN
  • 0009-7322 (ISSN-L)
  • 1524-4539
DOI
10.1161/circulationaha.112.108753
OpenAlex
W2769328074
Cited by
337
References
58
Citations by year
2026: 8 · 2025: 10 · 2024: 10 · 2023: 11 · 2022: 25 · 2021: 22 · 2020: 19 · 2019: 35 · 2018: 30 · 2017: 29 · 2016: 26 · 2015: 42 · 2014: 41 · 2013: 29
FWCI
25.46
Type
journal article
Language
en
Open access
Licence
other-oa
Locations
  • Circulation (publishedVersion)
  • PubMed (publishedVersion)
  • Zurich Open Repository and Archive (University of Zurich) (acceptedVersion, other-oa)
  • Zurich Open Repository and Archive (University of Zurich) (submittedVersion, other-oa)
  • Zurich Open Repository and Archive (University of Zurich)
Topics
  • Life Sciences › Immunology and Microbiology › Immunology › Atherosclerosis and Cardiovascular Diseases
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Biochemistry › Cholesterol and Lipid Metabolism
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Cell death mechanisms and regulation
Keywords
high-density lipoprotein, coronary artery disease, endothelial cell apoptosis, Bcl-xL, tBid, p38 MAPK, clusterin, apolipoprotein C-III, HDL proteome, endothelial dysfunction, acute coronary syndrome, ApoE-deficient mice, nitric oxide synthase, anti-apoptotic pathways
MeSH terms
Animals, Apolipoproteins E, Coronary Artery Disease, Endothelium, Vascular, Female, Flow Cytometry, Humans, Lipoproteins, HDL, Male, Mice, Inbred C57BL, Middle Aged, Signal Transduction, Apoptosis, Mice, Knockout, Proteome, Mice

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