Mapping the dynamic high-density lipoprotein synapse.

Aminopeptidase n CD13 Chemoproteomics HDL High-density lipoprotein Interactome Ligand-receptor interactions Scavenger receptor B1 Signaling Spacial proteotyping Surfaceome

Journal

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

Informations de publication

Date de publication:
09 2023
Historique:
received: 11 03 2023
revised: 27 07 2023
accepted: 28 07 2023
medline: 4 9 2023
pubmed: 25 8 2023
entrez: 24 8 2023
Statut: ppublish

Résumé

Heterogeneous high-density lipoprotein (HDL) particles, which can contain hundreds of proteins, affect human health and disease through dynamic molecular interactions with cell surface proteins. How HDL mediates its long-range signaling functions and interactions with various cell types is largely unknown. Due to the complexity of HDL, we hypothesize that multiple receptors engage with HDL particles resulting in condition-dependent receptor-HDL interaction clusters at the cell surface. Here we used the mass spectrometry-based and light-controlled proximity labeling strategy LUX-MS in a discovery-driven manner to decode HDL-receptor interactions. Surfaceome nanoscale organization analysis of hepatocytes and endothelial cells using LUX-MS revealed that the previously known HDL-binding protein scavenger receptor B1 (SCRB1) is embedded in a cell surface protein community, which we term HDL synapse. Modulating the endothelial HDL synapse, composed of 60 proteins, by silencing individual members, showed that the HDL synapse can be assembled in the absence of SCRB1 and that the members are interlinked. The aminopeptidase N (AMPN) (also known as CD13) was identified as an HDL synapse member that directly influences HDL uptake into the primary human aortic endothelial cells (HAECs). Our data indicate that preformed cell surface residing protein complexes modulate HDL function and suggest new theragnostic opportunities.

Sections du résumé

BACKGROUND AND AIMS
Heterogeneous high-density lipoprotein (HDL) particles, which can contain hundreds of proteins, affect human health and disease through dynamic molecular interactions with cell surface proteins. How HDL mediates its long-range signaling functions and interactions with various cell types is largely unknown. Due to the complexity of HDL, we hypothesize that multiple receptors engage with HDL particles resulting in condition-dependent receptor-HDL interaction clusters at the cell surface.
METHODS
Here we used the mass spectrometry-based and light-controlled proximity labeling strategy LUX-MS in a discovery-driven manner to decode HDL-receptor interactions.
RESULTS
Surfaceome nanoscale organization analysis of hepatocytes and endothelial cells using LUX-MS revealed that the previously known HDL-binding protein scavenger receptor B1 (SCRB1) is embedded in a cell surface protein community, which we term HDL synapse. Modulating the endothelial HDL synapse, composed of 60 proteins, by silencing individual members, showed that the HDL synapse can be assembled in the absence of SCRB1 and that the members are interlinked. The aminopeptidase N (AMPN) (also known as CD13) was identified as an HDL synapse member that directly influences HDL uptake into the primary human aortic endothelial cells (HAECs).
CONCLUSIONS
Our data indicate that preformed cell surface residing protein complexes modulate HDL function and suggest new theragnostic opportunities.

Identifiants

pubmed: 37619408
pii: S0021-9150(23)05107-9
doi: 10.1016/j.atherosclerosis.2023.117200
pii:
doi:

Substances chimiques

Membrane Proteins 0
Lipoproteins, HDL 0

Types de publication

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

Langues

eng

Sous-ensembles de citation

IM

Pagination

117200

Informations de copyright

Copyright © 2023 The Author(s). Published by Elsevier B.V. All rights reserved.

Déclaration de conflit d'intérêts

Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.

Auteurs

Kathrin Frey (K)

Institute of Translational Medicine, Department of Health Sciences and Technology, ETH Zurich, Zurich, Switzerland; Swiss Institute of Bioinformatics (SIB), Lausanne, Switzerland; Institute for Clinical Chemistry University Hospital Zurich, Zurich, Switzerland. Electronic address: kathrin.frey@usz.ch.

Lucia Rohrer (L)

Institute for Clinical Chemistry University Hospital Zurich, Zurich, Switzerland.

Fabian Frommelt (F)

Institute of Molecular Systems Biology, Department of Biology, ETH Zurich, Zurich, Switzerland.

Meret Ringwald (M)

Institute of Translational Medicine, Department of Health Sciences and Technology, ETH Zurich, Zurich, Switzerland.

Anton Potapenko (A)

Institute for Clinical Chemistry University Hospital Zurich, Zurich, Switzerland.

Sandra Goetze (S)

Institute of Translational Medicine, Department of Health Sciences and Technology, ETH Zurich, Zurich, Switzerland; Swiss Institute of Bioinformatics (SIB), Lausanne, Switzerland; ETH PHRT Swiss Multi-Omics Center (SMOC), Switzerland.

Arnold von Eckardstein (A)

Institute for Clinical Chemistry University Hospital Zurich, Zurich, Switzerland.

Bernd Wollscheid (B)

Institute of Translational Medicine, Department of Health Sciences and Technology, ETH Zurich, Zurich, Switzerland; Swiss Institute of Bioinformatics (SIB), Lausanne, Switzerland; ETH PHRT Swiss Multi-Omics Center (SMOC), Switzerland. Electronic address: wbernd@ethz.ch.

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