Regulation of CD163 Receptor in Patients with Abdominal Aortic Aneurysm and Associations with Antioxidant Enzymes HO-1 and NQO1-Reference-Cited by-同舟云学术

Regulation of CD163 Receptor in Patients with Abdominal Aortic Aneurysm and Associations with Antioxidant Enzymes HO-1 and NQO1

Published:2023-04-18 Issue:4 Volume:12 Page:947
ISSN:2076-3921
Container-title:Antioxidants
language:en
Short-container-title:Antioxidants

Author:

Hamann Bianca¹^ORCID,Klimova Anna²,Klotz Felicia¹,Frank Frieda¹,Jänichen Christian¹,Kapalla Marvin¹^ORCID,Sabarstinski Pamela¹^ORCID,Wolk Steffen¹,Morawietz Henning³^ORCID,Poitz David M.⁴^ORCID,Hofmann Anja¹^ORCID,Reeps Christian¹

Affiliation:

1. Division of Vascular and Endovascular Surgery, Department of Visceral, Thoracic and Vascular Surgery, Faculty of Medicine and University Hospital Carl Gustav Carus, Technische Universität Dresden, D-01307 Dresden, Germany

2. Core Unit Data Management and Analytics, National Center for Tumor Diseases Dresden (NCT/UCC), Faculty of Medicine and University Hospital Carl Gustav Carus, Technische Universität Dresden, D-01307 Dresden, Germany

3. Division of Vascular Endothelium and Microcirculation, Department of Medicine III, University Hospital and Medical Faculty Carl Gustav Carus, Technische Universität Dresden, D-01307 Dresden, Germany

4. Institute for Clinical Chemistry and Laboratory Medicine, University Hospital and Medical Faculty Carl Gustav Carus, Technische Universität Dresden, D-01307 Dresden, Germany

Abstract

Red blood cells are found within the abdominal aortic aneurysm (AAA), in the intraluminal thrombus (ILT), and in neovessels. Hemolysis promotes aortic degeneration, e.g., by heme-induced reactive oxygen species formation. To reduce its toxicity, hemoglobin is endocytosed by the CD163 receptor and heme is degraded by heme oxygenase-1 (HO-1). A soluble form (sCD163) is discussed as an inflammatory biomarker representing the activation of monocytes and macrophages. HO-1 and NAD(P)H quinone dehydrogenase 1 (NQO1) are antioxidant genes that are induced by the Nrf2 transcription factor, but their regulation in AAA is only poorly understood. The aim of the present study was to analyze linkages between CD163, Nrf2, HO-1, and NQO1 and to clarify if plasma sCD163 has diagnostic and risk stratification potential. Soluble CD163 was 1.3-fold (p = 0.015) higher in AAA compared to patients without arterial disease. The difference remained significant after adjusting for age and sex. sCD163 correlated with the thickness of the ILT (rs = 0.26; p = 0.02) but not with the AAA diameter or volume. A high aneurysmal CD163 mRNA was connected to increases in NQO1, HMOX1, and Nrf2 mRNA. Further studies are needed to analyze the modulation of the CD163/HO-1/NQO1 pathway with the overall goal of minimizing the detrimental effects of hemolysis.

Funder

Medical Faculty of the TU Dresden

Deutsche Gesellschaft für Gefäßchirurgie und Gefäßmedizin Gesellschaft für operative, endovaskuläre und präventive Gefäßmedizin e.V.

Publisher

MDPI AG

Subject

Cell Biology,Clinical Biochemistry,Molecular Biology,Biochemistry,Physiology

Link

https://www.mdpi.com/2076-3921/12/4/947/pdf

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