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C1q/TNF-related protein-1: an adipokine marking and promoting atherosclerosis

Lin Lu¹, Rui Yan Zhang², Xiao Qun Wang¹

¹Department of Cardiology, Rui Jin Hospital, Shanghai Jiaotong University School of Medicine, Shanghai, People's Republic of China Institute of Cardiovascular Diseases, Shanghai Jiaotong University School of Medicine, Shanghai 200025, People's Republic of China.

European Heart Journal

|December 26, 2015

Insights

C1q/TNF-related protein-1 (CTRP1) is elevated in coronary artery disease (CAD) patients and promotes atherosclerosis by increasing inflammation and monocyte adhesion. CTRP1 is a potential therapeutic target for preventing CAD progression.

Area of Science:

Cardiovascular Biology
Immunology
Molecular Medicine

Background:

Coronary artery disease (CAD) is a significant global health burden.
Adipokines, like C1q/TNF-related protein (CTRP) 1, play roles in metabolic and cardiovascular health.
The specific role of CTRP1 in the pathogenesis of CAD requires further elucidation.

Purpose of the Study:

To investigate the association between CTRP1 levels and CAD in humans.
To determine the biological effects of CTRP1 on vascular cells and its role in atherogenesis.
To explore CTRP1 as a potential biomarker and therapeutic target for CAD.

Main Methods:

Analysis of CTRP1 serum levels in CAD patients and controls.
Immunohistochemical assessment of CTRP1 expression in human atherosclerotic tissues.
In vitro studies on CTRP1's effects on endothelial cells and monocytes.
In vivo studies using mouse models (apoE-/- and CTRP1-/-/apoE-/-) to assess CTRP1's role in atherogenesis.

Main Results:

CTRP1 levels were significantly higher in CAD patients' sera and atherosclerotic tissues compared to controls.
CTRP1 induced inflammatory markers and adhesion molecules in vascular cells, promoting monocyte-endothelial adhesion.
CTRP1 administration promoted atherogenesis in apoE-/- mice, an effect attenuated in CTRP1 deficient mice.
CTRP1 deficiency reduced inflammatory responses and macrophage infiltration in atherosclerotic plaques.

Conclusions:

CTRP1 is a novel biomarker associated with CAD severity.
CTRP1 actively promotes atherogenesis through inflammatory pathways and leukocyte recruitment.
Targeting CTRP1 may offer a therapeutic strategy for mitigating atherosclerosis and CAD progression.

Read full analysis

Abstract

Aims:

We investigated the association of the adipokine C1q/TNF-related protein (CTRP) 1 with coronary artery disease (CAD), and the biological vascular effects of CTRP1.

Methods And Results:

We analysed CTRP1 levels in sera of CAD patients (n = 451) and non-CAD controls (n = 686), and in coronary endarterectomy specimens (n = 32), non-atherosclerotic internal mammary arteries (n = 26), aortic atherosclerotic plaques (n = 15), and non-atherosclerotic aortic samples (n = 10). C1q/TNF-related protein-levels were higher in sera, endarterectomy specimens, aortic atherosclerotic plaques, and peripheral blood mononuclear cells (PBMCs) from CAD patients compared with controls, and were related to CAD severity. The production of CTRP1 was profusely induced by inflammatory cytokines and itself caused a concentration-dependent expression of adhesion molecules and inflammatory markers in human endothelial cells, human peripheral blood monocytes, and THP-1 cells. C1q/TNF-related protein-1 induced p38-dependent monocyte-endothelium adhesion in vitro and the recruitment of leucocytes to mesenteric venules in C57BL/6 mice. Immunohistochemistry of atherosclerotic femoral arteries exhibited CD68 and VE-cadherin loci-associated increased CTRP1 expression in plaques. Compared with saline, intraperitoneal injection of recombinant CTRP1 protein (200 μg/kg) every other day promoted atherogenesis in apoE(-/-) mice at 24 weeks. However, pro-atherogenic effects were significantly attenuated in CTRP1(-/-)/apoE(-/-) double-knockout mice compared with apoE(-/-) mice, with a consistent decrease in vascular adhesion molecule, phospho-p38 and TNF-α expression and macrophage infiltration in plaque in CTRP1(-/-) and double-knockout mice. Tumour necrosis factor-α-induced expression of adhesion molecules and cytokines were lower in primary endothelial cells and macrophages from CTRP(-/-) mice than in those from C57BL/6 mice.

Conclusion:

C1q/TNF-related protein-1 is a marker of atherosclerosis in humans and promotes atherogenesis in mice.

Keywords:

Adipokines Atherosclerosis CTRP1 Coronary artery disease Endothelium

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