CTRP3 induces an intermediate switch of CD14++CD16+ monocyte subset with anti‑inflammatory phenotype

Zhu,Hongtao; Ding,Yuan; Zhang,Youming; Ding,Xiaojun; Zhao,Jianfeng; Ouyang,Weili; Gong,Junhui; Zou,Yuqin; Liu,Xueqing; Wu,Weidong

doi:10.3892/etm.2020.8467

March-2020 Volume 19 Issue 3

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March-2020 Volume 19 Issue 3

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Article Open Access

CTRP3 induces an intermediate switch of CD14++CD16+ monocyte subset with anti‑inflammatory phenotype

Authors:
- Hongtao Zhu
- Yuan Ding
- Youming Zhang
- Xiaojun Ding
- Jianfeng Zhao
- Weili Ouyang
- Junhui Gong
- Yuqin Zou
- Xueqing Liu
- Weidong Wu
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Affiliations: Department of Cardiology, People's Hospital of Danyang, The Affiliated Hospital of Nantong University, Danyang, Jiangsu 212300, P.R. China, Department of Clinical Laboratory, Danyang Hospital for Chinese Traditional Medicine, Danyang, Jiangsu 212300, P.R. China, Department of Anesthesiology, People's Hospital of Danyang, The Affiliated Hospital of Nantong University, Danyang, Jiangsu 212300, P.R. China

Copyright: © Zhu et al. This is an open access article distributed under the terms of Creative Commons Attribution License.
Pages: 2243-2251
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Published online on: January 23, 2020

https://doi.org/10.3892/etm.2020.8467
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Abstract

Acute myocardial infarction (AMI) evokes a temporally coordinated immune response, in which monocytes are critically involved in the clearance of cell debris; however, excessive inflammation induced by the classical sub‑population of monocytes frequently limits the endogenous reparative process. In the present study, the potential of the anti‑inflammatory adipokine complement C1q tumor necrosis factor (TNF)‑related protein‑3 (CTRP3) to induce intermediate switch of monocytes to an anti‑inflammatory phenotype was explored. Circulating monocytes were isolated from patients with AMI at various time‑points (3‑5 h, 3 days and 7 days) and categorized by flow cytometry/immunostaining into three sub‑divisions based on the expression of CD14 and CD16 epitopes: Classical (CD14++/CD16‑), non‑classical (CD14+/CD16++) and intermediate populations (CD14++/CD16+). The phagocytic activity was evaluated by the ingestion of FITC‑Zymosan and 19F‑nanoemulsion and the migratory activity using Thin Cert™ Transwell assay. Monocytes were cultured using autologous serum in the presence of CTRP3 (1 µg/ml) for 24 h and the expression of interleukin 6 (IL‑6) and TNF‑α was quantified by reverse‑transcription quantitative PCR. In addition, SB203580, a p38 mitogen‑activated protein kinase (MAPK)/ERK inhibitor, was used to examine the downstream pathways of CTRP3. AMI evoked a transient increase in monocyte counts of the classical subset after onset of the ischemic insult, while the non‑classical and intermediate subsets persistently expanded (P<0.01). The monocytes from patients at 3 days after AMI displayed enhanced phagocytic and migratory activities in comparison with those from healthy volunteers (P<0.01). Of note, addition of CTRP3 induced an intermediate switch of monocyte subsets and antagonized the enhanced expression of cytokines, particularly IL‑6, in monocytes stressed by lipopolysaccharides, likely by blunting the ERK1/2 and P38 MAPK signaling pathway. In conclusion, the present study demonstrated a dynamic fluctuation of monocyte subsets and enhanced phagocytic and migratory activities in patients with AMI. Furthermore, the ‘proof‑of‑concept' evidence pinpoints CTRP3 as an alternative candidate to modulate the ‘uncontrolled' inflammatory response and thus to augment cardiac reparative processes in patients with AMI.

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Journals

International Journal of Molecular Medicine

International Journal of Oncology

Molecular Medicine Reports

Oncology Reports

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Oncology Letters

Biomedical Reports

Molecular and Clinical Oncology

World Academy of Sciences Journal

International Journal of Functional Nutrition

International Journal of Epigenetics

Medicine International

CTRP3 induces an intermediate switch of CD14++CD16+ monocyte subset with anti‑inflammatory phenotype

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