Research Paper Volume 13, Issue 2 pp 2768—2779
PTPN2 negatively regulates macrophage inflammation in atherosclerosis
- 1 Department of Cardiology, Zhongnan Hospital of Wuhan University, Wuhan, Hubei, China
- 2 Department of Cardiology, The First College of Clinical Medical Sciences, China Three Gorges University, Yichang, Hubei, China
- 3 Department of Emergency, Renmin Hospital of Wuhan University, Wuhan, Hubei, China
- 4 Department of Cardiology, Jiangxi Provincial People's Hospital Affiliated to Nanchang University, Nanchang, JiangXi, China
Received: February 10, 2020 Accepted: October 27, 2020 Published: December 19, 2020https://doi.org/10.18632/aging.202326
How to Cite
Copyright: © 2020 Hu et al. This is an open access article distributed under the terms of the Creative Commons Attribution License (CC BY 3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Atherosclerosis is the main cause of cardiovascular disease. Systemic inflammation is one important characteristic in atherosclerosis. Pro-inflammatory macrophages can secrete inflammatory factors and promote the inflammation of atherosclerosis. It has a great value for the treatment of atherosclerosis by inhibiting the release of inflammatory factors in macrophages. However, the detailed mechanism of this process is still unclear. In this study, we constructed an APOE-/- mice model of atherosclerosis to research the molecular mechanism of atherosclerosis. Protein tyrosine phosphatase non-receptor type 2 (PTPN2), an anti-inflammatory gene, was dramatically decreased in inflammatory mice. Deletion of PTPN2 could significantly induce monocytes toward M1 phenotype of macrophages, enhance the secretion of IL-12 and IL-1, and promote cell proliferation, invasion and metastasis. Mechanism research showed that PTPN2-mediated p65/p38/STAT3 de-phosphorylation could block the process of macrophage inflammation. In vivo experiments showed that PTPN2 may effectively inhibit the inflammatory response during atherosclerosis. In conclusion, we uncovered the negative role of PTPN2 in the occurrence of atherosclerosis, and this study provides a new potential target for atherosclerosis treatment.