Excessive Neutrophil Extracellular Trap Formation Aggravates Acute Myocardial Infarction Injury in Apolipoprotein E Deficiency Mice via the ROS-Dependent Pathway
Joint Authors
Zou, Yunzeng
Ge, Junbo
Zhou, Zheliang
Zhang, Shuning
Ding, Suling
Abudupataer, Mieradilijiang
Zhang, Zhiwei
Zhu, Xiaowei
Zhang, Weiwei
Yang, Xiangdong
Hong, Tao
Source
Oxidative Medicine and Cellular Longevity
Issue
Vol. 2019, Issue 2019 (31 Dec. 2019), pp.1-15, 15 p.
Publisher
Hindawi Publishing Corporation
Publication Date
2019-05-21
Country of Publication
Egypt
No. of Pages
15
Main Subjects
Abstract EN
Genetically human apolipoprotein E (APOE) ε32 is associated with a decreased risk of ischemic heart disease.
ApoE deficiency in mice impairs infarct healing after myocardial infarction (MI).
After the ischemic injury, a large number of neutrophils are firstly recruited into the infarct zone and then degrade dead material and promote reparative phase transformation.
The role of ApoE in inflammation response in the early stage of MI remains largely unclear.
In this study, we investigated the effect of ApoE deficiency on neutrophils’ function and myocardial injury after myocardial infarction.
By left coronary artery ligation in ApoE-/- and wild-type (WT) mice, we observed increased infarct size and neutrophil infiltration in ApoE-/- mice.
Within the infarct zone, more neutrophil extracellular traps (NETs) were observed in ApoE-/- mice, while increased ex vivo NET formation was detected in ApoE-/- mouse-derived neutrophils through the NADPH oxidase-ROS-dependent pathway.
Suppressing overproduced NETs reduced myocardial injury in ApoE-/- mice after ligation.
In general, our findings reveal a critical role of apolipoprotein E in regulating Ly6G+ neutrophil activation and NET formation, resulting in limiting myocardial injury after myocardial infarction.
In such a process, apolipoprotein E regulates NET formation via the ROS-MAPK-MSK1 pathway.
American Psychological Association (APA)
Zhou, Zheliang& Zhang, Shuning& Ding, Suling& Abudupataer, Mieradilijiang& Zhang, Zhiwei& Zhu, Xiaowei…[et al.]. 2019. Excessive Neutrophil Extracellular Trap Formation Aggravates Acute Myocardial Infarction Injury in Apolipoprotein E Deficiency Mice via the ROS-Dependent Pathway. Oxidative Medicine and Cellular Longevity،Vol. 2019, no. 2019, pp.1-15.
https://search.emarefa.net/detail/BIM-1202039
Modern Language Association (MLA)
Zhou, Zheliang…[et al.]. Excessive Neutrophil Extracellular Trap Formation Aggravates Acute Myocardial Infarction Injury in Apolipoprotein E Deficiency Mice via the ROS-Dependent Pathway. Oxidative Medicine and Cellular Longevity No. 2019 (2019), pp.1-15.
https://search.emarefa.net/detail/BIM-1202039
American Medical Association (AMA)
Zhou, Zheliang& Zhang, Shuning& Ding, Suling& Abudupataer, Mieradilijiang& Zhang, Zhiwei& Zhu, Xiaowei…[et al.]. Excessive Neutrophil Extracellular Trap Formation Aggravates Acute Myocardial Infarction Injury in Apolipoprotein E Deficiency Mice via the ROS-Dependent Pathway. Oxidative Medicine and Cellular Longevity. 2019. Vol. 2019, no. 2019, pp.1-15.
https://search.emarefa.net/detail/BIM-1202039
Data Type
Journal Articles
Language
English
Notes
Includes bibliographical references
Record ID
BIM-1202039