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Published on: January 13, 2012
Acute Stress Activates Piezo1 to Drive NETs Formation and Aggravated Arterial Thrombosis
Chen Yu1, Xuewei Liu2, Sonlin Li3
1Department of Cardiology, Nanfang Hospital, Southern Medical University, Guangzhou, Guangdong, China; Department of Cardiology, The First Affiliated Hospital of Nanchang University, Nanchang, Jiangxi, China.
Acute stress drives arterial thrombosis by promoting neutrophil extracellular traps (NETs) formation via epinephrine and the Piezo1 channel. Targeting these pathways may prevent cardiovascular events.
Area of Science:
- Cardiovascular Science
- Immunology
- Neuroscience
Background:
- Acute stress is a key factor in arterial thrombosis, but its immune cell regulation is unclear.
- The neuro-immune axis links stress, inflammation, and thrombosis.
Purpose of the Study:
- To investigate how acute stress influences arterial thrombosis.
- Focus on neutrophil extracellular traps (NETs) and their regulatory mechanisms.
Main Methods:
- Used animal models of stress and thrombosis (FeCl3-induced carotid artery thrombosis, myocardial infarction).
- Investigated NETs formation in human and mouse neutrophils using SYTOX green, F-04 staining, immunofluorescence, and co-immunoprecipitation.
- Examined the role of epinephrine, calcium (Ca2+), reactive oxygen species (ROS), and the Piezo1 channel.
Main Results:
- Acute stress and epinephrine induce NETs formation and promote thrombosis.
- Epinephrine-induced NETs formation is mediated by Ca2+ influx via the Piezo1 channel, not ROS.
- Blocking the β2 adrenergic receptor with ICI-118551 reduced Ca2+ levels, suppressed NETs, and slowed thrombosis.
Conclusions:
- Acute stress exacerbates arterial thrombosis through epinephrine-induced NETs formation.
- The Piezo1 channel is crucial for intracellular Ca2+ elevation in this process.
- Targeting Piezo1 and NETs offers potential therapeutic strategies for cardiovascular events.
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