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Published on: April 24, 2021
SERP1 Alleviates Cerebral Ischemia/Reperfusion Injury by Inhibiting ER Stress-Mediated Apoptosis
Le Yin1, Dan Wang1, Xinyue Zhang1
1Department of Neurology, The Second Affiliated Hospital of Harbin Medical University, Harbin, China.
Stress-associated endoplasmic reticulum protein 1 (SERP1) protects against ischemic stroke by reducing brain damage. SERP1 mitigates endoplasmic reticulum stress and neuronal apoptosis, offering a potential therapeutic target for stroke.
Area of Science:
- Neuroscience
- Molecular Biology
- Cellular Biology
Background:
- Ischemic stroke causes significant central nervous system damage.
- Endoplasmic reticulum (ER) stress-induced apoptosis is a key mechanism in stroke-related brain injury.
- The role of Stress-associated endoplasmic reticulum protein 1 (SERP1) in ischemic stroke remains unclear.
Purpose of the Study:
- To investigate the protective effect of SERP1 against cerebral ischemia/reperfusion (I/R) injury.
- To elucidate the molecular mechanism by which SERP1 influences I/R injury.
Main Methods:
- In vivo studies utilized transient middle cerebral artery occlusion/reperfusion (tMCAO/R) in Sprague-Dawley rats.
- In vitro studies employed oxygen glucose deprivation/reperfusion (OGD/R) in PC12 cells.
- SERP1 expression, apoptosis, ER stress, and the PERK-EIF2α-ATF4-CHOP pathway were analyzed.
Main Results:
- SERP1 expression was upregulated following cerebral I/R injury in both in vivo and in vitro models.
- SERP1 knockdown exacerbated I/R-induced brain injury and apoptosis, while SERP1 overexpression conferred protection.
- SERP1 alleviated OGD/R-induced cell damage and inhibited ER stress-mediated neuronal apoptosis via the PERK-EIF2α-ATF4-CHOP pathway.
Conclusions:
- SERP1 exhibits a protective role against cerebral I/R injury.
- SERP1 mitigates neuronal apoptosis and ER stress during ischemic stroke.
- SERP1 represents a potential therapeutic target for treating cerebral I/R injury.
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