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TRIM37 exacerbates cerebral ischemic injury by regulating the PPARγ/NF-κB pathway
Guixin Shi1,2, Linyan Fu3, Hua Xiao2
1Department of Neurosurgery, the First Affiliated Hospital of Hainan Medical University, Haikou.
Neuroreport
|December 11, 2024
Summary
Tripartite motif 37 (TRIM37) knockdown protected against ischemic stroke by regulating the PPARγ/NF-κB pathway. This suggests TRIM37 is a potential therapeutic target for improving brain injury.
Area of Science:
- Neuroscience
- Molecular Biology
- Pathology
Background:
- Ischemic stroke is a leading cause of death and disability globally.
- Tripartite motif 37 (TRIM37) is involved in various cellular functions.
- The role of TRIM37 in ischemic stroke progression remains unclear.
Purpose of the Study:
- To investigate the impact of TRIM37 on ischemic stroke development.
- To elucidate the underlying molecular mechanisms involving TRIM37 in ischemic stroke.
Main Methods:
- Primary rat brain microvascular endothelial cells (BMECs) subjected to oxygen-glucose deprivation/reoxygenation (OGD/R).
- TRIM37 knockdown or overexpression using shRNA and plasmid vectors.
- In vivo middle cerebral artery occlusion (MCAO) model in rats.
Main Results:
- OGD/R increased TRIM37 expression, cell permeability, inflammation (TNF-α, ICAM-1), and altered NF-κB and PPARγ expression.
- TRIM37 knockdown reversed OGD/R-induced damage and inflammation by modulating the PPARγ/NF-κB pathway.
- TRIM37 interacted with PPARγ, promoting its ubiquitination; PPARγ agonist reversed TRIM37 overexpression effects.
Conclusions:
- TRIM37 knockdown mitigates ischemic stroke injury by regulating the PPARγ/NF-κB pathway and inflammatory response.
- TRIM37 emerges as a potential therapeutic target for treating ischemic stroke.
- Targeting TRIM37 may offer a novel strategy to improve outcomes in ischemic stroke patients.
