Abstract | BACKGROUND: METHODS AND RESULTS: The MCAO rats exhibited reduced body weight and motor ability, while increased neurological deficits and brain infarct volume. Gene ontology (GO) enrichment and KEGG pathway analyses revealed that differentially expressed genes were mainly enriched in the TLR4/NF-κB signaling. Moreover, ATF3 was the most differentially expressed gene in brain tissues of MCAO rats versus sham-operated rats, which could bind to CCL2. ATF3 was reduced in MCAO rats, and ATF3 inhibited CCL2 expression to mediate the TLR4/NF-κB signaling. Functionally, ATF3 inhibited neuronal apoptosis, microglia activation, and pro-inflammatory cytokine production to alleviate brain injury in rats. By contrast, CCL2 was overexpressed in neurons and microglia, and CCL2 mitigated the effects of ATF3 to exacerbate brain injury in rats. CONCLUSION: Our findings suggested that ATF3 repressed neuronal apoptosis and microglia activation caused by cerebral ischemia via targeting CCL2 and mediating the TLR4/NF-κB signaling.
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Authors | Na Ma, Gaixia Li, Xiuxin Fu |
Journal | Brain and behavior
(Brain Behav)
Vol. 12
Issue 4
Pg. e2522
(04 2022)
ISSN: 2162-3279 [Electronic] United States |
PMID | 35263513
(Publication Type: Journal Article)
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Copyright | © 2022 The Authors. Brain and Behavior published by Wiley Periodicals LLC. |
Chemical References |
- Activating Transcription Factor 3
- Cyclic AMP Response Element-Binding Protein
- NF-kappa B
- Toll-Like Receptor 4
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Topics |
- Activating Transcription Factor 3
(metabolism)
- Animals
- Brain Injuries
(metabolism)
- Brain Ischemia
(metabolism)
- Cyclic AMP Response Element-Binding Protein
(metabolism)
- Infarction, Middle Cerebral Artery
(metabolism)
- NF-kappa B
(metabolism)
- Neurons
(metabolism)
- Rats
- Rats, Sprague-Dawley
- Toll-Like Receptor 4
(metabolism)
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