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ILF3 downregulation by circMETTL9: Effect on traumatic brain injury-induced neuroinflammation
Lulu Sun1, Hao Huang2, Yonglin Hu3
1Department of Rehabilitation Medicine, Affiliated Hospital of Nantong University, Nantong 226001, Jiangsu, China.
Abstract:
Neuroinflammation is a pivotal component of the cascade of reactions that follow traumatic brain injury (TBI). Our previous reports have identified circular RNA METTL9 (circMETTL9) as a modulator of neuroinflammation following TBI. Further, interleukin enhancer binding factor 3 (ILF3) was identified as the most likely protein bound by circMETTL9, resulting in neuroinflammation. However, following TBI the precise role ILF3 and the regulatory pathways involved in neuroinflammation and neurological dysfunction are unknown. In this study, ILF3 expression was shown to be significantly reduced in injured brain cortices and in astrocytes. Overexpression of ILF3 improved neurological function and reduced neuronal apoptosis post-TBI. Mechanically, circMETTL9 was found to bind directly to ILF3, subsequently decreasing ILF3 levels. Reduced ILF3 levels led to the activation of p38 MAPK and increased levels of the chemokines CCL2, CCL3, CXCL1, and CXCL3 in astrocytes. Collectively, ILF3 may be a promising therapeutic target for post-TBI intervention.
Insights
Circular RNA METTL9 (circMETTL9) exacerbates neuroinflammation after traumatic brain injury (TBI) by reducing interleukin enhancer binding factor 3 (ILF3). Restoring ILF3 levels offers a potential therapeutic strategy for TBI recovery.
Area of Science:
- Neuroscience
- Molecular Biology
- Immunology
Background:
- Neuroinflammation is a key factor in traumatic brain injury (TBI) pathology.
- Circular RNA METTL9 (circMETTL9) has been implicated in modulating neuroinflammation post-TBI.
- Interleukin enhancer binding factor 3 (ILF3) is a potential binding protein for circMETTL9.
Purpose of the Study:
- To elucidate the role of ILF3 in neuroinflammation and neurological dysfunction following TBI.
- To investigate the regulatory pathways influenced by ILF3 in the context of TBI.
- To determine the therapeutic potential of targeting ILF3 for TBI intervention.
Main Methods:
- Analysis of ILF3 expression in injured brain cortices and astrocytes post-TBI.
- Overexpression of ILF3 to assess its impact on neurological function and neuronal apoptosis.
- Investigation of the interaction between circMETTL9 and ILF3 using molecular binding assays.
- Assessment of downstream signaling pathways, including p38 MAPK, and chemokine levels (CCL2, CCL3, CXCL1, CXCL3) in astrocytes.
Main Results:
- ILF3 expression was significantly reduced in injured brain tissues and astrocytes after TBI.
- Overexpression of ILF3 demonstrated neuroprotective effects, improving neurological function and reducing neuronal apoptosis.
- circMETTL9 directly binds to ILF3, leading to decreased ILF3 levels.
- Reduced ILF3 levels activate the p38 MAPK pathway and increase pro-inflammatory chemokine expression in astrocytes.
Conclusions:
- ILF3 plays a critical role in mitigating neuroinflammation and neurological deficits post-TBI.
- The circMETTL9/ILF3 interaction represents a novel regulatory mechanism in TBI-induced neuroinflammation.
- ILF3 emerges as a potential therapeutic target for managing TBI.
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