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miR-155 Is Essential for Inflammation-Induced Hippocampal Neurogenic Dysfunction.
Maya E Woodbury1, Robert W Freilich2, Christopher J Cheng3
1Department of Pharmacology and Experimental Therapeutics and Graduate Program in Neuroscience, Boston University, Boston, Massachusetts 02118, and.
Summary
MicroRNA-155 (miR-155) drives inflammation-induced neurogenesis deficits by activating microglia and inducing IL6. Inhibiting miR-155 or IL6 restores normal neural development.
Area of Science:
- Neuroscience
- Immunology
- Developmental Biology
Background:
- Inflammation impacts neurogenesis, but mechanisms are unclear.
- MicroRNAs (miRs) regulate inflammatory and neural processes.
- miR-155 is upregulated in microglia during inflammation.
Purpose of the Study:
- Investigate miR-155's role in inflammation-induced neurogenesis deficits.
- Elucidate miR-155's mechanism in microglial activation and IL6 induction.
- Determine miR-155's sufficiency in disrupting hippocampal development.
Main Methods:
- In vitro studies using lipopolysaccharide (LPS)-stimulated microglia and neural stem cells (NSCs).
- Genetic manipulation: miR-155 knockout mice and transgenic mice with elevated miR-155.
- In vivo assessments of neurogenesis, microglial activation, and hippocampal morphology.
Main Results:
- miR-155 is crucial for LPS-induced IL6 production in microglia.
- Microglial activation and IL6 mediate inflammation-induced neurogenic deficits.
- miR-155 knockout reversed LPS-induced neurogenic deficits and microglial activation.
- Elevated miR-155 in stem cells disrupted hippocampal development, increasing proliferation and causing ectopic neuron/glia localization.
Conclusions:
- miR-155 is essential for inflammation-induced neurogenic deficits via microglial IL6 induction.
- miR-155 dysregulation is sufficient to disrupt normal hippocampal development.
- Targeting miR-155 may offer therapeutic potential for neuroinflammatory conditions.
