Potential implication of SGK1-dependent activity change in BV-2 microglial cells
Hayato Asai1, Koichi Inoue1, Eisuke Sakuma1
1Department of Integrative Anatomy, Nagoya City University Graduate School of Medical Sciences Nagoya 467-8601, Japan.
Summary
Serum- and glucocorticoid-inducible kinase 1 (SGK1) inhibits microglial activation. SGK1 deficiency in microglia leads to toxic conversion, suggesting SGK1 as a therapeutic target for CNS inflammation.
Area of Science:
- Neuroscience
- Immunology
- Molecular Biology
Background:
- Microglial activation is implicated in neurological and psychiatric disorders.
- Pathological mechanisms of microglial activation are known, but inhibitory mechanisms are unclear.
- Serum- and glucocorticoid-inducible kinases (SGK1 and SGK3) are expressed in microglia.
Purpose of the Study:
- To elucidate the physiological mechanism that represses microglial activation.
- To investigate the role of SGK1 in microglial activation.
Main Methods:
- Generated a serum- and glucocorticoid-inducible kinase 1 (SGK1)-lacked microglial cell line (BV-2).
- Assessed microglial morphology, CD68 expression, proliferation, and susceptibility to ATP-induced cell death.
Main Results:
- SGK1 deficiency induced toxic conversion in microglia, characterized by amoeboid morphology and increased CD68 expression.
- SGK1-deficient microglia exhibited accelerated proliferation and increased susceptibility to ATP-induced cell death.
- Inhibiting SGK1 enhanced lipopolysaccharide's toxic effect on microglial inflammatory substance production.
Conclusions:
- SGK1 plays a crucial role in inhibiting pathological microglial activation.
- SGK1 represents a potential therapeutic target for central nervous system (CNS) inflammatory disorders.
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