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Published on: April 13, 2017
Serum- and glucocorticoid-inducible kinases in microglia
Koichi Inoue1, Eisuke Sakuma2, Hiroyuki Morimoto3
1Department of Integrative Anatomy, Nagoya City University Graduate School of Medical Sciences, Nagoya 467-8601, Japan; Neuroscience Institute, Morehouse School of Medicine, Atlanta, GA 30310, USA.
Abstract:
Microglia are derived from myelogenous cells and contribute to immunological and inflammatory responses in central nervous system. They play important roles not only in infectious diseases and inflammation after stroke, but also in psychiatric diseases such as schizophrenia. While recent studies suggest the significances of serum- and glucocorticoid-inducible kinases (SGKs) in other immune cells such as macrophages, T cells and dendritic cells, their role in microglia remains unknown. Here we, for the first time, report that SGK1 and SGK3 are expressed in multiple microglial cell lines. An SGK inhibitor, gsk650394, inhibits cell viability. In addition, lipopolysaccharide-induced expression of inflammatory regulators iNOS and TNFα was enhanced by gsk650394. Furthermore, translocation of NF-κB was enhanced by gsk650394. Taken together, these findings suggest that SGKs may play an important role in regulating microglial viability and inflammatory responses.
Insights
Serum- and glucocorticoid-inducible kinases (SGKs) are expressed in microglia and influence their inflammatory responses. Inhibiting SGKs can enhance microglial inflammatory activity and NF-κB translocation.
Area of Science:
- Neuroimmunology
- Cellular Immunology
Background:
- Microglia are key immune cells in the central nervous system, involved in inflammation and diseases like schizophrenia.
- Serum- and glucocorticoid-inducible kinases (SGKs) are implicated in immune cell function, but their role in microglia is unexplored.
Purpose of the Study:
- To investigate the expression and function of SGK1 and SGK3 in microglial cells.
- To determine the effect of SGK inhibition on microglial viability and inflammatory responses.
Main Methods:
- Expression analysis of SGK1 and SGK3 in microglial cell lines.
- Treatment with an SGK inhibitor (gsk650394) to assess effects on cell viability.
- Evaluation of lipopolysaccharide-induced inflammatory markers (iNOS, TNFα) and NF-κB translocation.
Main Results:
- SGK1 and SGK3 were found to be expressed in microglial cell lines.
- SGK inhibition reduced microglial cell viability.
- Inhibition of SGKs enhanced lipopolysaccharide-induced expression of iNOS and TNFα.
- SGK inhibition promoted the translocation of NF-κB.
Conclusions:
- SGKs are expressed in microglia and play a role in regulating their viability.
- SGKs appear to modulate microglial inflammatory responses, potentially through the NF-κB pathway.
