Microglial Activation in Neuroinflammation: Implications for the Etiology of Neurodegeneration

• Published in: Neuro-degenerative diseases Vol. 10; no. 1-4; pp. 100 - 103
• Main Authors: Kaneko, Yoko S., Nakashima, Akira, Mori, Keiji, Nagatsu, Toshiharu, Nagatsu, Ikuko, Ota, Akira
• Format: Journal Article
• Language: English
• Published: Basel, Switzerland S. Karger AG 01.01.2012
• Subjects: Animals; Apoptosis - drug effects; Apoptosis - physiology; bcl-2-Associated X Protein - metabolism; bcl-X Protein - metabolism; Brain - cytology; Caspase 3 - metabolism; Cells, Cultured; Cytokines - metabolism; Lipopolysaccharides - pharmacology; Mice; Microglia - drug effects; Signal Transduction - drug effects; Lipopolysaccharide; Life span; Autophagy; Apoptosis; Microglia
• ISBN: 9783318021721; 3318021725
• ISSN: 1660-2854; 1660-2862
• DOI: 10.1159/000332936

Background: Activated microglia secrete inflammatory cytokines and may play roles in the progression of neurodegenerative diseases. However, the mechanism underlying microglial activation remains unclear. Objective: Our aim was to examine the regulation of activated microglia through their cell death and survival pathways. Methods: We used mouse primary-cultured microglia, which are destined to die within a few days under ordinary culture conditions. The microglia live for longer than 1 month, without any measurable increase in apoptotic or necrotic cell death, when kept activated by sublethal concentrations of lipopolysaccharide (LPS). Results: LPS-treated microglia showed changes in shape. LPS treatment had no effect on the level of the proapoptotic Bcl-2-associated X protein but increased the level of the antiapoptotic protein Bcl-xL at day 1. Furthermore, the level of microtubule-associated light chain 3-II, a marker protein for autophagy, was decreased 3 h after exposure to LPS.Conclusion:An increase in Bcl-xL seems to inhibit both apoptosis and autophagy. Our results suggest that long-lived microglia resulting from exposure to the optimal dose of LPS may play critical roles in the progression of neurodegeneration.