Journal
CELL STRESS & CHAPERONES
Volume 20, Issue 2, Pages 321-331Publisher
SPRINGER
DOI: 10.1007/s12192-014-0552-1
Keywords
BV2 microglia; TLR4; PC12 cell; Lipopolysaccharide; Interleukin-1 beta
Categories
Funding
- National Natural Science of China [81171041]
- Natural Science foundation of Jiangsu Province [BK2011197]
- Key Subject of Colleges and Universities Natural Science Foundation of Jiangsu Province [13KJA320001]
- Natural Science fund for colleges and universities of Jiangsu Province [12KJD320005]
- Innovation Project of Nanjing Military Region [ZD13]
- University Graduate Student Science and Technology Innovation Project of Jiangsu Province [XYYC-1214]
- Qing Lan Project
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Microglia play an important role in neuronal protection and damage. However, the molecular and cellular relationship between microglia and neurons is unclear. We carried out a prospective study to detect that activation of BV2 microglia induced PC12 cell apoptosis in vitro through the TLR4/adapter protein myeloid differentiation factor 88 (MyD88)/nuclear factor-kappa B (NF-kappa B) signaling pathway. BV2 microglia were treated with different concentrations of LPS for 24 h. Western blot was utilized to detect the expression of TLR4 and the downstream signaling pathway. The level of inflammatory mediator was quantified using a specific ELISA kit. The supernatant of 10 mu g/ml LPS-treated BV2 cells was used as conditioned medium (CM). PC12 cells were co-culture with CM for 24 h. Cell viability was determined by MTT assay and cell apoptosis was tested by flow cytometry. BV2 microglia were treated with 10, 20, or 30 mu g/ml LPS for 24 h. The expression of TLR4, MyD88, and NF-kappa B significantly increased. When PC12 cells were co-cultured with CM for 24 h, cell viability decreased. CM up-regulated the Bax level and down-regulated the Bcl-2 protein level in PC12 cells. PC12 cells pretreated with interleukin-1 receptor antagonist (IL-1RA) for 30 min, significantly alleviated CM-induced PC12 cell apoptosis. These results suggest that BV2 microglia activated by LPS triggered TLR4/MyD88/NF-kappa B signaling pathway that induced the release of IL-1 beta and could participate in the PC12 cells injury.
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