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BV-2 stimulation by lactacystin results in a strong inflammatory reaction and apoptotic neuronal death in SH-SY5Y cells

Cited 13 time in Web of Science Cited 16 time in Scopus
Authors
Kwon, Seon-Joo; Ahn, Tae-Beom; Yoon, Min-Yung; Jeon, Beom S
Issue Date
2008-03-21
Publisher
Elsevier
Citation
Brain Res. 1205, 116-121
Keywords
Acetylcysteine/*analogs & derivatives/pharmacologyAnimalsAnti-Bacterial Agents/pharmacologyApoptosis/*physiologyCell LineCell SurvivalCulture Media, Conditioned/chemistry/*pharmacologyCysteine Proteinase Inhibitors/*pharmacologyEnzyme Inhibitors/pharmacologyEnzyme-Linked Immunosorbent AssayHumansI-kappa B Proteins/metabolismInflammation/*pathologyMacrophage Activation/physiologyMiceMicroglia/*physiologyMinocycline/pharmacologyNG-Nitroarginine Methyl Ester/pharmacologyNeurons/*physiologyNitric Oxide/metabolismNitric Oxide Synthase Type I/antagonists & inhibitorsProteasome Endopeptidase Complex/genetics
Abstract
Neuroinflammation plays a role in the pathomechanism of many neurodegenerative diseases, including Parkinson disease (PD). Proteasome inhibition has also been known to be involved in the pathology of PD. Recent studies have reported that microglial activation and dopaminergic cell death were observed in in vivo lactacystin-induced models of PD. In the present study, we investigated whether proteasome inhibition had a direct effect on the inflammatory reaction. Lactacystin treatment increased the amount of nitric oxide and tumor necrosis factor alpha (TNF-alpha) in culture media containing murine microglia (BV-2). Neuronal cell death was more pronounced when the culture media containing BV-2 cells (BV-2 conditioned media; BV-2 CM) were harvested and treated with human dopaminergic neurons (SH-SY5Y) than when treated with lactacystin alone. Apoptosis was markedly increased by treatment with BV-2 CM, which could be mitigated by pretreatment with minocycline and N(omega)-nitro-l-arginine methyl ester (L-NAME). These results suggest that proteasome inhibition can directly trigger neuroinflammation, which leads to neuronal death.
ISSN
0006-8993 (Print)
Language
English
URI
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=18353281

http://www.sciencedirect.com/science?_ob=MImg&_imagekey=B6SYR-4RX0755-1-F&_cdi=4841&_user=168665&_orig=search&_coverDate=04%2F18%2F2008&_sk=987949999&view=c&wchp=dGLbVzW-zSkzV&md5=9d5c7e64a4f69be080dd3c2804cec49a&ie=/sdarticle.pdf

http://hdl.handle.net/10371/68425
DOI
https://doi.org/10.1016/j.brainres.2008.02.030
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College of Medicine/School of Medicine (의과대학/대학원)Dept. of Neurology (신경과학교실)Journal Papers (저널논문_신경과학교실)
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