The effects of okadaic acid-treated SH-SY5Y cells on microglia activation and phagocytosis
Issued Date
2022-02-01
Resource Type
ISSN
10656995
eISSN
10958355
Scopus ID
2-s2.0-85119015941
Pubmed ID
34748253
Journal Title
Cell Biology International
Volume
46
Issue
2
Start Page
234
End Page
242
Rights Holder(s)
SCOPUS
Bibliographic Citation
Cell Biology International Vol.46 No.2 (2022) , 234-242
Suggested Citation
Amonruttanapun P., Chongthammakun S., Chamniansawat S. The effects of okadaic acid-treated SH-SY5Y cells on microglia activation and phagocytosis. Cell Biology International Vol.46 No.2 (2022) , 234-242. 242. doi:10.1002/cbin.11722 Retrieved from: https://repository.li.mahidol.ac.th/handle/20.500.14594/83851
Title
The effects of okadaic acid-treated SH-SY5Y cells on microglia activation and phagocytosis
Author's Affiliation
Other Contributor(s)
Abstract
The activation of microglia is found to be associated with neurodegenerative disorders including Alzheimer's disease (AD). Several studies have shown that okadaic acid (OA) induced deposition of tau hyperphosphorylation, and subsequent neuronal degeneration, loss of synapses, and memory impairment, all of which resemble the pathology of AD. Although OA is a powerful tool available for mechanisms of the neurotoxicity associated with AD, the exact mechanism underlying the activation of microglial cells remains unrevealed. The aim of this study was to determine the effect of both OA and OA-treated neuroblastoma SH-SY5Y cells on microglial HAPI cell viability, activation, and phagocytosis. The results showed that both OA and OA-treated neurons did not induce any detectable cytotoxicity of microglial cells. Furthermore, incubation with OA-treated SH-SY5Y cells could increase the expression of ionized calcium-binding adapter molecule 1 (Iba1) on microglial HAPI cells. This result indicated that OA may induce microglial activation through the toxicity of neurons. Moreover, we also demonstrated that OA-treated SH-SY5Y cells were engulfed by CD11b/c-labeled microglial HAPI cells, which were abolished after treatment with 10 mM O-phospho- l-serine (L-SOP) for 30 min before co-culture with OA-treated SH-SY5Y cells, indicating cells experiencing phagocytic activity. We also confirmed that OA treatment for 24 h significantly increased tau hyperphosphorylation at S396 in SH-SY5Y cells. In conclusion, our findings indicate that OA is a potential toxic inducer underlying the role of microglia in AD pathogenesis.
