Activation of peroxisome proliferator-activated receptor-delta attenuates glutamate-induced neurotoxicity in HT22 mouse hippocampal cells
- Authors
- Jin, Hana; Ham, Sun Ah; Kim, Min Young; Woo, Im Sun; Kang, Eun Sil; Hwang, Jung Seok; Lee, Ko-Woon; Kim, Hye Jung; Roh, Gu Seob; Lim, Dae-Seog; Kang, Dawon; Seo, Han Geuk
- Issue Date
- Aug-2012
- Publisher
- WILEY
- Keywords
- calcium; glutamate; HT22 mouse hippocampal cells; peroxisome proliferator-activated receptor-d; ROS
- Citation
- JOURNAL OF NEUROSCIENCE RESEARCH, v.90, no.8, pp.1646 - 1653
- Indexed
- SCIE
SCOPUS
- Journal Title
- JOURNAL OF NEUROSCIENCE RESEARCH
- Volume
- 90
- Number
- 8
- Start Page
- 1646
- End Page
- 1653
- URI
- https://scholarworks.bwise.kr/gnu/handle/sw.gnu/22087
- DOI
- 10.1002/jnr.23053
- ISSN
- 0360-4012
- Abstract
- Glutamate-induced neurotoxicity has been implicated in the pathogenesis of neurodegenerative disorders; however, little is known about the cellular events that underlie neurotoxicity or how to impede these events. This study demonstrates that peroxisome proliferator-activated receptor (PPAR)-d regulates glutamate-induced neurotoxicity in HT22 mouse hippocampal cells. Activation of PPARd by GW501516, a specific ligand, significantly inhibited glutamate-induced cell death and reactive oxygen species (ROS) production in HT22 cells. The siRNA-mediated knockdown of PPARd abrogated the effects of GW501516 in neuronal toxicity and ROS production induced by glutamate. In addition, ligand-activated PPARd reduced the glutamate-induced level of intracellular calcium ions (Ca2+) by modulating the influx of Ca2+ from the extracellular space. Similarly, glutamate-induced cell death and intracellular Ca2+ levels were attenuated in the presence of LY83583, an inhibitor of soluble guanylyl cyclase. Taken together, these results suggest that PPARd plays an important role in glutamate-induced neurotoxicity by modulating oxidative stress and Ca2+ influx. (c) 2012 Wiley Periodicals, Inc.
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