Abstract
ARC is a caspase recruitment domain-containing molecule that plays an important role in the regulation of apoptosis. We examined ARC expression during neuronal cell death following ischemic injury in vivo and in vitro. After exposure to transient global ischemic conditions, the expression of ARC was substantially reduced in the CA1 region of hippocampus in a time-dependent manner with concomitant increase of TUNEL-positive cells. Quantitative analysis using Western blotting exhibited that most of ARC protein disappeared in the cultured hippocampal neurons exposed to hypoxia for 12 h and showing 60% cell viability. Forced expression of ARC in the primary cultures of hippocampal neurons or B103 neuronal cells significantly reduced hypoxia-induced cell death. Further, the C-terminal P/E rich region of ARC was effective to attenuate hypoxic insults. These results suggest that down-regulation of ARC expression in hippocampal neurons may contribute to neuronal death induced by ischemia/hypoxia.
| Original language | English (US) |
|---|---|
| Pages (from-to) | 170-173 |
| Number of pages | 4 |
| Journal | FEBS Letters |
| Volume | 543 |
| Issue number | 1-3 |
| DOIs | |
| State | Published - May 22 2003 |
Bibliographical note
Funding Information:Y.-M.H. was partially supported by Brain Korea 21. This work was supported by a grant from the National Research Laboratory program (to Y.-K.J.) and Life Phenomena and Function Research Group Program (2000) of the Ministry of Science and Technology.
Keywords
- Apoptosis repressor with caspase recruitment domain
- Hippocampal neuron
- Hypoxia
- Ischemia
- Rat brain