Phosphatidylethanolamine-binding protein 1 protects CA1 neurons against ischemic damage via ERK-CREB signaling in Mongolian gerbils
- Authors
- Jung, Hyo Young; Cho, Su Bin; Kim, Woosuk; Yoo, Dae Young; Won, Moo-Ho; Choi, Goang-Min; Cho, Tack-Geun; Kim, Dae Won; Hwang, In Koo; Choi, Soo Young; Moon, Seung Myung
- Issue Date
- Sep-2018
- Publisher
- Elsevier BV
- Keywords
- Phosphatidylethanolamine-binding protein 1; Hippocampus; Gerbil; Oxidative stress; PEP-1 fusion protein; MAPK
- Citation
- Neurochemistry International, v.118, pp 265 - 274
- Pages
- 10
- Journal Title
- Neurochemistry International
- Volume
- 118
- Start Page
- 265
- End Page
- 274
- URI
- https://scholarworks.bwise.kr/sch/handle/2021.sw.sch/5662
- DOI
- 10.1016/j.neuint.2018.05.005
- ISSN
- 0197-0186
1872-9754
- Abstract
- In the present study, we made a PEP-1-phosphatidylethanolamine-binding protein 1 (PEP-1-PEBP1) fusion protein to facilitate the transduction of PEBP1 into cells and observed significant ameliorative effects of PEP-1-PEBP1 against H2O2-induced neuronal damage and the formation of reactive oxygen species in the HT22 hippocampal cells. In addition, administration of PEP-1-PEBP1 fusion protein ameliorated H2O2-induced phosphorylation of extracellular signal-regulated kinases (ERK1/2) and facilitated the phosphorylation of cyclic-AMP response element binding protein (CREB) in HT22 cells after exposure to H2O2. We also investigated the temporal and spatial changes of phosphorylated phosphatidylethanolamine-binding protein 1 (pPEBP1) in the hippocampus, after 5 min of transient forebrain ischemia in gerbils. In the sham-operated animals, pPEBP1 immunoreactivity was not detectable in the hippocampal CA1 region. pPEBP1 immunoreactivity was significantly increased in the hippocampal CA1 region, 1-2 days after ischemia, compared to that in the sham operated group and pPEBP1 immunoreactivity was returned to levels in sham-operated group at 3-4 days after ischemia. pPEBP1 immunoreactivity significantly increased at day 7 after ischemia and decreased to sham operated group levels by day 10 after ischemia/reperfusion. In addition, administration of PEP-1-PEBP1 fusion protein significantly reduced the ischemia-induced hyperactivity of locomotion, 1 day after ischemia and PEP-1-PEBP1 reduced neuronal damage and reactive gliosis (astrocytosis and microgliosis) in the gerbil hippocampal CA1 region, 4 days after ischemia. Administration of PEP-1-PEBP1 fusion protein ameliorated the ischemia-induced phosphorylation of ERK at 3 h and 6 h after ischemia/reperfusion and accelerated the phosphorylation of CREB in ischemic hippocampus at 6 h after ischemia. These results suggest that the increase in PEBP1 phosphorylation causes neuronal damage in the hippocampus and treatment with PEP-1-PEBP1 fusion protein provides neuroprotection from increasing phosphorylation of ERK-CREB pathways in the hippocampal CA1 region, during ischemic damage.
- Files in This Item
- There are no files associated with this item.
- Appears in
Collections - College of Medicine > Department of Anatomy > 1. Journal Articles
![qrcode](https://api.qrserver.com/v1/create-qr-code/?size=55x55&data=https://scholarworks.bwise.kr/sch/handle/2021.sw.sch/5662)
Items in ScholarWorks are protected by copyright, with all rights reserved, unless otherwise indicated.