PMID- 29720605
OWN - NLM
STAT- MEDLINE
DCOM- 20191015
LR  - 20231112
IS  - 2045-2322 (Electronic)
IS  - 2045-2322 (Linking)
VI  - 8
IP  - 1
DP  - 2018 May 2
TI  - EAAC1 gene deletion reduces adult hippocampal neurogenesis after transient 
      cerebral ischemia.
PG  - 6903
LID - 10.1038/s41598-018-25191-4 [doi]
LID - 6903
AB  - Several studies have demonstrated that excitatory amino acid carrier-1 (EAAC1) 
      gene deletion exacerbates hippocampal and cortical neuronal death after ischemia. 
      However, presently there are no studies investigating the role of EAAC1 in 
      hippocampal neurogenesis. In this study, we tested the hypothesis that reduced 
      cysteine transport into neurons by EAAC1 knockout negatively affects adult 
      hippocampal neurogenesis under physiological or pathological states. This study 
      used young mice (aged 3-5 months) and aged mice (aged 11-15 months) of either the 
      wild-type (WT) or EAAC1 (-/-) genotype. Ischemia was induced through the 
      occlusion of bilateral common carotid arteries for 30 minutes. Histological 
      analysis was performed at 7 or 30 days after ischemia. We found that both young 
      and aged mice with loss of the EAAC1 displayed unaltered cell proliferation and 
      neuronal differentiation, as compared to age-matched WT mice under ischemia-free 
      conditions. However, neurons generated from EAAC1 (-/-) mice showed poor survival 
      outcomes in both young and aged mice. In addition, deletion of EAAC1 reduced the 
      overall level of neurogenesis, including cell proliferation, differentiation, and 
      survival after ischemia. The present study demonstrates that EAAC1 is important 
      for the survival of newly generated neurons in the adult brain under 
      physiological and pathological conditions. Therefore, this study suggests that 
      EAAC1 plays an essential role in modulating hippocampal neurogenesis.
FAU - Choi, Bo Young
AU  - Choi BY
AD  - Department of Physiology, Hallym University, College of Medicine, Chuncheon, 
      24252, South Korea.
FAU - Won, Seok Joon
AU  - Won SJ
AD  - Department of Neurology, University of California San Francisco and Veterans 
      Affairs Medical Center, San Francisco, CA, 94121, USA.
FAU - Kim, Jin Hee
AU  - Kim JH
AD  - Department of Physiology, Hallym University, College of Medicine, Chuncheon, 
      24252, South Korea.
FAU - Sohn, Min
AU  - Sohn M
AD  - Department of Nursing, Inha University, Incheon, 22212, South Korea.
FAU - Song, Hong Ki
AU  - Song HK
AD  - Department of Neurology, Hallym University, College of Medicine, Chuncheon, 
      24252, South Korea.
FAU - Chung, Tae Nyoung
AU  - Chung TN
AD  - Department of Emergency Medicine, CHA University School of Medicine, Seongnam, 
      13496, South Korea.
FAU - Kim, Tae Yul
AU  - Kim TY
AD  - Department of Physiology, Hallym University, College of Medicine, Chuncheon, 
      24252, South Korea.
FAU - Suh, Sang Won
AU  - Suh SW
AUID- ORCID: 0000-0002-7492-579X
AD  - Department of Physiology, Hallym University, College of Medicine, Chuncheon, 
      24252, South Korea. swsuh@hallym.ac.kr.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20180502
PL  - England
TA  - Sci Rep
JT  - Scientific reports
JID - 101563288
RN  - 0 (Excitatory Amino Acid Transporter 3)
RN  - 0 (Slc1a1 protein, mouse)
SB  - IM
MH  - Animals
MH  - Cell Count
MH  - Cell Differentiation/genetics
MH  - Cell Survival/genetics
MH  - Disease Models, Animal
MH  - Excitatory Amino Acid Transporter 3/*genetics
MH  - *Gene Deletion
MH  - Hippocampus/*blood supply/*metabolism/physiopathology
MH  - Immunohistochemistry
MH  - Ischemic Attack, Transient/*genetics/*metabolism/physiopathology
MH  - Male
MH  - Mice
MH  - Models, Biological
MH  - Neural Stem Cells/cytology/metabolism
MH  - Neurogenesis/*genetics
MH  - Neurons/cytology/metabolism
MH  - Oxidative Stress
PMC - PMC5932005
COIS- The authors declare no competing interests.
EDAT- 2018/05/04 06:00
MHDA- 2019/10/16 06:00
PMCR- 2018/05/02
CRDT- 2018/05/04 06:00
PHST- 2017/09/21 00:00 [received]
PHST- 2018/04/17 00:00 [accepted]
PHST- 2018/05/04 06:00 [entrez]
PHST- 2018/05/04 06:00 [pubmed]
PHST- 2019/10/16 06:00 [medline]
PHST- 2018/05/02 00:00 [pmc-release]
AID - 10.1038/s41598-018-25191-4 [pii]
AID - 25191 [pii]
AID - 10.1038/s41598-018-25191-4 [doi]
PST - epublish
SO  - Sci Rep. 2018 May 2;8(1):6903. doi: 10.1038/s41598-018-25191-4.