PMID- 21040763
OWN - NLM
STAT- MEDLINE
DCOM- 20110118
LR  - 20101220
IS  - 1879-3169 (Electronic)
IS  - 0378-4274 (Linking)
VI  - 200
IP  - 1-2
DP  - 2011 Jan 15
TI  - Nonlethal aluminum maltolate can reduce brain-derived neurotrophic factor-induced 
      Arc expression through interrupting the ERK signaling in SH-SY5Y neuroblastoma 
      cells.
PG  - 67-76
LID - 10.1016/j.toxlet.2010.10.016 [doi]
AB  - Although many studies have demonstrated that aluminum (Al) exposure impairs 
      learning and memory, its underlying mechanism is still uncertain. Long-lasting 
      forms of synaptic plasticity that underlie memory are dependent on new protein 
      synthesis. In particular, activity-regulated cytoskeleton-associated protein 
      (Arc) has a versatile role in synaptic plasticity, and its synthesis can be 
      induced by brain-derived neurotrophic factor (BDNF). BDNF-induced Arc expression 
      has been suggested to play a fundamental role in the stabilization of synaptic 
      plasticity. In the present study, the pretreatment of Al(malt)(3) at nonlethal 
      level (200 muM, 24 h) significantly reduced BDNF (10 ng/ml, 1h)-induced Arc 
      expression in SH-SY5Y human neuroblastoma cells. BDNF-induced activation of ERK 
      but not PI3K signaling pathway was interfered with the Al(malt)(3) pretreatment, 
      resulting in the subsequent reduction of BDNF-induced phosphorylation of 4EBP1, 
      p70S6K, and eIF4E. Reduced phospho-4EBP1 and phospho-eIF4E hindered the 
      initiation step of translation, which may lead to a reduction in BDNF-induced Arc 
      expression. However, reduced phospho-p70S6K did not influence the phosphorylation 
      of eEF2K and eEF2, indicating no significant effect on BDNF-enhanced translation 
      elongation. Therefore, even at nonlethal level, Al(malt)(3) pretreatment reduced 
      BDNF-induced Arc expression, which was caused by interrupting the ERK signaling 
      pathway as well as the subsequent translation initiation.
CI  - Copyright (c) 2010 Elsevier Ireland Ltd. All rights reserved.
FAU - Chen, Tsan-Ju
AU  - Chen TJ
AD  - Department of Physiology, College of Medicine, Kaohsiung Medical University, 
      Kaohsiung 807, Taiwan. tsanju@kmu.edu.tw
FAU - Cheng, Hsiu-Min
AU  - Cheng HM
FAU - Wang, Dean-Chuan
AU  - Wang DC
FAU - Hung, Hui-Shan
AU  - Hung HS
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20101030
PL  - Netherlands
TA  - Toxicol Lett
JT  - Toxicology letters
JID - 7709027
RN  - 0 (Brain-Derived Neurotrophic Factor)
RN  - 0 (Cytoskeletal Proteins)
RN  - 0 (Nerve Tissue Proteins)
RN  - 0 (Organometallic Compounds)
RN  - 0 (Pyrones)
RN  - 0 (activity regulated cytoskeletal-associated protein)
RN  - 23058-19-7 (aluminum maltolate)
RN  - EC 2.7.1.- (Phosphatidylinositol 3-Kinases)
RN  - EC 2.7.11.24 (Extracellular Signal-Regulated MAP Kinases)
SB  - IM
MH  - Blotting, Western
MH  - Brain-Derived Neurotrophic Factor/*pharmacology
MH  - Cell Line, Tumor
MH  - Cell Survival/drug effects
MH  - Cytoskeletal Proteins/*biosynthesis
MH  - Extracellular Signal-Regulated MAP Kinases/*drug effects
MH  - Humans
MH  - Nerve Tissue Proteins/*biosynthesis
MH  - Neuroblastoma/*metabolism
MH  - Neuronal Plasticity/drug effects
MH  - Organometallic Compounds/*pharmacology
MH  - Phosphatidylinositol 3-Kinases/drug effects
MH  - Phosphorylation
MH  - Pyrones/*pharmacology
MH  - Signal Transduction/*drug effects
EDAT- 2010/11/03 06:00
MHDA- 2011/01/19 06:00
CRDT- 2010/11/03 06:00
PHST- 2010/07/26 00:00 [received]
PHST- 2010/10/22 00:00 [revised]
PHST- 2010/10/25 00:00 [accepted]
PHST- 2010/11/03 06:00 [entrez]
PHST- 2010/11/03 06:00 [pubmed]
PHST- 2011/01/19 06:00 [medline]
AID - S0378-4274(10)01741-8 [pii]
AID - 10.1016/j.toxlet.2010.10.016 [doi]
PST - ppublish
SO  - Toxicol Lett. 2011 Jan 15;200(1-2):67-76. doi: 10.1016/j.toxlet.2010.10.016. Epub 
      2010 Oct 30.