PMID- 29305263
OWN - NLM
STAT- MEDLINE
DCOM- 20180222
LR  - 20180222
IS  - 1090-2104 (Electronic)
IS  - 0006-291X (Linking)
VI  - 495
IP  - 4
DP  - 2018 Jan 22
TI  - S-adenosylmethionine reduces the inhibitory effect of Abeta on BDNF expression 
      through decreasing methylation level of BDNF exon Ⅳ in rats.
PG  - 2609-2615
LID - S0006-291X(17)32578-0 [pii]
LID - 10.1016/j.bbrc.2017.12.166 [doi]
AB  - The structure of brain-derived neurotrophic factor (BDNF) gene is complex, which 
      is composed of eight non-coding exons and one coding exon, each of them has its 
      own unique promoter. Multiple BDNF transcripts have distinct functional 
      properties and epigenetic modulation of BDNF gene transcription is implicated in 
      the neurological disorders. In the present study, rat models with amyloid-beta (Abeta) 
      intrahippocampal injection and PC12 cells were used to explore the role of DNA 
      methylation in the promoters of BDNF exon Ⅳ and exon Ⅵ in BDNF suppression caused 
      by Abeta. We found that Abeta inhibited BDNF expression accompanying with 
      hypermethylation in BDNF exon Ⅳ promoter, meanwhile, S-adenosylmethionine (SAM), 
      primary methyl donor, reversed the low BDNF expression through demethylation in 
      BDNF exon Ⅳ promoter. No methylation change was observed in BDNF exon Ⅵ promoter. 
      The alteration of DNA methylation caused by Abeta or SAM was mediated by DNA 
      methyltransferase 3A (DNMT3A). These data suggest that methylation change in BDNF 
      exon Ⅳ is involved in the regulation of BDNF expression by Abeta or SAM, and further 
      support the view of specific epigenetic modifications of a certain BDNF gene 
      transcript.
CI  - Copyright (c) 2018 Elsevier Inc. All rights reserved.
FAU - Cao, Dandan
AU  - Cao D
AD  - Department of Pathology, Capital Medical University, Beijing 100069, China.
FAU - Cui, Jing
AU  - Cui J
AD  - Department of Pathology, Capital Medical University, Beijing 100069, China.
FAU - Cao, Dandan
AU  - Cao D
AD  - Department of Pathology, Capital Medical University, Beijing 100069, China.
FAU - Guo, Chenjia
AU  - Guo C
AD  - Department of Pathology, Capital Medical University, Beijing 100069, China.
FAU - Min, Guowen
AU  - Min G
AD  - Department of Pathology, Capital Medical University, Beijing 100069, China.
FAU - Liu, Min
AU  - Liu M
AD  - Department of Pathology, Capital Medical University, Beijing 100069, China.
FAU - Li, Liang
AU  - Li L
AD  - Department of Pathology, Capital Medical University, Beijing 100069, China. 
      Electronic address: liliang8698@yeah.net.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20180102
PL  - United States
TA  - Biochem Biophys Res Commun
JT  - Biochemical and biophysical research communications
JID - 0372516
RN  - 0 (Amyloid beta-Peptides)
RN  - 0 (Brain-Derived Neurotrophic Factor)
RN  - 7LP2MPO46S (S-Adenosylmethionine)
SB  - IM
MH  - Amyloid beta-Peptides/genetics/*metabolism
MH  - Animals
MH  - Brain-Derived Neurotrophic Factor/*genetics/*metabolism
MH  - DNA Methylation/genetics
MH  - Exons/*genetics
MH  - Gene Expression Regulation/genetics
MH  - Hippocampus/*metabolism
MH  - Male
MH  - Rats
MH  - Rats, Sprague-Dawley
MH  - S-Adenosylmethionine/*metabolism
OTO - NOTNLM
OT  - Amyloid-beta
OT  - Brain-derived neurotrophic factor
OT  - DNA methylation
OT  - Rat
OT  - S-adenosylmethionine
EDAT- 2018/01/07 06:00
MHDA- 2018/02/23 06:00
CRDT- 2018/01/07 06:00
PHST- 2017/12/23 00:00 [received]
PHST- 2017/12/30 00:00 [accepted]
PHST- 2018/01/07 06:00 [pubmed]
PHST- 2018/02/23 06:00 [medline]
PHST- 2018/01/07 06:00 [entrez]
AID - S0006-291X(17)32578-0 [pii]
AID - 10.1016/j.bbrc.2017.12.166 [doi]
PST - ppublish
SO  - Biochem Biophys Res Commun. 2018 Jan 22;495(4):2609-2615. doi: 
      10.1016/j.bbrc.2017.12.166. Epub 2018 Jan 2.