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Epigenetic regulation of HDAC1 SUMOylation as an endogenous neuroprotection against Aβ toxicity in a mouse model of Alzheimer's disease.

Abstract Amyloid-β (Aβ) produces neurotoxicity in the brain and causes neuronal death, but the endogenous defense mechanism that is activated on Aβ insult is less well known. Here we found that acute Aβ increases the expression of PIAS1 and Mcl-1 via activation of MAPK/ERK, and Aβ induction of PIAS1 enhances HDAC1 SUMOylation in rat hippocampus. Knockdown of PIAS1 decreases endogenous HDAC1 SUMOylation and blocks Aβ induction of Mcl-1. Sumoylated HDAC1 reduces it association with CREB, increases CREB binding to the Mcl-1 promoter and mediates Aβ induction of Mcl-1 expression. Transduction of SUMO-modified lenti-HDAC1 vector to the hippocampus of APP/PS1 mice rescues spatial learning and memory deficit and long-term potentiation impairment in APP/PS1 mice. It also reduces the amount of amyloid plaque and the number of apoptotic cells in CA1 area of APP/PS1 mice. Meanwhile, HDAC1 SUMOylation decreases HDAC1 binding to the neprilysin promoter. These results together reveal an important role of HDAC1 SUMOylation as a naturally occurring defense mechanism protecting against Aβ toxicity and provide an alternative therapeutic strategy against AD.Cell Death and Differentiation advance online publication, 10 February 2017; doi:10.1038/cdd.2016.161.
PMID
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Authors

Mayor MeshTerms
Keywords
Journal Title cell death and differentiation
Publication Year Start




PMID- 28186506
OWN - NLM
STAT- Publisher
DA  - 20170210
LR  - 20170210
IS  - 1476-5403 (Electronic)
IS  - 1350-9047 (Linking)
DP  - 2017 Feb 10
TI  - Epigenetic regulation of HDAC1 SUMOylation as an endogenous neuroprotection
      against Abeta toxicity in a mouse model of Alzheimer's disease.
LID - 10.1038/cdd.2016.161 [doi]
AB  - Amyloid-beta (Abeta) produces neurotoxicity in the brain and causes neuronal
      death, but the endogenous defense mechanism that is activated on Abeta insult is 
      less well known. Here we found that acute Abeta increases the expression of PIAS1
      and Mcl-1 via activation of MAPK/ERK, and Abeta induction of PIAS1 enhances HDAC1
      SUMOylation in rat hippocampus. Knockdown of PIAS1 decreases endogenous HDAC1
      SUMOylation and blocks Abeta induction of Mcl-1. Sumoylated HDAC1 reduces it
      association with CREB, increases CREB binding to the Mcl-1 promoter and mediates 
      Abeta induction of Mcl-1 expression. Transduction of SUMO-modified lenti-HDAC1
      vector to the hippocampus of APP/PS1 mice rescues spatial learning and memory
      deficit and long-term potentiation impairment in APP/PS1 mice. It also reduces
      the amount of amyloid plaque and the number of apoptotic cells in CA1 area of
      APP/PS1 mice. Meanwhile, HDAC1 SUMOylation decreases HDAC1 binding to the
      neprilysin promoter. These results together reveal an important role of HDAC1
      SUMOylation as a naturally occurring defense mechanism protecting against Abeta
      toxicity and provide an alternative therapeutic strategy against AD.Cell Death
      and Differentiation advance online publication, 10 February 2017;
      doi:10.1038/cdd.2016.161.
FAU - Tao, Chih Chieh
AU  - Tao CC
AD  - Graduate Institute of Life Sciences, National Defense Medical Center, Taipei,
      Taiwan.
FAU - Hsu, Wei Lun
AU  - Hsu WL
AD  - Institute of Biomedical Sciences, Academia Sinica, Taipei, Taiwan.
FAU - Ma, Yun Li
AU  - Ma YL
AD  - Institute of Biomedical Sciences, Academia Sinica, Taipei, Taiwan.
FAU - Cheng, Sin Jhong
AU  - Cheng SJ
AD  - Institute of Biomedical Sciences, Academia Sinica, Taipei, Taiwan.
AD  - Neuroscience Program in Academia Sinica, Taipei, Taiwan.
FAU - Lee, Eminy Hy
AU  - Lee EH
AD  - Graduate Institute of Life Sciences, National Defense Medical Center, Taipei,
      Taiwan.
AD  - Institute of Biomedical Sciences, Academia Sinica, Taipei, Taiwan.
LA  - eng
PT  - Journal Article
DEP - 20170210
PL  - England
TA  - Cell Death Differ
JT  - Cell death and differentiation
JID - 9437445
EDAT- 2017/02/12 06:00
MHDA- 2017/02/12 06:00
CRDT- 2017/02/11 06:00
PHST- 2016/08/18 [received]
PHST- 2016/12/04 [revised]
PHST- 2016/12/13 [accepted]
AID - cdd2016161 [pii]
AID - 10.1038/cdd.2016.161 [doi]
PST - aheadofprint
SO  - Cell Death Differ. 2017 Feb 10. doi: 10.1038/cdd.2016.161.

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