PMID- 22766501
OWN - NLM
STAT- MEDLINE
DCOM- 20121119
LR  - 20161125
IS  - 1090-2104 (Electronic)
IS  - 0006-291X (Linking)
VI  - 424
IP  - 3
DP  - 2012 Aug 3
TI  - Deletion of microsomal prostaglandin E synthase-1 protects neuronal cells from 
      cytotoxic effects of beta-amyloid peptide fragment 31-35.
PG  - 409-13
LID - 10.1016/j.bbrc.2012.06.121 [doi]
AB  - Epidemiological studies have suggested that the long-term use of nonsteroidal 
      anti-inflammatory drugs that inhibit cyclooxygenase (COX) activity moderates the 
      onset or progression of Alzheimer's disease (AD). Thus it has been suggested that 
      prostaglandin E(2) (PGE(2)), a major end-product of COX, may play a pathogenic 
      role in AD, but the involvement of PGE synthase (PGES), a terminal enzyme 
      downstream from COX, has not been fully elucidated. To examine the involvement in 
      AD pathology of microsomal PGES-1 (mPGES-1), a PGES enzyme, we here prepared 
      primary cerebral neuronal cells from the cerebri of wild-type and 
      mPGES-1-deficient mice and then treated them with beta-amyloid (Abeta) fragment 31-35 
      (Abeta(31-35)), which represents the shortest sequence of native Abeta peptide required 
      for neurotoxicity. Treatment of wild-type neuronal cells with Abeta(31-35) induced 
      mPGES-1 gene expression and PGE(2) production, followed by significant apoptotic 
      cell death, but apoptosis was not induced in mPGES-1-deficient cells. 
      Furthermore, the combined treatment of Abeta(31-35) and PGE(2) induced apoptosis in 
      mPGES-1-deficient neuronal cells. These results indicated that mPGES-1 is induced 
      during Abeta-mediated neuronal cell death and is involved in Abeta-induced 
      neurotoxicity associated with AD pathology.
CI  - Copyright (c) 2012 Elsevier Inc. All rights reserved.
FAU - Kuroki, Yukiko
AU  - Kuroki Y
AD  - Department of Health Chemistry, School of Pharmacy, Showa University, Tokyo 
      142-8555, Japan.
FAU - Sasaki, Yuka
AU  - Sasaki Y
FAU - Kamei, Daisuke
AU  - Kamei D
FAU - Akitake, Yoshiharu
AU  - Akitake Y
FAU - Takahashi, Mitsuo
AU  - Takahashi M
FAU - Uematsu, Satoshi
AU  - Uematsu S
FAU - Akira, Shizuo
AU  - Akira S
FAU - Nakatani, Yoshihito
AU  - Nakatani Y
FAU - Kudo, Ichiro
AU  - Kudo I
FAU - Hara, Shuntaro
AU  - Hara S
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20120702
PL  - United States
TA  - Biochem Biophys Res Commun
JT  - Biochemical and biophysical research communications
JID - 0372516
RN  - 0 (Amyloid beta-Peptides)
RN  - 0 (Peptide Fragments)
RN  - EC 5.3.- (Intramolecular Oxidoreductases)
RN  - EC 5.3.99.3 (Prostaglandin-E Synthases)
RN  - EC 5.3.99.3 (Ptges protein, mouse)
SB  - IM
MH  - Alzheimer Disease/*genetics/pathology
MH  - Amyloid beta-Peptides/*metabolism/toxicity
MH  - Animals
MH  - Apoptosis
MH  - Cells, Cultured
MH  - Gene Deletion
MH  - Intramolecular Oxidoreductases/*genetics
MH  - Mice
MH  - Microsomes/enzymology
MH  - Neurons/drug effects/metabolism/pathology
MH  - Peptide Fragments/*metabolism/toxicity
MH  - Prostaglandin-E Synthases
EDAT- 2012/07/07 06:00
MHDA- 2012/12/10 06:00
CRDT- 2012/07/07 06:00
PHST- 2012/06/15 00:00 [received]
PHST- 2012/06/24 00:00 [accepted]
PHST- 2012/07/07 06:00 [entrez]
PHST- 2012/07/07 06:00 [pubmed]
PHST- 2012/12/10 06:00 [medline]
AID - S0006-291X(12)01223-5 [pii]
AID - 10.1016/j.bbrc.2012.06.121 [doi]
PST - ppublish
SO  - Biochem Biophys Res Commun. 2012 Aug 3;424(3):409-13. doi: 
      10.1016/j.bbrc.2012.06.121. Epub 2012 Jul 2.