PMID- 9282919
OWN - NLM
STAT- MEDLINE
DCOM- 19970925
LR  - 20190630
IS  - 0022-3042 (Print)
IS  - 0022-3042 (Linking)
VI  - 69
IP  - 3
DP  - 1997 Sep
TI  - Beta-amyloid-induced neurotoxicity of a hybrid septal cell line associated with 
      increased tau phosphorylation and expression of beta-amyloid precursor protein.
PG  - 978-85
AB  - Recent evidence suggests that beta-amyloid peptide (beta-AP) may induce tau 
      protein phosphorylation, resulting in loss of microtubule binding capacity and 
      formation of paired helical filaments. The mechanism by which beta-AP increases 
      tau phosphorylation, however, is unclear. Using a hybrid septal cell line, SN56, 
      we demonstrate that aggregated beta-AP(1-40) treatment caused cell injury. 
      Accompanying the cell injury, the levels of phosphorylated tau as well as total 
      tau were enhanced as detected immunochemically by AT8, PHF-1, Tau-1, and Tau-5 
      antibodies. Alkaline phosphatase treatment abolished AT8 and PHF-1 
      immunoreactivity, confirming that the tau phosphorylation sites were at least at 
      Ser(199/202) and Ser396. In association with the increase in tau phosphorylation, 
      the immunoreactivity of cell-associated and secreted beta-amyloid precursor 
      protein (beta-APP) was markedly elevated. Application of antisense 
      oligonucleotide to beta-APP reduced expression of beta-APP and immunoreactivity 
      of phosphorylated tau. Control peptide beta-AP(1-28) did not produce significant 
      effects on tau phosphorylation, although it slightly increased cell-associated 
      beta-APP. These results suggest that betaAP(1-40)-induced tau phosphorylation may 
      be associated with increased beta-APP expression in degenerated neurons.
FAU - Le, W D
AU  - Le WD
AD  - Department of Neurology, Baylor College of Medicine, Houston, Texas 77030, U.S.A.
FAU - Xie, W J
AU  - Xie WJ
FAU - Kong, R
AU  - Kong R
FAU - Appel, S H
AU  - Appel SH
LA  - eng
GR  - AG08664/AG/NIA NIH HHS/United States
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - England
TA  - J Neurochem
JT  - Journal of neurochemistry
JID - 2985190R
RN  - 0 (Amyloid beta-Peptides)
RN  - 0 (Amyloid beta-Protein Precursor)
RN  - 0 (Neurotoxins)
RN  - 0 (Oligonucleotides, Antisense)
RN  - 0 (Peptide Fragments)
RN  - 0 (amyloid beta-protein (1-28))
RN  - 0 (amyloid beta-protein (1-40))
RN  - 0 (tau Proteins)
RN  - EC 3.1.3.1 (Alkaline Phosphatase)
SB  - IM
MH  - Alkaline Phosphatase/pharmacology
MH  - Amyloid beta-Peptides/*toxicity
MH  - Amyloid beta-Protein Precursor/*biosynthesis
MH  - Animals
MH  - Cell Survival/*drug effects
MH  - Hybrid Cells
MH  - Mice
MH  - Nerve Degeneration/drug effects
MH  - Neuroblastoma
MH  - *Neurotoxins
MH  - Oligonucleotides, Antisense/pharmacology
MH  - Peptide Fragments/*toxicity
MH  - Phosphorylation
MH  - tau Proteins/*metabolism
EDAT- 1997/09/01 00:00
MHDA- 1997/09/01 00:01
CRDT- 1997/09/01 00:00
PHST- 1997/09/01 00:00 [pubmed]
PHST- 1997/09/01 00:01 [medline]
PHST- 1997/09/01 00:00 [entrez]
AID - 10.1046/j.1471-4159.1997.69030978.x [doi]
PST - ppublish
SO  - J Neurochem. 1997 Sep;69(3):978-85. doi: 10.1046/j.1471-4159.1997.69030978.x.