PMID- 9413580
OWN - NLM
STAT- MEDLINE
DCOM- 19980129
LR  - 20220223
IS  - 0065-2598 (Print)
IS  - 0065-2598 (Linking)
VI  - 429
DP  - 1997
TI  - Estrogens influence growth, maturation, and amyloid beta-peptide production in 
      neuroblastoma cells and in a beta-APP transfected kidney 293 cell line.
PG  - 261-71
AB  - During development in vivo and in vitro, estrogens: a) increase brain 
      excitability, particularly in limbic structures; b) are responsible for the 
      maturation and cyclicity of limbic-hypothalamic interrelations; c) enhance 
      myelinogenesis; and d) may act with NGF to stimulate neurite formation. In 
      senescence, estrogen administration would improve memory in postmenopausal women. 
      The absence or low levels of estrogens after menopause would increase prevalence 
      of Alzheimer's dementia (AD) more in women than men, irrespective of age or 
      ethnicity. In the present study, addition of 17-beta estradiol to cultured human 
      neuroblastoma cells affected growth slightly, but stimulated cell maturation as 
      shown by increased tyrosine hydroxylase activity. The extracellular deposition in 
      brain tissue and around blood vessels of the amyloid beta-peptide (A beta), a 4.3 
      kD fragment of the larger integral membrane protein, beta-amyloid precursor 
      protein (beta-APP), is considered an important characteristic of AD. We 
      investigated whether 17-beta estradiol may influence the formation of the A beta 
      (thus the abnormal accumulation of amyloid proteins) in neuroblastoma cells and 
      in a beta-APP transfected human kidney 293 cell line. Two doses of 17 
      beta-estradiol were added to the cultures of both cell lines. Cells were grown 
      until confluence, metabolically labeled with 35S-methionine, immunoprecipitated 
      with the rabbit antiserum R1282, gel electrophoresed and autoradiographed in 
      order to compare levels of A beta under the different estradiol concentrations. 
      While in neuroblastoma cells, levels of A beta were only slightly reduced after 
      estradiol and a dose-effect relationship with the hormone could not be 
      demonstrated, in the 293 cells, A beta band intensity decreased as concentration 
      of estradiol increased. These data support the role of estrogen in normal and 
      abnormal brain metabolism and suggest potential hormonal interventions which may 
      reduce or prevent the formation of amyloid deposits occur in AD.
FAU - Chang, D
AU  - Chang D
AD  - Department of Molecular and Cell Biology, University of California, Berkeley 
      94720-3202, USA.
FAU - Kwan, J
AU  - Kwan J
FAU - Timiras, P S
AU  - Timiras PS
LA  - eng
PT  - Journal Article
PL  - United States
TA  - Adv Exp Med Biol
JT  - Advances in experimental medicine and biology
JID - 0121103
RN  - 0 (Amyloid beta-Peptides)
RN  - 0 (Amyloid beta-Protein Precursor)
RN  - 4TI98Z838E (Estradiol)
RN  - EC 1.14.16.2 (Tyrosine 3-Monooxygenase)
SB  - IM
MH  - Alzheimer Disease/metabolism
MH  - Amyloid beta-Peptides/metabolism
MH  - Amyloid beta-Protein Precursor/metabolism
MH  - Amyloidosis/metabolism
MH  - Animals
MH  - Brain/drug effects/metabolism
MH  - Cell Line
MH  - Cellular Senescence/drug effects
MH  - Estradiol/*pharmacology
MH  - Female
MH  - Humans
MH  - Kidney/*drug effects
MH  - Male
MH  - Neuroblastoma
MH  - PC12 Cells
MH  - Rats
MH  - *Transfection
MH  - Tumor Cells, Cultured
MH  - Tyrosine 3-Monooxygenase/metabolism
EDAT- 1997/01/01 00:00
MHDA- 1997/12/31 00:01
CRDT- 1997/01/01 00:00
PHST- 1997/01/01 00:00 [pubmed]
PHST- 1997/12/31 00:01 [medline]
PHST- 1997/01/01 00:00 [entrez]
AID - 10.1007/978-1-4757-9551-6_19 [doi]
PST - ppublish
SO  - Adv Exp Med Biol. 1997;429:261-71. doi: 10.1007/978-1-4757-9551-6_19.