Oxidative stress has been implicated in a variety of
neurodegenerative diseases such as Alzheimer's disease (AD),
Parkinson's disease (PD) and stroke. Estrogens are gonadal steroid
hormones that have been shown to be neuroprotective against
numerous in vitro and in vivo challenges. Evidence from
epidemiological studies has shown the beneficial effects of
estrogens against cognitive decline and memory loss. Integrins are
cell surface receptors shown to have an important role in neural
development and synaptic plasticity. This study hypothesized
integrins to be one of the molecular targets for estrogen-mediated
effects in the brain. The hypothesis was tested with a set of in
vitro experiments using HT-22 cells and an in vivo study using an
ovariectomized rodent model. In the in vitro study, oxidative
stress induced by H2O2 caused an increase in the expression of
beta1-integrin protein while 17beta-estradiol (E2) treatment along
with H2O2 attenuated the increase in integrin expression. Nanomolar
concentrations of E2 treatment increased the expression of
integrins and showed a time-dependent increase in expression of
integrins in HT-22 cells. In the in vivo study, E2 treatment caused
an increase in the expression of post-synaptic proteins,
post-synaptic density-95 (PSD-95) and N-methyl D-aspartate receptor
subunit 1 (NMDAR1) in hippocampus and no significant differences
were observed in the expression of pre-synaptic protein,
synaptophysin and beta1-integrins. Collectively, H2O2 and
physiological concentrations of E2 affected the expression of
beta1-integrins in vitro but E2 did not have an effect on the
expression of integrins in vivo. Effects of E2 on synaptic proteins
do not appear to be mediated by beta1-integrins.
Proquest, Umi Dissertation Publishing
|Country of origin:
||254 x 203 x 5mm (L x W x T)
||Paperback - Trade
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