http://www.sciencedirect.com/science/article/pii/S0925443913001312
Abstract
Astrocytes
play a crucial role in proper iron handling within the central nervous
system. This competence can be fundamental, particularly during
neuroinflammation, and neurodegenerative processes, where an increase in
iron content can favour oxidative stress, thereby worsening disease
progression. Under these pathological conditions, astrocytes undergo a
process of activation that confers them either a beneficial or a
detrimental role on neuronal survival.
Our work
investigates the mechanisms of iron entry in cultures of quiescent and
activated hippocampal astrocytes. Our data confirm that the main source
of iron is the non-transferrin-bound iron (NTBI) and show the
involvement of two different routes for its entry: the resident
transient receptor potential (TRP) channels in quiescent astrocytes and
the de novo expressed divalent metal transporter 1 (DMT1) in activated
astrocytes, which accounts for a potentiation of iron entry.
Overall,
our data suggest that at rest, but even more after activation,
astrocytes have the potential to buffer the excess of iron, thereby
protecting neurons from iron overload. These findings further extend our
understanding of the protective role of astrocytes under the conditions
of iron-mediated oxidative stress observed in several neurodegenerative
conditions.
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