Research Reports - Increased expression of ferritin in cerebral cortex after human traumatic brain injury

Neurol Sci. 2013 Jul;34(7):1173-80

Liu HD, Li W, Chen ZR, Zhou ML, Zhuang Z, Zhang DD, Zhu L, Hang CH

Despite numerous researches and improvements in the past few years, the precise
mechanisms underlying secondary brain injury after trauma remain obscure. Iron is
essential for almost all types of cells, including nerve cells. However, excess
of iron has been proved to contribute to the brain injury following trauma in
animal models. As a key iron-handling protein in the brain, ferritin might be
involved in iron-induced pathophysiological process of various brain disorders.
Therefore, the current study was aimed to investigate the expression of ferritin
in the human contused brain. Nineteen contused brain samples were obtained from
19 patients undergoing surgery for brain contusions 3 h-17 d after trauma, and
three normal temporal pole samples from 3 patients with petroclival meningioma
were collected as controls. Expression of ferritin-H-chain was measured by
quantitative real-time polymerase chain reaction (PCR), western blot and
immunohistochemistry, respectively. Perl's reaction was taken for iron staining.
The results showed that human traumatic brain injury (TBI) could up-regulate
ferritin-H-chain in pericontusional cortex. A marked increase of ferritin was
detected in the early group (≤12 h), and remained elevated for a long time till
after 48 h post-injury. The location of ferritin-H-chain was found mainly at the
neuron-like cells and seldom at glia-like cells. Perl's reaction showed that most
of the iron-positive cells were glia-like cells. These findings suggested that
iron and ferritin might be involved in the secondary brain injury and could be
therapeutic targets for patients with TBI.

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