Kazanis, E., Filippidou, H., Stylianopoulou, F. and Kazanis, I. 2001. Molecular mechanisms involved in the response of brain tissue to trauma molecular mechanisms involved in the response of brain tissue to trauma. Archives of Hellenic Medicine. 18 (4), pp. 363-374.
| Title | Molecular mechanisms involved in the response of brain tissue to trauma molecular mechanisms involved in the response of brain tissue to trauma |
|---|---|
| Type | Journal article |
| Authors | Kazanis, E., Filippidou, H., Stylianopoulou, F. and Kazanis, I. |
| Abstract | OBJECTIVE: Brain trauma is a major medical problem. It is a primary cause of death, and in the event of survival it leads to long-term ill-health, as well as social and economic problems. The elucidation of the molecular mechanisms involved in the destruction of brain tissue after trauma and in the induction of permanent changes in brain function is necessary for the development of rational therapeutic approaches. METHOD: A model of focal, mechanical, penetrating injury was employed in adult rats. In this model the expression of certain proteins was studied in order to investigate the response of the brain tissue to trauma. The expression of Heat-shock protein-70 (Hsp-70), Brain-Derived Neurotrophic Factor (BDNF), Neurotrophin-3 (NT-3), the astrocytic marker Glial Fibrillary Acidic Protein (GFAP) and Insulin-like Growth Factor-I (IGF-I) were studied immunohistochemically. The occurrence of apoptotic cell death was investigated by the TUNEL reaction. In addition, IGF-I was administered to the injured rats and its neuroprotective properties were determined. RESULTS: 4 and 12 hours after the injury, an increase in Hsp-70 expression, limited induction of IGF-I and activation of astroglia around the core of the injury were observed. Neurotrophin expression was severely reduced in a restricted peritraumatic zone and scattered apoptotic cells were detected, mainly in the injured hemisphere but to a lesser degree in the contralateral hemisphere. One week later, an astroglial scar had been formed at the site of the injury and Hsp-70 expression was limited. BDNF levels remained low, while the reduction in NT-3 was no longer visible. IGF-I expression as well as the number of apoptotic cells were further increased. The local administration of IGF-I following the injury restored the normal tissue patterns to a significant degree, as evidenced by the maintenance of normal neurotrophin expression and the reduction of the apoptosis in the injured hemisphere. CONCLUSIONS: Focal mechanical injury of the brain induces significant local changes in BDNF, NT-3 and IGF-I expression, which remain detectable at least one week after the injury. With time, degenerative cellular phenomena, as reflected by Hsp-70 expression and apoptotic cell death, spread beyond the site of tissue damage. Administration of IGF-I after the injury reverses some of these phenomena and is able to help maintain homeostasis of the brain tissue. |
| Journal | Archives of Hellenic Medicine |
| Journal citation | 18 (4), pp. 363-374 |
| ISSN | 1105-3992 |
| Year | 2001 |
| Publisher | Athens Medical Society |
| Web address (URL) | https://www.mednet.gr/archives/2001-4/363abs.html |
| Publication dates | |
| Published | 2001 |
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Giannakopoulou, M., Mansour, M., Kazanis, E., Bozas, E., Philpipidis, H., Stylianopoulou, F. and Kazanis, I. 2000. NMDA receptor mediated changes in IGF-II gene expression in the rat brain after injury and the possible role of nitric oxide. Neuropathology and Applied Neurobiology. 26 (6), pp. 513-521. https://doi.org/10.1046/j.0305-1846.2000.00286.x
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