The Insulin-like Growth Factor-I Receptor and the Central Nervous System: Mechanisms Involved in the Prevention of Apoptosis
Apoptosis or programmed cell death is an essential element in the regulation and behavior of mammalian cells [1, 2]. The process is a genetically controlled response for cells to commit suicide and is orchestrated by mechanisms involving various proteins. The purpose of apoptosis is to kill unwanted cells. This process is important in the developing nervous system where a large excess of redundant neurons die off during the period when synapses are being formed between the neurons and their target cells [3, 4]. Apparently, the surviving neurons represent those that receive survival signals from the target cells. Apoptosis is also important in the nervous system following injury. Traumatic injury to the nervous system initially causes necrosis at the injury site, followed by secondary processes which cause spreading of the damage beyond this initial site of damage . This secondary event is apoptosis, and occurs hours after the initial injury. Following spinal cord injury, for example, the apoptotic cells were found to be oligodendrocytes in the spinal white matter as well as in the fiber tracts, which became demyelinated as a result of apoptosis. The process of apoptosis in this model apparently occurs secondary to the release of cytokines such as tumor necrosis factor and certain interleukins. In a separate study of hypoxic-ischemic injury to the brain in rats, insulin-like growth factor-I (IGF-I) was protective against neuronal cell death .
KeywordsSpinal Cord Injury PC12 Cell Nerve Growth Factor p70S6 Kinase Differentiate PC12 Cell
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