Abstract
This article reviews the wealth of papers dealing with the different effects of epidermal growth factor (EGF) on oligodendrocytes, astrocytes, neurons, and neural stem cells (NSCs). EGF induces the in vitro and in vivo proliferation of NSCs, their migration, and their differentiation towards the neuroglial cell line. It interacts with extracellular matrix components. NSCs are distributed in different CNS areas, serve as a reservoir of multipotent cells, and may be increased during CNS demyelinating diseases. EGF has pleiotropic differentiative and proliferative effects on the main CNS cell types, particularly oligodendrocytes and their precursors, and astrocytes. EGF mediates the in vivo myelinotrophic effect of cobalamin on the CNS, and modulates the synthesis and levels of CNS normal prions (PrPCs), both of which are indispensable for myelinogenesis and myelin maintenance. EGF levels are significantly lower in the cerebrospinal fluid and spinal cord of patients with multiple sclerosis (MS), which probably explains remyelination failure, also because of the EGF marginal role in immunology. When repeatedly administered, EGF protects mouse spinal cord from demyelination in various experimental models of autoimmune encephalomyelitis. It would be worth further investigating the role of EGF in the pathogenesis of MS because of its multifarious effects.
Highlights
Introduction and Historical BenchmarksEpidermal growth factor (EGF) was first isolated from mouse submaxillary glands (Cohen 1962)
The traditional neuropathological view of the multiple sclerosis (MS) pathogenesis highlights the role of central nervous system (CNS) myelin loss, because it leads to the impaired propagation of action potentials across the areas of demyelinated axons and is the major cause of neurological disability
If MS demyelination is likely caused by a local deficiency in myelinotrophic molecules combined with a local ODC paucity, a local ODC differentiation block, and a local excess of remyelination-impeding agents, it is of primary importance to redress this imbalance by stimulating the search for a means of remyelination: findings showing epidermal growth factor (EGF), NRG, and P rPC-deficiency in MS spinal cord (SC) support this need (Viehover et al 2001; Scalabrino et al 2010, 2015)
Summary
Epidermal growth factor (EGF) was first isolated from mouse submaxillary glands (Cohen 1962). In relation to the central nervous system (CNS), the first demonstration of the EGF presence in human cerebrospinal fluid (CSF) was in 1982 (Hirata et al 1982), the first evidence of EGF crossreacting material in rat brain was provided in 1984 (Fallon et al 1984), and the presence of EGF mRNA in the mouse brainstem and striatum was shown in 1992 (Lazar and Blum 1992). The importance of EGF in CNS development and preservation is clearly shown by the fact that EGFmRNA and the membrane-bound EGF receptors (EGFRs) appear very early in mouse embryonic brain and remain in. The picture is further complicated by the fact that EGF is produced by glial cells of the enteric nervous system (Gulbransen and Sharkey 2012)
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