Does Thymosin β4 Enhance Oligodendrogenesis by up-regulating Epidermal Growth Factor Receptor?
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Treatment of neurological injury remains to be an exceedingly difficult task. Current treatments focus on neuroprotection (mitigating immediate damage) and have a small window for delivery in order to be effective. The field of neurorestorative treatments for neurological illnesses has been gaining momentum in modern research. These new therapies focus on reversing the damage caused by neurological injury by treating the intact tissue. The focus of this research is the endogenously present (already inside of you) peptide, Thymosin β4 (Tβ4). Tβ4 is a 43 amino acid peptide involved in multiple healing processes throughout the body. Tβ4 has significant neuronal regenerative abilities and has been shown to enhance oligodendrogenesis (the transition from oligodendrocyte progenitor cells to mature oligodendrocytes) as well as improve functional neurological outcome after injury. Tβ4 has also been shown to promote stem cell migration, recruitment, proliferation and differentiation. Currently, the method by which Tβ4 expression is regulated is unknown. This study looks at the possibility of an interaction between Tβ4 and epidermal growth factor receptor (EGFR). EGFR is a tyrosine kinase that has been proven to be involved in cell survival, differentiation and proliferation. It has also been shown that there is a distinct functional relationship between cellular expression of EGFR and re-myelination after neuronal injury. Since both EGFR and Tβ4 are heavily involved in neuronal repair, it is reasonable to explore if a connection between them exists.