Does Thymosin 𝛽4 Enhance Oligodendrogenesis by up-regulating Epidermal Growth Factor Receptor?
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Thymosin p 4 (T𝛽4) is an endogenous 43 amino acid peptide involved in multiple healing processes throughout the body. T𝛽4 has significant regenerative abilities in neuronal models and has been consistently shown to enhance oligodendrogenesis as well as improve functional neurological outcome after injury. The molecular mechanism behind these abilities remains unclear. This study aims to examine a possible mechanism that could explain how Tl34 enhances oligodendrogenesis in an oligodendrocyte progenitor cell culture model. We hypothesize that the epidermal growth factor receptor (EGFR) is a pivotal receptor in T𝛽4 enhanced oligodendrogenesis. EGFR is a known regulator of proliferation, migration and differentiation and it has been shown to be involved in both myelination and re-myelination. Furthermore, upregulation of EGFR has consistently shown an increase in myelination. Our results are still in a preliminary stage and at this point provide inconclusive evidence to prove or dis-prove the hypothesis. To test our hypothesis we treated oligodendrocyte progenitor cells (OPC's) with TP4 and analyzed the cells with standard techniques such as western blots and PCR. We observed inconsistent results that generally showed both fluctuating levels of myelin basic protein (MBP) and EGFR. There was a general elevation in MBP with most testing methods and an elevation of EGFR with only a few. Almost every method of testing showed inconsistency and fluctuation with different samples of the same origin and cohort. Future study and larger sample size will be necessary to definitively disprove or confirm our hypothesis. On a positive note, this study was able to develop methods for testing this hypothesis and will allow for future studies to build off of the developments.