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Transplantation of embryonic stem cells (ESCs) is a promising therapeutic approach for the treatment of neurodegenerative diseases. However, ESCs are not usable clinically due to immunological and ethical limitations. The identification of an alternative safe cell source opens novel options via autologous transplantation in neuro-regeneration circumventing these problems. Here, we examined the neurogenic capacity of embryonic stem-like cells (ES-like cells) derived from the testis using neural growth factor inducers and utilized them to generate functional mature neurons. The neuronal differentiation of ES-like cells is induced in three stages. Stage 1 is related to embryoid body (EB) formation. To induce neuroprogenitor cells, EBs were cultured in the presence of retinoic acid, N supplement and fibroblast growth factor followed by culturing in a neurobasal medium containing B, N supplements for additional 10 days, to allow the maturation and development of neuronal progenitor cells. The neurogenic differentiation was confirmed by immunostaining for markers of mature neurons. The differentiated neurons were positive for Tuj1 and Tau1. Real-time PCR dates indicated the expression of Nestin and Neuro D (neuroprogenitor markers) in induced cells at the second stage of the differentiation protocol. The differentiated mature neurons exhibited the specific neuron markers Map2 and β-tubulin. The functional maturity of neurons was confirmed by an electrophysiological analysis of passive and active neural membrane properties. These findings indicated a differentiation capacity of ES-like cells derived from the testis to functionally mature neurons, which proposes them as a novel cell source for neuroregenerative medicine.

Induction of demyelination in the central nervous system induce the oligodendrocyte progenitors to proliferate, migrate, and differentiate for restoring new myelin sheathes around demyelinated axons. Factors which increase the response of endogenous progenitor cells could be used to improve remyelination. In the current study, the effect of bFGF on lysolecithin-induced demyelination and remyelination processes in mouse optic chiasm and nerves was investigated. Lysolecithin was injected into the optic chiasm of Balb/C mice. Two groups of animals received doses of bFGF (1 or 5 ng/kg i.p.) just before and every 3 days after lysolecithin injection. Delay and amplitude of visual evoked potential (VEP) waves were recorded as indices of axonal demyelination at 7th, 13th, and 28th days post-lesion. Myelin basic protein (MBP) and Olig2 gene expressions were studied as indices of myelination and oligodendrocyte precursors' recruitment into the lesion. Lysolecithin elongated delay of P1 wave and declined the amplitude of P1-N1 wave. Lysolecithin decreased MBP and increased Olig2 expression in different days post-lesion. Lysolecithin-induced changes in VEPs were partially ameliorated by endogenous repair. bFGF reduced the increased delay, increased the reduced amplitude of P1-N1 wave, increased MBP gene expression, and accelerated the increasing pattern of Olig2. bFGF seems to be able to potentiate the endogenous repair mechanisms of myelin. Its effect on demyelination and remyelination processes seems to be mediated by oligodendrocyte progenitor cells and their differentiation to myelinating cells.

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