NG2-expressing neural progenitors can produce neurons in the central nervous system, providing a potential cell resource of therapy for neurological disorders. However, the mechanism underlying neuronal differentiation of NG2 cells remains largely unknown. In this report, we found that a thrombospondin (TSP) family member, TSP4, is involved in the neuronal differentiation of NG2 cells. When TSP4 was overexpressed, NG2 cells underwent spontaneous neuronal differentiation, as demonstrated by the induction of various neuronal differentiation markers such as NeuN, Tuj1, and NF200, at the messenger RNA and protein levels. In contrast, TSP4 silencing had an opposite effect on the expression of neuronal differentiation markers in NG2 cells. Next, the signaling pathway responsible for TSP4-mediated NG2 cell differentiation was investigated. We found that ERK but not p38 and AKT signaling was affected by TSP4 overexpression. Furthermore, when ERK signaling was blocked by the inhibitor U0126, the neuronal marker expression of NG2 cells was substantially increased. Together, these findings suggested that TSP4 promoted neuronal differentiation of NG2 cells by inhibiting ERK/MAPK signaling, revealing a novel role of TSP4 in cell fate specification of NG2 cells.

Oligodendrocytes (OLs) are derived oligodendrocyte progenitor cells (OPCs), and their differentiation is a tightly regulated process. It is known that cyclin-dependent kinases (CDKs) play an essential role as regulators of OPC differentiation. Here, we newly identified a CDK-like protein, PFTK1, to be involved in OPC differentiation. With serum-deprivation, OLN-93 undergoes OL differentiation, and PFTK1 expression is markedly decreased during differentiation. When PFTK1 is silenced, OL differentiation is potentiated, as suggested by the increase of various differentiation markers CNPase, MOG, CGT, and MBP, by qPCR and Western blotting analysis. Vice versa, PTTK1 overexpression has opposite effects on OL differentiation of OLN-93 in vitro. Next, the modulation mechanism underlying OL differentiation of OLN-93 was investigated. Significantly, PFTK1 silencing leads to the activation of PI3K/AKT pathway, but no activation of MAPK/ERK pathway. The inhibition of AKT by its specific inhibitor abrogates PFTK1 silencing-promoted OL differentiation, indicating that PFTK1 negatively regulates OL differentiation through PI3K/AKT pathway. Together, these findings indicate a novel role played by PFTK1 in OL development, thus presenting opportunities to establish therapeutic approaches in improving neurological recovery related to demyelinating disorders.

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In this paper, we discuss the excitation module in the magnetic induction system. First, we start from the traditional sinusoidal input resonant excitation circuit and give the frequency domain equation of its excitation current. Then, we propose a new module based on pulse excitation and give the corresponding excitation equation in the frequency domain. After that, we deduce the mathematical model of excitation gain of new and old modules using application and technology and finally obtain intuitive mathematical analysis graphics for engineering promotion.