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To further analyze the role of Foxg1 in differentiation of OPCs, we seeded isolated OPCs on poly-L-lysine-coated coverslips in the presence of PDGF-AA and bFGF for 3 days and then cultured them in the presence of PDGF-AA and bFGF for 7 days.
To further analyze the role of Foxg1 in the differentiation of OPCs, we seeded isolated OPCs on poly-L-lysine-coated coverslips in the presence of PDGF-AA and bFGF for 3 days and then cultured them in the presence of PDGF-AA and bFGF for 7 days. The results showed that Foxg1 knockdown in OPCs led to an inhibition of oligodendrocyte maturation, as revealed by the downregulation of MBP, CNPase, and MAG (Fig. 4I, J, K). Taken together, these results demonstrated that Foxg1 cKO prevented the decrease in OPC proliferation and the promotion of OPC differentiation caused by CPZ. It was also demonstrated that Foxg1 cKO could promote OPC differentiation into mature OLs, which is accompanied by remyelination.
To further investigate the role of Foxg1 in differentiation of OPCs, we seeded isolated OPCs on poly-L-lysine-coated coverslips in the presence of PDGF-AA and bFGF for 3 days and then cultured them in the presence of PDGF-AA and bFGF for 7 days. The results showed that the percentage of MBP+ cells, CNPase+ cells, and MAG+ cells in the WT+CPZ group was lower than that in the WT group (Fig. 5A-C). However, the percentage of MBP+ cells, CNPase+ cells, and MAG+ cells in the Foxg1 cKO+CPZ group was higher than that in the WT+CPZ group (Fig. 5A-C). These data suggested that Foxg1 knockdown in OPCs promoted OPC differentiation into mature OLs, which was accompanied by remyelination.
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