Dystroglycan modulates the ability of insulin-like growth factor-1 to promote oligodendrocyte differentiation.
Dystroglycan modulates the ability of insulin-like growth factor-1 to promote oligodendrocyte differentiation.
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DOI：
10.1002/jnr.22484
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发表时间：
2010-11-15
影响因子：
4.2
通讯作者：
Colognato, Holly
中科院分区：
文献类型：
--
作者：
Galvin, Jason;Eyermann, Christopher;Colognato, Holly
The adhesion receptor dystroglycan positively regulates terminal differentiation of oligodendrocytes, however the mechanism by which this occurs remains unclear. Using primary oligodendrocyte cultures, we identified and examined a connection between dystroglycan expression and the ability of insulin-like growth factor-1 (IGF-1) to promote oligodendrocyte differentiation. Consistent with previous reports, treatment with exogenous IGF-1 caused an increase in MBP protein that was preceded by activation of PI3K (AKT) and MAPK (ERK) signaling pathways. The extracellular matrix protein laminin was furthermore shown to potentiate the effect of IGF-1 on oligodendrocyte differentiation. Depletion of the laminin receptor dystroglycan using siRNA, however, blocked the ability of IGF-1 to promote oligodendrocyte differentiation of cells grown on laminin, suggesting a role for dystroglycan in IGF-1-mediated differentiation. Indeed, loss of dystroglycan led to a reduction in the ability of IGF-1 to activate MAPK, but not PI3K, signaling pathways. Pharmacological inhibition of MAPK signaling also prevented IGF-1-induced increases in MBP, indicating that MAPK signaling was necessary to drive IGF-1-mediated enhancement of oligodendrocyte differentiation. Using immunoprecipitation, we found that dystroglycan, the adaptor protein Grb2, and insulin receptor substrate-1 (IRS1), were associated in a protein complex. Taken together, our results suggest that the positive regulatory effect of laminin on oligodendrocyte differentiation may be attributed, at least in part, to dystroglycan’s ability to promote IGF-1-induced differentiation.
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