Figure 1. Diagram showing the different mechanisms by which ECs and oligodendrocytes have been shown to interact.

OPCs that are hypoxic secrete Wnt7a and Wnt7b, which act cell autonomously to prevent OPC differentiation, and on the EC, where they up-regulate the expression of Lef1, increasing EC proliferation and angiogenesis [104]. As EC proliferation leads to a leakier BBB [115,116], a similar mechanism could explain how OPCs undergoing oxidative stress cause BBB leakiness [99]. ECs also signal to OPCs, both through secreted factors including FGF and BDNF that increase OPC survival [95], and through cell contact interactions through Cxcl12 and Cxcr4 that allow OPC attachment for migrating along blood vessels [103]. Pericytes, which appose and support ECs, also demonstrate bidirectional signalling with OPCs through secreted pro-survival factors [112].