Leukemia inhibitory factor is an autocrine survival factor for Schwann cells

Schwann cells play a major role in promoting nerve survival and regeneratio n after injury. Their activities include providing neurotrophic factors and increasing the production of extracellular matrix components and cell surf ace adhesion molecules to promote axon regeneration. Following nerve transe ction, leukemia inhibitory factor (LIF) is up-regulated by Schwann cells at the injury site. LIF receptors are also up-regulated at the nerve injury s ite, but their cellular localization and function have not been fully chara cterized. We demonstrate that Schwann cells express mRNAs for LIF and the L IF receptor components LIF receptor subunit beta and glycoprotein 130 in vi tro. We also show that although LIF is not required for the genesis of Schw ann cells, it can potentiate the survival of differentiated Schwann cells i n the context of neuregulin support. Not only does exogenous LIF promote su rvival under these conditions, but addition of the soluble LIF receptor (LI F binding protein) and anti-LIF antibodies significantly reduced cell survi val, suggesting that LIF exerts autocrine effects. These results suggest th at Schwann cell survival following nerve injury is potentially modulated by LIF.