Q.-L.F., B.H. and X.L. contributed equally to this work.
LINGO-1 negatively regulates TrkB phosphorylation after ocular hypertension
Article first published online: 3 MAR 2010
© The Authors (2010). Journal Compilation © Federation of European Neuroscience Societies and Blackwell Publishing Ltd
European Journal of Neuroscience
Volume 31, Issue 6, pages 1091–1097, March 2010
How to Cite
Fu, Q.-L., Hu, B., Li, X., Shao, Z., Shi, J.-B., Wu, W., So, K.-F. and Mi, S. (2010), LINGO-1 negatively regulates TrkB phosphorylation after ocular hypertension. European Journal of Neuroscience, 31: 1091–1097. doi: 10.1111/j.1460-9568.2010.07127.x
- Issue published online: 16 MAR 2010
- Article first published online: 3 MAR 2010
- Received 26 August 2009, revised 20 December 2009, accepted 4 January 2010
- brain-derived neurotrophic factor;
- intraocular pressure;
- neuronal survival;
- retinal ganglion cell
The antagonism of LINGO-1, a CNS-specific negative regulator of neuronal survival, was shown to promote short-term survival of retinal ganglion cell (RGC) in an ocular hypertension model. LINGO-1 antagonists, combined with brain-derived neurotrophic factor (BDNF), can increase the length of neuron survival through an unclear molecular mechanism. To determine the relationship between LINGO-1 and BDNF/TrkB receptor in neuronal protection, we show here that LINGO-1 forms a receptor complex with TrkB and negatively regulates its activation in the retina after ocular hypertension injury. LINGO-1 antagonist antibody 1A7 or soluble LINGO-1 (LINGO-1-Fc) treatment upregulates phospho-TrkB phosphorylation and leads to RGC survival after high intraocular pressure injury. This neuronal protective effect was blocked by anti-BDNF antibody. LINGO-1 antagonism therefore promotes RGC survival by regulating the BDNF and TrkB signaling pathway after ocular hypertension.