Skip to main content
. Author manuscript; available in PMC: 2012 Dec 1.
Published in final edited form as: Nat Neurosci. 2012 Jun;15(6):862–870. doi: 10.1038/nn.3109

Figure 5.

Figure 5

Inhibition of HGF signaling with cMet or anti-HGF antibodies blocks the ability of MSC-CM100kD and HGF to alter the development and migration of neural cells from neurospheres. A. The proportions of A2B5+, O4+, β tubulin + and GFAP+ cells are altered in the presence of MSC-CM100kD and HGF and reversed by cMet and anti-HGF. B. Quantification of different cell types in the presence and absence of MSC-CM100kD and HGF± cMet antibodies. Compared to controls the proportion of O4+ and β tubulin + cells is increased by MSC-CM and HGF (p=<0.05 for both) and blocked by cMet antibodies (p=<0.01 for both) C. Treatment with HGF stimulates migration of neuronal precursors from adult SVZ derived neurospheres of EAE animals and is blocked by cMet antibodies. D. Treatment with MSC-CM100kD stimulates migration of OPCs and neuronal precursors from adult EAE SVZ derived neurospheres and is blocked by cMet and anti-HGF. E. The mobilization of PLP+ OPCs into EAE lesions is enhanced in animals treated with HGF. The number of EGFP-PLP cells which populate lesions increase following HGF treatment.. Bars = 20μm in A and 100μm in C and D. and 50μm in E. Data in B represent the mean±SD of the proportion of individual cell types taken from 5 random fields from at least 2 independent experiments. Lesion areas are outlined in E. Note that in B there is both unlabeled and overlap of antigen expression on individual cells.