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. Author manuscript; available in PMC: 2019 Dec 1.
Published in final edited form as: Neurobiol Dis. 2018 Aug 24;120:1–11. doi: 10.1016/j.nbd.2018.08.013

Figure 2: GPNMB is elevated in mouse brain following complete pharmacological inhibition of glucocerebrosidase activity.

Figure 2:

Tissue homogenates of freshly dissected striatum (STR), cerebellum (CB), motor cortex (MCtx), hippocampus (HP) and substantia nigra (SN) from mice receiving daily (for 28 days) i.p. injections of DMSO (0.1%, n=4–6) or CBE (100mg/kg, n=3–6) were prepared. (A) Glucocerebrosidase activity levels were determined using the artificial substrate 4-methylumbelliferyl-β-D-glucopyranoside (4-MU-Glc). GCase activity levels were significantly diminished in all brain regions in CBE-treated mice. (B) Levels of GPNMB across these brain regions were determined by ELISA, with significantly elevated GPNMB measured in the MCtx, HP, and SN of CBE-treated mice. GPNMB levels in the STR and CB were not affected by CBE-treatment. For panels A and B, results are means ±SEM, ** p <0.01, **** p <0.0001 (two-way ANOVA, with Sidak’s multiple comparison post-hoc test).