Skip to main content
Fig. 6 | Molecular Neurodegeneration

Fig. 6

From: Pathological α-synuclein recruits LRRK2 expressing pro-inflammatory monocytes to the brain

Fig. 6

Lrrk2 kinase inhibition attenuates chemotactic responses to α-synuclein fibrils. A In the experimental paradigm, mouse BV-2 microglial cells were treated for 24 h with human α-synuclein fibrils (+) or monomer (−) control (both at 1 μg・mL− 1), and cell culture media was applied (1/10th volume) to the bottom chamber in Boyden transwell assays. Chemotaxis of bone-marrow derived macrophages (MCSF) cells from the indicated mouse strain were compared, with or without the Lrrk2 small molecule inhibitor MLi2 (100 nM). B After 2 h, cells that failed to migrate into the transwell membrane were removed with a cotton swab. Migrated cells were stained with DAPI, counted across the filter, and representative images from three independent experiments from three mice (male) are shown, and C relative chemotaxis calculated as a fold of the number of WT(nTg) cells from three different experiments. Each dot represents one independent experiment. D Human α-synuclein fibrils (1 μg・mL− 1) were added into the bottom chamber of Boyden transwell assays. Chemotaxis of bone-marrow derived macrophages cells were counted after 2 h. CCL5 (500 ng・mL− 1) was used as the positive control. Data are group means ± SEM. Significance was assessed by one-way ANOVA with Tukey’s post-hoc test where *p < 0.05, **p < 0.01, and ***P < 0.001

Back to article page