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Fig. 6 | Cell & Bioscience

Fig. 6

From: Microglia degrade Tau oligomers deposit via purinergic P2Y12-associated podosome and filopodia formation and induce chemotaxis

Fig. 6

P2Y12-activation and blockage influence Tau deposit degradation through the Arp2-mediated podosome and filopodia formation. A P2Y12 activation by ADP has induced more filopodia formation for Tau deposit degradation. While, microglia, which degrade Tau, deposits by P2Y12.+ podosome formation, were independent of P2Y12 signaling activation/blockage. Microglia have been shown to degrade Tau deposits as scattered spots at the cell surface upon Clopidogrel treatment. While upon ADP exposure, microglia degraded the Tau deposits throughout the cell surface (Scale bar 10 μm). B The percentage of cells with Tau deposit degradation has been reduced by Clopidogrel exposure. While the ADP-mediated P2Y12 activation showed unaltered Tau deposit degradation compared to the control. (No. of experiment = 3) (n = 33). C P2Y12 activation resulted in more Arp2-localized filopodia formation that leads to Tau degradation, while Clopidogrel treatment did not alter the membrane-associated actin and Tau deposit degradation (Scale bar 10 μm). D Similarly, TKS5 localization was reduced in podosome and filopodia during Tau deposit degradation upon P2Y12-activated microglia (Scale bar 10 μm). E P2Y12 activation leads to the Arp2-associated filopodia formation at the site of Tau deposit degradation. At the same time, the blockage of P2Y12 signaling by clopidogrel resulted in more accumulation of Arp2-orchestrated podosome and filopodia at the Tau degradation site. (No. of experiment = 3) (n = 25). F ADP-mediated P2Y12 activation lead to the reduced TKS5 colocalization at podosome and filopodia while P2Y12 blockage did not alter TKS5 localization in remodeled actin network. (No. of experiment = 3) (n = 25)

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