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Fig. 7 | Molecular Neurodegeneration

Fig. 7

From: Inactivation of NLRP3 inflammasome by dephosphorylation at Serine 658 alleviates glial inflammation in the mouse model of Parkinson’s disease

Fig. 7

S658A mutation blocks the inhibitory effect of Psoralen on NLRP3 inflammasome activation. Effects of Psoralen treatment on the release of IL-1β (A), IL-6 (B), and TNF-α (C) from LPS + ATP-stimulated WT and S658A mutant BMDMs. (D) IL-1β and caspase-1 from SN and pro-IL-1β/pro-caspase-1 from Lysates were analyzed by immunoblotting after BMDMs were transfected with wtNLRP3 or mutNLRP3-S658A plasmids. (E) Immunoblots showed the binding of Pso and wtNLRP3 but not Pso and mutNLRP3-S658A in HEK-293T cells. (F-G) Phos-tag assay and quantification of NLRP3 phosphorylation in BMDMs pretreated with Pso followed by transfection with wtNLRP3 or mutNLRP3-S658A plasmids. (H-I) Immunostaining and quantification for ASC speck (red) in Nlrp3 KO BMDMs pretreated with Pso followed by transfection with wtNLRP3 or mutNLRP3-S658A plasmids. DAPI stains the nucleus (blue). The scale bar represents 5 μm. Data were analyzed by one-way ANOVA, followed by Tukey post-tests. *P < 0.05, **P < 0.01 and ***P < 0.001

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Molecular Neurodegeneration

ISSN: 1750-1326