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. 2021 May 11;12:2674. doi: 10.1038/s41467-021-22987-3

Fig. 8. YAP promotes NLRP3 inflammasome activation in vivo.

Fig. 8

a, b Yapfl/fl lyz2-Cre or Yapfl/fl mice were intraperitoneal injected 20 mg/kg LPS for 6 h, ELISA analysis of serum levels of IL-1β and TNF-α (a), H&E staining of lung tissue sections(b) Scale bars, 50 μm (mean ± SEM, two-way ANOVA with Bonferroni test, Yapfl/fl lyz2-Cre vs. Yapfl/fl, ***P < 0.0001, n = 10 biologically independent mice). c, d Yapfl/fl lyz2-Cre or Yapfl/fl mice were intraperitoneally injected with 1 mg monosodium urate for 6 h, ELISA analysis of IL-1β (c) and quantification of neutrophils (d) in the peritoneal cavity fluid (mean ± SEM, two-way ANOVA with Bonferroni test, Yapfl/fl lyz2-Cre vs. Yapfl/fl, ***P < 0.0001 (c), ***P < 0.0001 (d) in sequence, n = 8 biologically independent mice). e The model of YAP in NLRP3 inflammasome activation. YAP maintains the stability of NLRP3 by blocking/masking the interaction between NLRP3 and the E3 ligase β-TrCP1, which promotes the proteasomal degradation of NLRP3 via K27-linked ubiquitination at lys380. Cellular nutrient/density status, activating the Hippo-YAP pathway, impairs NLRP3 inflammasome activation in a YAP-dependent manner. Source data are provided as a Source Data file.