Fig. 3

SHP2 deficiency leads to mitochondrial dysfunction and excessive NLRP3 inflammasome activation. a, b Flow cytometry analysis of mitochondrial membrane potential by JC-1 staining a or mitochondrial ROS by MitoSOX staining b in peritoneal macrophages from conditional SHP2 knockout (cSHP2-KO) and wild-type (WT) mice, and left untreated or treated with ATP (5 mM) for indicated times. c Quantitative real-time PCR analysis of mtDNA released from peritoneal macrophages from cSHP2-KO and WT mice and left unstimulated (medium) or primed with LPS (100 ng ml⁻¹) for 3 h and stimulated with ATP (5 mM, 1 h) and Nigericin (10 µM, 2 h). d ELISA of IL-1β in supernatants of peritoneal macrophages from cSHP2-KO and WT mice, which were primed with LPS (100 ng ml⁻¹) for 3 h, and left untreated or treated with Ac-YVAD-cmk (30 μM), NAC (5 mM), or E-64d (20 μM) for 1 h, followed by stimulation of ATP (5 mM) for 1 h. *P < 0.05, **P < 0.01, one-way ANOVA for multiple comparisons; NS represents no significance. Data are presented as mean ± SEM of three independent experiments in a–d