Extended Data Fig. 2: Hypoxia promotes RIPK1 activity in vivo.
(a-i) Mice of indicated genotypes were challenged to hypoxia for 72 h. Histological analysis on brain sections (n = 10) (a), immunostaining for p-RIPK1(S166) on brain sections (n = 10) (b), brain and liver sections (n = 10) (c), qRT-PCR analysis of the mRNA expression of the indicated cytokines and chemokines from brains (n = 6). Data are mean ± s.e.m. One-way ANOVA, post hoc Dunnett’s test (d), TUNEL assays and immunostaining for Cleaved caspase-3 (CC3) on liver sections (n = 6). Scale bars, 100 μm. DAPI for nuclei. Microscopic quantification of TUNEL and CC3 positive cells (right). Data are mean ± s.e.m. Unpaired two-tailed t-test (e), serum ALT and AST levels (f), Bilirubin levels (g) were measured from wild type mice (n = 6). Data are mean ± s.e.m. Unpaired two-tailed t-test, immunostaining for p-RIPK1(S166) (h), CD68 and Ly6G (i) on lung sections (n = 6). Scale bars, 100 μm. DAPI for nuclei. Microscopic quantification of p-S166, CD68 and Ly6G positive cells (right). Data are mean ± s.e.m. One-way ANOVA, post hoc Dunnett’s test.
