Skip to main content
. 2021 May 13;12:2776. doi: 10.1038/s41467-021-23086-z

Fig. 4. Inhibition of HMGB1 and NETs improves overall RT response.

Fig. 4

a Schematic representation of tumor growth experiment where C57BL/6 or PAD4−/− mice were injected subcutaneously (s.c) in the right flank with MB49 (500,000 cells). Mice were randomized into two groups: non-irradiated (control) or irradiated (RT). Tumors were irradiated with two fractions of 5 Gy and DNAse I was administered intramuscularly (i.m.) to degrade NETs or GLZ was administered intraperitoneally (i.p) to inhibit extracellular HMGB1. b MB49 tumor growth 11 days post-RT (n = 8 mice per arm for all groups except n = 10 for C57BL/6 RT + DNAse I, n = 9 C57BL/6 + RT + GLZ + DNAse I). c Kaplan–Meier percent survival. d Immunofluorescence of tissues obtained at endpoint staining for PMNs and NETs through NE (green) and H3Cit (red) staining, nuclei (blue), 20×, scale bar 50 μm, representative of three independent experiments. e Quantification of PMN infiltration and NETs in tumors, data represented as percent positive of total cells per field of view (n = 6 mice). Data represented as mean ± SEM. Statistical significance was assessed using two-way ANOVA with Bonferroni’s multiple comparison’s test (b) log rank (Mantel-cox) test (c) unpaired two-tailed students t-test (e). NS not significant (compared to C57BL/6: C57BL/6 + GLZ p > 0.05, PAD4−/− + GLZ p = 0.053, PAD4−/− p = 0.13), ***p < 0.001.