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. 2019 Oct 16;294(48):18057–18068. doi: 10.1074/jbc.RA119.008925

Figure 4.

Figure 4.

Knockdown of TSG101 exacerbates LPS-triggered animal mortality, cardiac dysfunction, and inflammation. A, experimental procedure and biochemical assays for LPS (10 μg/g) treatment in CTRL (TSG101fl/+) and TSG101 KD (MerCreMer-TSG101fl/+) mice. wk, week. B, Western blots and quantification analysis showing the expression of TSG101 in hearts of CTRL and KD mice. GAPDH was used as a loading control for total protein. n = 6 for all groups. *, p < 0.05 versus CTRL. C, survival curve of CTRL and KD mice when challenged with LPS (10 μg/g) and monitored over 5 days. n = 10 for CTRL, n = 8 for KD. *, p < 0.05 versus CTRL. D–F, cardiac function in CTRL and KD mice subjected to PBS or LPS treatment was determined by echocardiography. n = 5 for PBS CTRL, n = 6 for PBS KD, n = 6 for LPS CTRL, n = 7 for LPS KD. *, p < 0.05 versus PBS CTRL; #, p < 0.05 versus PBS KD; &, p < 0.05 versus LPS CTRL. G and H, levels of the pro-inflammatory cytokines TNFα (G) and IL-6 (H) in CTRL and KD mice subjected to PBS or LPS treatment were determined by qRT-PCR. n = 4 for all groups. *, p < 0.05 versus PBS CTRL; #, p < 0.05 versus PBS KD; &, p < 0.05 versus LPS CTRL. I and J, levels of the pro-inflammatory cytokines TNFα (I) and IL-6 (J) in CTRL and KD mice subjected to PBS or LPS treatment were measured by ELISA. n = 6 for all groups. *, p < 0.05 versus PBS CTRL; #, p < 0.05 versus PBS KD; &, p < 0.05 versus LPS CTRL.