Skip to main content
. Author manuscript; available in PMC: 2019 Sep 9.
Published in final edited form as: J Mol Cell Cardiol. 2018 Jul 5;121:107–123. doi: 10.1016/j.yjmcc.2018.07.003

Fig. 8.

Fig. 8.

TRAF3IP2 gene deletion blunts TWEAK-induced NF-κB, AP-1 and p38 MAPK activation, TWEAK and its receptor upregulation, and induction of other inflammatory mediators in the hypertrophied heart. Both wild type and TRAF3IP2-KO mice were continuously infused with TWEAK (10 μg/kg body weight/day) for 7 days via subcutaneously implanted osmotic minipumps (A). TWEAK significantly increased oxidative stress, as evidenced by increased lipid peroxides (B). Further, TWEAK upregulated TRAF3IP2 expression (C), NF-κB (p65), AP-1 (c-Jun) and p38 MAPK activation (C), and proinflammatory cytokine (TNF-α, IL-18), chemokine (MCP-1), adhesion molecule (ICAM1) and iNOS expression (C). These TWEAK-induced pro-oxidant and proinflammatory effects were blunted by TRAF3IP2 gene deletion (C). While all the immunoblots in C include three individual animals selected at random in each group, the corresponding summarized semi-quantification data in panel D includes all 5 animals/group. B, D, *P < 0.05 versus untreated, †P < 0.05 versus TWEAK (n = 5/group).