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- W1454804774 abstract "Tumor necrosis factor-α (TNFα), a pro-inflammatory cytokine can cause either vascular smooth muscle cell (VSMC) apoptosis (JNK-dependent) or proliferation (NF-κB-dependent). We hypothesized that TNFα receptor 1 (TNFR1) endocytosis balances these two pathways. We quantified NF-κB activation and MAPK (JNK, p38, ERK1/2) phosphorylation by TNFα in the presence of siRNA targeting TNFR1 or 2 in cultured murine mesenteric VSMC. Both NF-κB activation (Fig. 1, n=3–4) and JNK phosphorylation are TNFR1-dependent, and NF-κB activation is potentiated by JNK inhibition (SP600125, 3μM). Impairing endocytosis (Dynasore, 15μM) reduced NF-κB activation by TNFα (1.5-fold, n=5) and prevented this effect of SP600125 (2.2-fold, n=4). TNFα also caused phosphorylation of p38 and ERK1/2. JNK and ERK1/2 phosphorylation were TNFR1-dependent while p38 activation was altered by both TNFR1 and 2 siRNA. Thus, TNFR1 activates both NF-κB and JNK activation and JNK modulates endocytosis-dependent NF-κB activation in VSMC." @default.
- W1454804774 created "2016-06-24" @default.
- W1454804774 creator A5019806106 @default.
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- W1454804774 date "2013-04-01" @default.
- W1454804774 modified "2023-09-23" @default.
- W1454804774 title "TNFα receptor 1 causes endocytosis‐dependent NF‐κB and ‐ independent JNK activation in vascular smooth muscle cells" @default.
- W1454804774 doi "https://doi.org/10.1096/fasebj.27.1_supplement.1139.6" @default.
- W1454804774 hasPublicationYear "2013" @default.
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