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TNF activates SCN10A. 19 / 20
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"TNF-α mediated increase in Nav1.8 current density increases neuronal excitability, likely contributing to increased mechanical allodynia following motor nerve injury (Chen et al., 2011)."

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"Furthermore, peri-sciatic exogenous TNF-α, which leads to lasting mechanical allodynia [71], upregulates Nav1.3 and Nav1.8 in DRG in vivo."

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"Interestingly, both Nav 1.3 and Nav 1.8 up-regulation was mediated by cytokine TNFα, as was shown by inhibition of TNFα synthesis [26,38]."

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"Here, we found that Nav1.8 was upregulated by TNFα and induced ROS accumulation and production of pro-inflammatory factors in keratinocytes."

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"First, as shown in Fig. 1C, mouse SNs were stimulated by a pro-inflammatory cytokine, TNF-α, to induce neuronal inflammation."

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"In cultured DRG neurons, TNF-α upregulates Nav1.3, Nav1.8 and Nav1.7 in a dose-dependent manner ( Chen et al., 2011; He et al., 2010; Tamura et al., 2014 )."

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"Moreover, TNF-α was reported to induce Nav1.8 upregulation in uninjured sciatic nerve fibers following L5 ventral root transection (L5-VRT) [66]."

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"Inhibition of TNF-α synthesis blocks the upregulation of Nav1.8 and prevents the development of neuropathic pain [66]."

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"Furthermore, inhibition of TNF-α synthesis, which prevented neuropathic pain, strongly inhibited the up-regulation of Nav1.3 and Nav1.8."

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"These data suggest that increased TNF-α may be responsible for up-regulation of Nav1.3 and Nav1.8 in uninjured DRG neurons following nerve injury."

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"Inhibition of TNF-α synthesis or genetic ablation of TNFR1 significantly attenuates the upregulation of Nav1.3 and Nav1.8 in uninjured DRG neurons induced by L5-VRT ( He et al, 2010, Chen et al 2011 )[MISSING/INVALID CREDENTIALS: limited to 200 char for Elsevier]"

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"Moreover , TNF-alpha was reported to induce Nav1.8 upregulation in uninjured sciatic nerve fibers following L5 ventral root transection ( L5-VRT ) [ 66 ] ."

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"Indeed, recombinant rat TNF (rrTNF) enhanced the current densities of TTX-S and Nav1.8 in cultured DRG neurons dose-dependently."

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"In cultured DRG neurons, TNF-α dose-dependently upregulates Nav1.3, Nav1.8 and Nav1.7 ( He et al., 2010; Tamura et al., 2014 )."

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"Furthermore, the inhibition of TNF-α synthesis inhibited the up-regulation of Nav1.3 and Nav1.8 and prevented neuropathic pain."

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"In particular, TNF-α and IL-1β have been shown to increase the sensitivity and excitability of sensory neurons by activating the TTX-resistant sodium channels Nav1.8 [16, 17]."

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"A previous study demonstrated that TNF-α increased the current densities of Nav1.8 in DRG neurons (Chen et al., 2011)."

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"Also, while IL-1β generally inhibits voltage-gated ion channels to limit excitability, TNF-α can increase the excitability of neurons by enhancing the transcription or Nav1.3 and Nav1.8 upon in vivo."

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"Meanwhile, the amplification of TTX-R and NaV1.8 currents induced by TNF-α was attenuated in DRG neurons with pre-incubation with respective inhibitors of the intracellular signaling pathwaysp38-MAPK, JNK, and ERK."