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TNF increases the amount of TRPV1. 43 / 44
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"TNF-α increased spontaneous EPSC frequency by increasing transient receptor potential subtype V1 (TRPV1)-mediated glutamate release in presynaptic terminal (Park et al., 2011)."
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"Previous studies have shown that TNF-α can enhance the expression and activity of TRPA1, TRPV1, and TRPV4 [45,46]."
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"Furthermore, in endometrial epithelial mesenchymal cells with EMs, TNF-α and PGE2 can stimulate the expression of TRPV1, and TRPV1 further induces the release of factors such as nitric oxide (NO) and interleukin IL-1β to promote the development of inflammation [34]."
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"This cytokine increases TRPV1 expression on dorsal root ganglion and trigeminal ganglion neurons via the extracellular signal-regulated kinase pathway.96,97 Additionally, tumor necrosis factor alpha rapidly sensitizes TRPV1 activity and enhances the Ca influx induced by capsaicin."
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"TNF-α activates the trigeminal ganglion by enhancing the expression of TRPV1 channels and many cytokines, including IL-1b and brain-derived neurotrophic factor (BDNF)."
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"The expressions of TRPA1, TRPV1 and IL-31 mRNA in HaCaT cells were increased by TNF-α treatment and partially decreased by luteolin 7-methyl ether (4) treatment."
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"TNF-α enhances the expression and trafficking of TRPV1 and TRPA1 to the surface of trigeminal neurons, and such trafficking is required for CGRP exocytosis [81]."
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"TNF-α could up-regulate the expression of TRPV1 receptor, thus causing thermal hyperalgesia (156)."
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"In addition, TNF-α was also able to produce subsequent upregulation of TRPV1 protein expression when applied to cultured DRG neurons employing a pathway involving extracellular-signal-related kinase rather than p38 signaling."
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"In cultured sensory neurons, TNF-α and IL-1β have been shown to upregulate TRPV1 expression and neutralization of TNF-α and IL-1β in vivo reduces thermal hyperalgesia (Schaible, 2014), consistent with their involvement in neuro-immune underlying thermal hyperalgesia (Pinho-Ribeiro et al., 2017; Schaible, 2014)."
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"Moreover, the inflammatory response caused by the viral invasion and the concomitant release of proinflammatory cytokines (i.e., TNF-α) may enhance the expression and trafficking of TRPV1 receptors, which may help to enhance CGRP synthesis and release, a process that seems to be involved in odor inhibition."
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"In addition, TNF increases the TRPV1 protein level and number of TRPV1-expressing neurons."
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"TNF is known to increase the expression level of TRPV1 by activating TRPV1-dependent ERK signaling, but the influence of this overexpression on the effect of RTX is still unclear [40]."
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"Supporting the view that the activation of TRPV1 and TRPA1 in immune cells also promotes the upregulation of their own expression in the same cell type, the enhanced expression of TRPV1 (at both prote[MISSING/INVALID CREDENTIALS: limited to 200 char for Elsevier]"
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"Furthermore, vincristine administration induced the upregulation of tumor necrosis factor (TNF)-alpha production in DRGs, and inhibition of TNF-alpha synthesis with thalidomide in vivo reversed TRPV1 protein expression, as well as pain hypersensitivity induced by vincristine in rats."
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"Obviously, TNF-α not only promotes TRPV1 expression at a translational level, but may also induce the directed TRPV1 trafficking to the surface membrane in DRGs in vincristine-treated rats."
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"Under inflammatory conditions, TNF-α increases the transcription and expression of TRPV1 by activating transcription factors such as nuclear factor-kappa B (NF-κB), thereby enhancing the inflammatory response of cells."
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"This would lead to increased activation of tetrodotoxin-resistant sodium ion channels, which in turn would sensitize DRG neurons to mechanical stimulation.19 TNF-α can also promote the expression of transient receptor potential vanilloid-1 (TRPV1) on the surface of DRG neurons via the ERK-MAPK signaling pathway.20 TRPV1 is a sensor for noxious heat and plays an important role in the pathogenesis of heat hyperalgesia."
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"It has been shown previously that TRPV1 receptor expression and sensitivity to capsaicin may be modulated by TNFα pretreatment [4,29-31]."
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"This long-term up-regulation of TRPV1 expression by TNFalpha correlated with enhancement in capsaicin-induced calcitonin gene-related peptide release (P<0.05)."
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"In summary, our data demonstrate that TNFalpha directly enhances the sensitivity of rat trigeminal neurons to capsaicin via both rapid, non-genomic mechanisms as well as sustained genomic regulation in TRPV1 expression."
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"As an example, TNF-α activates the TNF-α receptor 1 (TNFR1) to promote Na 1.9 phosphorylation, while IL-6, by activating the gp130 channel, increases the expression of TRPV1 and TRPA1 (reviewed in [41])."
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"Interestingly, itching that remains still a significant nuisance in atopic dermatitis could be potentially an aim for luteolin, as luteolin 7-methyl ether significantly decreased the TNF-α-induced TRPV1 expression and slightly diminished the expression of TRPA1 and IL-31 induced by the same cytokine as well [ xref ]."
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"Remarkably, our data clearly demonstrated that IL-3 (p = 0.0007), IL-31 (p = 0.0022), IL-33 (p < 0.001), TSLP (p = 0.0105), TNF-α (p < 0.001), NGF-β (p = 0.0014), and BDNF (p = 0.0111) induced a higher expression of TRPV1 on the surface than in the unstimulated eosinophils (Figure 5A)."
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"In a model of cancer-related pain, TNFα acted via TNFR2 to increase TRPV1 expression resulting in thermal hyperalgesia [39]."
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"Although there are reports that TNF-alpha increases TRPV1 expression through TNF-alpha receptors and TRPV1 induced activity is enhanced by TNF-alpha administration [XREF_BIBR - XREF_BIBR], it would be interesting to know if they can reciprocally regulate one another."
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"Expression of TRPV1 in synovial fibroblasts from patients with rheumatoid arthritis and OA14 and in the synoviocyte cell line SW98220 has been shown to be upregulated by TNFα."
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"It should be noted that inhibition of TNF-α has been reported to decrease expression of TRPV1 and/or TRPA1 and attenuate the effects of these receptors’ activation in sensory nerves in the processing of inflammatory responses (Hu et al., 2010; El Karim et al., 2015; Meng et al., 2016)."
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"Similarly, proinflammatory chemokine, CCL3 sensitizes TRPV1 [44] and TNF-α increases cell surface expression of TRPV1 in ganglion neurons [45] ."
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"Long-term exposure of TNFα was shown to enhance TRPV1R-mediated currents in DRG neurons through the production of PGE2 (Nicol et al. 1997) and to upregulate TRPV1 expression through ERK activation (Hensellek et al. 2007)."
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"The Th1 cytokine TNF-α which, in turn, triggers secretion of TSLP in human keratinocytes [57] also potentiates TRPV1 expression in eosinophils."
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"Furthermore, TNF-α increases expression of TRPV1 in DRG via TNFR1 receptor with a requirement for ERK signaling [11]."
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"It has been reported that TNF-α partly increases activity of TRPV1 and sustainably upregulates TRPV1 expression ( Khan et al., 2008; Rozas et al., 2016 ) by acting directly on TNF-R1 ( Ma and Quirion,[MISSING/INVALID CREDENTIALS: limited to 200 char for Elsevier]"
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"TNF and IL-6 elevate gene expression or membrane expression of TRPV1 ."
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"TNF-alpha increases TRPV1 (8 hr peak) and TRPV4 (12 hr peak) immunostaining, mRNA and protein expression, with a TRPV1 shift to membrane fractions."
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"TNF-alpha increases expression of TRPV1 and TRPV4 mRNA, protein and immunostaining in synoviocytes after 8 hr."
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"The treatment of TNF-α increased the expression of TRPV1 and TRPA1 in THP-1 cells at both protein ( Fig. 9 B&C) and mRNA levels ( Fig. 9 D)."
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"It is highly likely that TNF-α increases expression of TRPV1 and TRPV4 by mediating the up-regulation directly and/or through initiation of downstream events since the inhibitor reduced the immunostaining increase."
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"Supporting the view that the activation of TRPV1 and TRPA1 in immune cells also promotes the upregulation of their own expression in the same cell type, the enhanced expression of TRPV1 (at both prote[MISSING/INVALID CREDENTIALS: limited to 200 char for Elsevier]"
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"For example, IL-6 and TNF-α upregulate TRPV1 expression in sensory neurons, leading to sustained hyperalgesia [27,28,29,30,31]."
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"Khan et al and Hensellek et al, using PCR, immunostaining, and calcium signaling, showed that TNF-alpha increased TRPV1 expression in rat trigeminal neurons and dorsal root ganglia, respectively [13, 14]."
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"In the present study, we investigated in cultured dorsal root ganglion (DRG) neurones, the somata of primary afferent fibres, whether TNFalpha increases TRPV1 receptor expression."
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"Furthermore, we found that activation of ERK but not of p38 kinase or cyclooxygenases is critically involved in the TNFalpha induced increase of TRPV1 receptor expression."
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