INT98621
From wiki-pain
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Sentences Mentioned In
Key: | Protein | Mutation | Event | Anatomy | Negation | Speculation | Pain term | Disease term |
An emerging concept with important implications for drug development is that TRPV1 may be differentially regulated under physiological and pathological conditions. | |||||||||||||||
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Activity of TRPV1 is modulated by actions of various kinases such as protein kinase A and C. | |||||||||||||||
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Cisplatin induced significant up-regulation of TRPV1 and TRPA1 mRNA (3-fold) in cultured DRG neurons at 6 h (Figure 2A and 2C). | |||||||||||||||
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We also illustrate that up-regulation of TRPV1 and TRPA1 mRNA reflects increases in TRPV1 and TRPA1 responsiveness in the nociceptors that contribute to the molecular mechanisms of the thermal hyperalgesia and mechanical allodynia observed in cisplatin-treated mice. | |||||||||||||||
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While our results illustrate that changes in the relative levels of TRPV1 and TRPA1 mRNA in vivo were similar to those observed in vitro (Figure 2), the increase in TRPM8 mRNA that was observed in oxaliplatin-treated mice was less than that seen in vitro. | |||||||||||||||
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Our objectives were to examine whether propofol modulates TRPV1 function in dorsal root ganglion neurons via activation of PKCepsilon. | |||||||||||||||
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In this study, we selected miogadial (MD), miogatrial (MT), and polygodial (PG) from the terpenoids with an alpha,beta-unsaturated 1,4-dialdehyde moiety and examined the effects of these 3 terpenoids on TRPA1 or TRPV1. | |||||||||||||||
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The reason that there has been no study describing the involvement of a PKC-dependent pathway in the regulation of TRPV1 following prostaglandin receptor activation is not clear. | |||||||||||||||
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VR1 activity is regulated both directly and indirectly by endogenous factors. | |||||||||||||||
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More importantly, we show that the shRNA and miRNA sequences targeting trpV1 have no effect on the expression levels of the closely related trpA1 gene or stat1, which is another gene involved in the INF response, when expressed in neurons in vivo. | |||||||||||||||
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Overall, the regulation of Trpv1 did not correlate significantly with any of the pain parameters considered. | |||||||||||||||
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Regardless, BH4-induced intracellular calcium increase in primary cultured DRG neurons is partly dependent on NOS [19], and essentially dependent on TRPV1 and TRPA1 (Fig. 5). | |||||||||||||||
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The plasticity of A-fiber neurons is an important mechanism that causes hyperalgesia following inflammation, therefore, increased TDAG8 expression in A-fiber could be involved in mechanical and thermal hyperalgesia by regulating TRPV1 function. | |||||||||||||||
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The functional regulation of TRPV1 and its role in pain sensitization. | |||||||||||||||
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Recently, advances have been made at the molecular and biochemical level to understand how phosphorylation by protein kinases regulates TRPV1 desensitization. | |||||||||||||||
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The TRPV1 channel is known to be a critical molecular transducer of heat and is modulated by protons [19]. | |||||||||||||||
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Therefore, we examined the effects of a selective TRPV1 antagonist, 5-iodoresiniferatoxin (I-RTX), on mouse body temperature. | |||||||||||||||
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TRPV1: a therapeutic target for novel analgesic drugs? | |||||||||||||||
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To determine if changes in TRPV1 staining among DRG might be due to either ectopic expression or neuronal loss, we determined the average percentage of neurons expressing TRPV1 per section (Fig. 7C). | |||||||||||||||
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We have used near saturating concentrations of capsaicin and the differences in current amplitude suggest that the TRPV1 protein content as a result of altered transcriptional regulation is higher and lower in hyper and hypoalgesic mice, respectively rather than phosphorylation state of TRPV1, where they showed prolongation of decay phase [41].
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