Paclitaxel Induces Upregulation of Transient Receptor Potential Vanilloid 1 Expression in the Rat Spinal Cord

Kamata, Yukako; Kambe, Toshie; Chiba, Toshinori; Yamamoto, Ken; Kawakami, Kazuyoshi; Abe, Kenji; Taguchi, Kyoji

doi:10.3390/ijms21124341

Cited by 25 publications

(21 citation statements)

References 53 publications

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“…Involvement in paclitaxel-induced peripheral neuropathy TRPV1 [59][60][61][62][63][64][65] Increased expression in DRG and superficial layers of SDH [59][60][61][62][63][64] and increased levels of sensitization [64,65].…”

Section: Name Channel Direction Of Regulationmentioning

confidence: 99%

Neuro-immune interactions in paclitaxel-induced peripheral neuropathy

et al. 2021

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Background: Paclitaxel is a taxane-based chemotherapeutic agent used as a treatment in breast cancer. There is no effective prevention or treatment strategy for the most common side effect of peripheral neuropathy. In this manuscript, we reviewed the molecular mechanisms that contribute to paclitaxel-induced peripheral neuropathy (PIPN) with an emphasis on immune-related processes. Methods: A systematic search of the literature was conducted in PubMed, EMBASE and Cochrane Library. The SYRCLE's risk of bias tool was used to assess internal validity. Results: 156 studies conducted with rodent models were included. The risk of bias was high due to unclear methodology. Paclitaxel induces changes in myelinated axons, mitochondrial dysfunction, and mechanical hypersensitivity by affecting ion channels expression and function and facilitating spinal transmission. Paclitaxel-induced inflammatory responses are important contributors to PIPN. Conclusion: Immune-related processes are an important mechanism contributing to PIPN. Studies in humans that validate these mechanistic data are highly needed to facilitate the development of therapeutic strategies.

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Section: Name Channel Direction Of Regulationmentioning

confidence: 99%

Neuro-immune interactions in paclitaxel-induced peripheral neuropathy

et al. 2021

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“…Treatment with oxaliplatin increases the expression of TRPV1, TRPV4, TRPA1, and TRPM8, and the upregulation of TRPA1 and TRPM8 in mice and rats is associated with oxaliplatin-induced cold allodynia [ 51 , 52 , 53 ]. Furthermore, TRPV1 and TRPV4 are involved in paclitaxel-induced cold and mechanical allodynia in rats and mice [ 54 , 55 , 56 ]. In addition, ERK activation in DRG nociceptive neurons promotes TRPV1 expression [ 57 ].…”

Section: Discussionmentioning

confidence: 99%

Gabapentin and Duloxetine Prevent Oxaliplatin- and Paclitaxel-Induced Peripheral Neuropathy by Inhibiting Extracellular Signal-Regulated Kinase 1/2 (ERK1/2) Phosphorylation in Spinal Cords of Mice

et al. 2020

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Chemotherapy-induced peripheral neuropathy is a common factor in limiting therapy which can result in therapy cessation or dose reduction. Gabapentin, a calcium channel inhibitor, and duloxetine, a serotonin noradrenaline reuptake inhibitor, are used to treat a variety of pain conditions such as chronic low back pain, postherpetic neuralgia, and diabetic neuropathy. It has been reported that administration of gabapentin suppressed oxaliplatin- and paclitaxel-induced mechanical hyperalgesia in rats. Moreover, duloxetine has been shown to suppress oxaliplatin-induced cold allodynia in rats. However, the mechanisms by which these drugs prevent oxaliplatin- and paclitaxel-induced neuropathy remain unknown. Behavioral assays were performed using cold plate and the von Frey test. The expression levels of proteins were examined using western blot analysis. In this study, we investigated the mechanisms by which gabapentin and duloxetine prevent oxaliplatin- and paclitaxel-induced neuropathy in mice. We found that gabapentin and duloxetine prevented the development of oxaliplatin- and paclitaxel-induced cold and mechanical allodynia. In addition, our results revealed that gabapentin and duloxetine suppressed extracellular signal-regulated protein kinase 1/2 (ERK1/2) phosphorylation in the spinal cord of mice. Moreover, PD0325901 prevented the development of oxaliplatin- and paclitaxel-induced neuropathic-like pain behavior by inhibiting ERK1/2 activation in the spinal cord of mice. In summary, our findings suggest that gabapentin, duloxetine, and PD0325901 prevent the development of oxaliplatin- and paclitaxel-induced neuropathic-like pain behavior by inhibiting ERK1/2 phosphorylation in mice. Therefore, inhibiting ERK1/2 phosphorylation could be an effective preventive strategy against oxaliplatin- and paclitaxel-induced neuropathy.

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“…Temperature-sensitive cation channels (e.g., transient receptor potential vanilloid 4 (TRPV4), transient receptor potential vanilloid 1 (TRPV1), and transient receptor potential ankyrin 1 (TRPA1)) have been reported to be involved in PIPN [61,[107][108][109]. Many drugs have also been reported to improve PIPN by downregulating or inhibiting TRP channels [55,[60][61][62][63][64].…”

Section: Transient Receptor Potential (Trp) Modulatorsmentioning

confidence: 99%

Preclinical and Clinical Evidence of Therapeutic Agents for Paclitaxel-Induced Peripheral Neuropathy

Kawashiri

Inoue

Mori

et al. 2021

IJMS

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Paclitaxel is an essential drug in the chemotherapy of ovarian, non-small cell lung, breast, gastric, endometrial, and pancreatic cancers. However, it frequently causes peripheral neuropathy as a dose-limiting factor. Animal models of paclitaxel-induced peripheral neuropathy (PIPN) have been established. The mechanisms of PIPN development have been elucidated, and many drugs and agents have been proven to have neuroprotective effects in basic studies. In addition, some of these drugs have been validated in clinical studies for their inhibitory PIPN effects. This review summarizes the basic and clinical evidence for therapeutic or prophylactic effects for PIPN. In pre-clinical research, many reports exist of neuropathy inhibitors that target oxidative stress, inflammatory response, ion channels, transient receptor potential (TRP) channels, cannabinoid receptors, and the monoamine nervous system. Alternatively, very few drugs have demonstrated PIPN efficacy in clinical trials. Thus, enhancing translational research to translate pre-clinical research into clinical research is important.

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Paclitaxel Induces Upregulation of Transient Receptor Potential Vanilloid 1 Expression in the Rat Spinal Cord

Cited by 25 publications

References 53 publications

Neuro-immune interactions in paclitaxel-induced peripheral neuropathy

Neuro-immune interactions in paclitaxel-induced peripheral neuropathy

Gabapentin and Duloxetine Prevent Oxaliplatin- and Paclitaxel-Induced Peripheral Neuropathy by Inhibiting Extracellular Signal-Regulated Kinase 1/2 (ERK1/2) Phosphorylation in Spinal Cords of Mice

Preclinical and Clinical Evidence of Therapeutic Agents for Paclitaxel-Induced Peripheral Neuropathy

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