Activation of transient receptor potential ankyrin 1 by hydrogen peroxide

Sawada, Yosuke; Hosokawa, Hiroshi; Matsumura, Kiyoshi; Kobayashi, Shígeo

doi:10.1111/j.1460-9568.2008.06093.x

Cited by 212 publications

(175 citation statements)

References 46 publications

Supporting

Mentioning

160

Contrasting

Order By: Relevance

“…Covalent modification of TRPA1 by allyl-isothiocyanate or alkylating agents excites pain fibers, evoking acute pain and nocifensive behaviors. Hydrogen peroxide (H 2 O 2 ) and ␣,␤-unsaturated aldehydes acutely activate TRPA1 (12)(13)(14)(15). The reactive compound allicin from garlic and nitric oxide activate TRPA1 and TRPV1 via covalent modification (16)(17)(18)(19)(20)(21)(22), providing examples for oxidative stress-related pain or hyperalgesia.…”

mentioning

confidence: 99%

Oxidative challenges sensitize the capsaicin receptor by covalent cysteine modification

Chuang

Lin

2009

Proc. Natl. Acad. Sci. U.S.A.

166

119

View full text Add to dashboard Cite

The capsaicin receptor TRPV1, one of the major transduction channels in the pain pathway, integrates information from extracellular milieu to control excitability of primary nociceptive neurons. Sensitization of TRPV1 heightens pain sensation to moderately noxious or even innocuous stimuli. We report here that oxidative stress markedly sensitizes TRPV1 in multiple species' orthologs. The sensitization can be recapitulated in excised insideout membrane patches, reversed by strong reducing agents, and blocked by pretreatment with maleimide that alkylates cysteines. We identify multiple cysteines required for full modulation of TRPV1 by oxidative challenges. Robust oxidative modulation recovers the agonist sensitivity of receptors desensitized by prolonged exposure to capsaicin. Moreover, oxidative modulation operates synergistically with kinase or proton modulations. Thus, oxidative modulation is a robust mechanism tuning TRPV1 activity via covalent modification of evolutionarily conserved cysteines and may play a role in pain sensing processes during inflammation, infection, or tissue injury.covalent modification ͉ pain

show abstract

mentioning

confidence: 99%

Oxidative challenges sensitize the capsaicin receptor by covalent cysteine modification

Chuang

Lin

2009

Proc. Natl. Acad. Sci. U.S.A.

166

119

View full text Add to dashboard Cite

show abstract

“…1C), we tested whether TRPA1 mediates the UVR photocurrent. TRPA1 is activated by numerous noxious compounds, pungent chemicals, and GPCRs (27)(28)(29)(30)(31), and was recently implicated in an extraocular UVR phototransduction system mediating light avoidance responses in Drosophila larvae (32).…”

mentioning

confidence: 99%

UV light phototransduction activates transient receptor potential A1 ion channels in human melanocytes

Bellono

Kammel

Zimmerman

et al. 2013

Proc. Natl. Acad. Sci. U.S.A.

123

139

View full text Add to dashboard Cite

Human skin is constantly exposed to solar ultraviolet radiation (UVR), the most prevalent environmental carcinogen. Humans have the unique ability among mammals to respond to UVR by increasing their skin pigmentation, a protective process driven by melanin synthesis in epidermal melanocytes. The molecular mechanisms used by melanocytes to detect and respond to longwavelength UVR (UVA) are not well understood. We recently identified a UVA phototransduction pathway in melanocytes that is mediated by G protein-coupled receptors and leads to rapid calcium mobilization. Here we report that in human epidermal melanocytes physiological doses of UVR activate a retinal-dependent current mediated by transient receptor potential A1 (TRPA1) ion channels. The TRPA1 photocurrent is UVA-specific and requires G protein and phospholipase C signaling, thus contributing to UVAinduced calcium responses to mediate downstream cellular effects and providing evidence for TRPA1 function in mammalian phototransduction. Remarkably, TRPA1 activation is required for the UVR-induced and retinal-dependent early increase in cellular melanin. Our results show that TRPA1 is essential for a unique extraocular phototransduction pathway in human melanocytes that is activated by physiological doses of UVR and results in early melanin synthesis.

show abstract

“…Similarly, whether or not TRPA1 functions as a sensor of noxious cold remains an unresolved question. Several studies demonstrated that noxious cold activates TRPA1 channels, both directly [118][119][120] and indirectly [121]. However, negative results were obtained in mouse TRPA1 channels heterologously expressed in human embryonic kidney cells [122], and neuronal activation by cold temperatures was found to be similar between wild-type and TRPA1 knock-out mice [123].…”

Section: Trpa1mentioning

confidence: 78%

Transient Receptor Potential Channels in Chemotherapy-Induced Neuropathy

Nassini¹,

Benemei²,

Fusi³

et al. 2013

TOPAINJ

View full text Add to dashboard Cite

Chemotherapy-Induced Peripheral Neuropathy (CIPN) is a common dose-limiting side effect of many chemotherapeutic drugs, including platinum-based compounds (e.g., cisplatin and oxaliplatin), taxanes (e.g., paclitaxel), vinca alkaloids (e.g., vincristine), and the first-in-class proteasome inhibitor, bortezomib. Among the various sensory symptoms of CIPN, paresthesia, dysesthesia, spontaneous pain, and mechanical and thermal hypersensitivity are prominent. Inflammation, oxidative stress, loss of intraepidermal nerve fibers, modifications of mitochondria, and various ion channels alterations are part of the several mechanisms contributing to CIPN. Because attempts to mitigate chemotherapeutic-induced acute neuronal hyperexcitability and the subsequent peripheral neuropathy have yielded unsatisfactory results, a more in-depth understanding of the mechanism(s) responsible for the neurotoxic action of anticancer drugs is required.Some members of the transient receptor potential (TRP) family of channels, as the TRPV1 and TRPV4 (vanilloid), TRPA1 (ankyrin) and TRPM8 (melastatin) are expressed on the plasma membrane of primary sensory neurons (nociceptors), where they are activated by an unprecedented series of physical and chemical stimuli. There is evidence that TRPV1, TRPV4, TRPA1 and TRPM8 are prominent contributors of mechanical and thermal hypersensitivity in models of CIPN. In particular, in vitro and in vivo studies have pointed out the unique role of TRPA1 and oxidative stress in the mechanism responsible for cold and mechanical hyperalgesia in rodent models of CIPN.

show abstract

Activation of transient receptor potential ankyrin 1 by hydrogen peroxide

Cited by 212 publications

References 46 publications

Oxidative challenges sensitize the capsaicin receptor by covalent cysteine modification

Oxidative challenges sensitize the capsaicin receptor by covalent cysteine modification

UV light phototransduction activates transient receptor potential A1 ion channels in human melanocytes

Transient Receptor Potential Channels in Chemotherapy-Induced Neuropathy

Contact Info

Product

Resources

About