Differentiation dependent expression of TRPA1 and TRPM8 channels in IMR‐32 human neuroblastoma cells

Louhivuori, Lauri; Bart, Geneviève; Larsson, Kim; Louhivuori, Verna; Näsman, Johnny; Nordström, Tommy; Koivisto, Ari; Åkerman, Karl E.O.

doi:10.1002/jcp.21828

Cited by 31 publications

(19 citation statements)

References 37 publications

(75 reference statements)

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“…2A, B) and differentiated IMR-32 human neuroblastoma cells (Fig. 2D, E), which have been previously reported to express the TRPA1 channel (27). Calcium responses to NAPQI and cinnamaldehyde in human TRPA1 were abated by HC-030031 ( Fig.…”

Section: Napqi Selectively Activates the Recombinant And The Native Tmentioning

confidence: 84%

Acetaminophen,viaits reactive metaboliteN-acetyl-p-benzo-quinoneimine and transient receptor potential ankyrin-1 stimulation, causes neurogenic inflammation in the airways and other tissues in rodents

Nassini¹,

Materazzi²,

André³

et al. 2010

The FASEB Journal

101

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Acetaminophen [N-acetyl-p-aminophenol (APAP)] is the most common antipyretic/analgesic medicine worldwide. If APAP is overdosed, its metabolite, N-acetyl-p-benzo-quinoneimine (NAPQI), causes liver damage. However, epidemiological evidence has associated previous use of therapeutic APAP doses with the risk of chronic obstructive pulmonary disease (COPD) and asthma. The transient receptor potential ankyrin-1 (TRPA1) channel is expressed by peptidergic primary sensory neurons. Because NAPQI, like other TRPA1 activators, is an electrophilic molecule, we hypothesized that APAP, via NAPQI, stimulates TRPA1, thus causing airway neurogenic inflammation. NAPQI selectively excites human recombinant and native (neuroblastoma cells) TRPA1. TRPA1 activation by NAPQI releases proinflammatory neuropeptides (substance P and calcitonin gene-related peptide) from sensory nerve terminals in rodent airways, thereby causing neurogenic edema and neutrophilia. Single or repeated administration of therapeutic (15-60 mg/kg) APAP doses to mice produces detectable levels of NAPQI in the lung, and increases neutrophil numbers, myeloperoxidase activity, and cytokine and chemokine levels in the airways or skin. Inflammatory responses evoked by NAPQI and APAP are abated by TRPA1 antagonism or are absent in TRPA1-deficient mice. This novel pathway, distinguished from the tissue-damaging effect of NAPQI, may contribute to the risk of COPD and asthma associated with therapeutic APAP use.

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Section: Napqi Selectively Activates the Recombinant And The Native Tmentioning

confidence: 84%

Acetaminophen,viaits reactive metaboliteN-acetyl-p-benzo-quinoneimine and transient receptor potential ankyrin-1 stimulation, causes neurogenic inflammation in the airways and other tissues in rodents

Nassini¹,

Materazzi²,

André³

et al. 2010

The FASEB Journal

101

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show abstract

“…Therefore, the identification of a safe, effective and low toxicity anticancer drug has attracted interest from researchers, and the development of these drugs from natural sources has become an important strategy in the development of antitumor drugs. As a type of plant chemical that is prevalent in the natural diet of humans, AITC may affect the proliferation of a variety of tumor cells (19,20), and has attracted extensive attention from researchers. The anticancer effect of AITC has been verified by studies in vivo and in vitro (21,22), but the function of AITC in the treatment of cervical cancer has not been reported.…”

Section: Discussionmentioning

confidence: 99%

Effect of allyl isothiocyanate on the viability and apoptosis of the human cervical cancer HeLa cell line inï¿½vitro

Qin

Xue

2018

Oncol Lett

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Abstract. The present study aimed to investigate the effect of allyl isothiocyanate (AITC) on the viability and apoptosis of the human cervical cancer HeLa cell line in vitro, and to explore the potential underlying mechanisms of this. HeLa cells were treated with varying concentrations of AITC for different durations. The cell viability was then measured using a Cell Counting kit-8 assay and the apoptosis rate of the cells was detected using flow cytometry. Additionally, the B cell lymphoma-2 (Bcl-2) and Bcl-2-associated X protein (Bax) mRNA expression levels were determined by reverse transcription-quantitative polymerase chain reaction, while the Bax and Bcl-2 protein expression levels in cells were detected by western blot analysis. AITC was revealed to inhibit the viability of HeLa cells. AITC was revealed to induce the apoptosis of HeLa cells, as the apoptosis rate increased gradually with an increase in the dose. As the concentration of AITC increased, the Bax mRNA expression level increased, whilst the Bcl-2 mRNA expression level decreased. Furthermore, the Bax protein expression intensity increased whilst Bcl-2 protein expression intensity decreased, thereby resulting in a decrease in the ratio of Bcl-2/Bax proteins. AITC may inhibit cell viability by inducing the apoptosis of HeLa cells and this may be accounted for by the imbalance in the Bcl-2/Bax expression ratio.

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“…We discarded cells without response to MO. When differentiated to neuronal cells (nIMR-32), IMR-32 human neuroblastoma (IMR-32) cells were treated with 5 M 5-bromo-2=-deoxyuridine (BrdU) and were then cultured for 12 days in BrdUcontaining medium that was exchanged every 2 days (24).…”

Section: Methodsmentioning

confidence: 99%

Stimulation of human TRPA1 channels by clinical concentrations of the antirheumatic drug auranofin

Hatano

Suzuki

Muraki

et al. 2013

American Journal of Physiology-Cell Physiology

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Gold compounds, which were widely used to treat rheumatoid arthritis, have been recently used as experimental agents for tumor treatment. Transient receptor potential (TRP) ankyrin repeat 1 (TRPA1) is a Ca(2+)-permeable ion channel that senses acute and inflammatory pain signals. Electrophilic compounds such as mustard oil and cinnamaldehyde activate TRPA1 by interacting with TRPA1 cysteine residues. Here we investigate the effects of the gold compound auranofin (AUR) on TRPA1 channels. Intracellular Ca(2+) and whole cell patch-clamp recordings were performed on human embryonic kidney cells transiently expressed with TRPA1, TRP melastatin 8 (TRPM8), and vanilloid type TRP (TRPV1-4) channels. AUR stimulated TRPA1 in a concentration-dependent manner with a half-maximum potency of around 1.0 μM. The AUR-induced response was effectively blocked by HC030031, a TRPA1 antagonist. On the other hand, AUR failed to activate TRPM8 and TRPV1-4 channels, which are highly expressed in sensory neurons as nociceptors. The stimulatory effect on TRPA1 channels depended on the C414, C421, C621, and C633 cysteine residues and not on the inhibition of thioredoxin reductase by AUR. Moreover, AUR effectively activated TRPA1 channels expressed in human differentiated neuroblastoma cell lines. The study shows that AUR is a potent stimulator of TRPA1 channels.

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Differentiation dependent expression of TRPA1 and TRPM8 channels in IMR‐32 human neuroblastoma cells

Cited by 31 publications

References 37 publications

Acetaminophen,viaits reactive metaboliteN-acetyl-p-benzo-quinoneimine and transient receptor potential ankyrin-1 stimulation, causes neurogenic inflammation in the airways and other tissues in rodents

Acetaminophen,viaits reactive metaboliteN-acetyl-p-benzo-quinoneimine and transient receptor potential ankyrin-1 stimulation, causes neurogenic inflammation in the airways and other tissues in rodents

Effect of allyl isothiocyanate on the viability and apoptosis of the human cervical cancer HeLa cell line inï¿½vitro

Stimulation of human TRPA1 channels by clinical concentrations of the antirheumatic drug auranofin

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