Cigarette smoke extract (CSE) induces transient receptor potential ankyrin 1(TRPA1) expression via activation of HIF1αin A549 cells

Nie, Yichu; Huang, Chuqin; Zhong, Shan; Wortley, Michael A.; Luo, Yu-Long; Luo, Wei; Xie, Yanqing; Lai, Kefang; Zhong, Nanshan

doi:10.1016/j.freeradbiomed.2016.07.028

Cited by 27 publications

(24 citation statements)

References 35 publications

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“…These data are supported by findings, that 4-week CSE increases TRPA1 mRNA level in the nodose and jugular ganglia, positively correlating with the inflammatory cell infiltration in the BALF [84]. Moreover, cigarette smoke extract also increased the expression of TRPA1 in airway epithelial cells in a hypoxia-inducible factor-1α-mediated manner [17,85]. Mostly in vitro data using cigarette smoke extract are available about the role of TRPA1 in cigarette smoke-induced airway inflammation.…”

Section: Endotoxin-induced Acute Inflammationsupporting

confidence: 60%

Complex Regulatory Role of the TRPA1 Receptor in Acute and Chronic Airway Inflammation Mouse Models

Hajna

Csekő

Kemény

et al. 2020

IJMS

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The Transient Receptor Potential Ankyrin 1 (TRPA1) cation channel expressed on capsaicin-sensitive afferents, immune and endothelial cells is activated by inflammatory mediators and exogenous irritants, e.g., endotoxins, nicotine, crotonaldehyde and acrolein. We investigated its involvement in acute and chronic pulmonary inflammation using Trpa1 gene-deleted (Trpa1−/−) mice. Acute pneumonitis was evoked by intranasal Escherichia coli endotoxin (lipopolysaccharide: LPS) administration, chronic bronchitis by daily cigarette smoke exposure (CSE) for 4 months. Frequency, peak inspiratory/expiratory flows, minute ventilation determined by unrestrained whole-body plethysmography were significantly greater, while tidal volume, inspiratory/expiratory/relaxation times were smaller in Trpa1−/− mice. LPS-induced bronchial hyperreactivity, myeloperoxidase activity, frequency-decrease were significantly greater in Trpa1−/− mice. CSE significantly decreased tidal volume, minute ventilation, peak inspiratory/expiratory flows in wildtypes, but not in Trpa1−/− mice. CSE remarkably increased the mean linear intercept (histopathology), as an emphysema indicator after 2 months in wildtypes, but only after 4 months in Trpa1−/− mice. Semiquantitative histopathological scores were not different between strains in either models. TRPA1 has a complex role in basal airway function regulation and inflammatory mechanisms. It protects against LPS-induced acute pneumonitis and hyperresponsiveness, but is required for CSE-evoked emphysema and respiratory deterioration. Further research is needed to determine TRPA1 as a potential pharmacological target in the lung.

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Section: Endotoxin-induced Acute Inflammationsupporting

confidence: 60%

Complex Regulatory Role of the TRPA1 Receptor in Acute and Chronic Airway Inflammation Mouse Models

Hajna

Csekő

Kemény

et al. 2020

IJMS

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“…Moreover, CSE upregulates expression of TRPA1 in A549 cells (Nie et al. ). However, the limitation of this study is that the final concentration of 9,10‐PQ around airway organs has not been determined when exposed to cigarette smoke and pollutant air.…”

Section: Discussionmentioning

confidence: 99%

“…Since 9,10-PQ is included in CSE and DEP, it is likely that 9,10-PQ acutely activates TRPA1 in airway organs when inhaled. Moreover, CSE upregulates expression of TRPA1 in A549 cells (Nie et al 2016). However, the limitation of this study is that the final concentration of 9,10-PQ around airway organs has not been determined when exposed to cigarette smoke and pollutant air.…”

Section: Discussionmentioning

confidence: 99%

An environmental pollutant, 9,10‐phenanthrenequinone, activates human TRPA1 via critical cysteines 621 and 665

Muraki

Sekine

Ando

et al. 2017

Pharmacology Res & Perspec

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Transient receptor potential ankyrin 1 (TRPA1) is activated by noxious cold, mechanical stimulation, and irritant chemicals. In our recent study, 9, 10‐phenanthrenequinone (9,10‐PQ) is the most potent irritant for activation of NRF2 among 1395 cigarette smoke components and it may be, therefore, important to find its additional targets. Here, we show that 9,10‐PQ functions as an activator of TRPA1 in human embryonic kidney (HEK) cells expressing human wild‐type TRPA1 (HEK‐wTRPA1) and human alveolar A549 (A549) cells. Application of 9,10‐PQ at 0.1–10 μmol/L induced a concentration‐dependent Ca2+ response as well as inward currents at −50 mV in HEK‐wTRPA1 cells. The current response was blocked by TRPA1 antagonists, HC‐030031 (HC) and A‐967079. To test whether 9,10‐PQ affects the cysteine residues of TRPA1, we expressed mutant TRPA1 channels in HEK cells (HEK‐muTRPA1) in which six different cysteine residues were replaced with serine. Among them, a mutation of cysteine 621 (C621S) abolished the 9,10‐PQ‐induced Ca2+ and current responses. The channel activity induced by 9,10‐PQ was also abolished in excised inside‐out patches isolated from HEK‐muTRPA1 cells with the C621S substitution. Although a mutation of cysteine 665 (C665S) reduced the 9,10‐PQ‐induced response, channel sensitization by pretreatment with Cu2+ plus 1,10‐phenanthroline and by internal dialysis of 3 μmol/L Ca2+ restored the response. However, a double mutant with C621S and C665S substitutions had little response to 9,10‐PQ, even when sensitized by Ca2+ dialysis. In A549 cells, 9,10‐PQ induced an HC‐sensitive Ca2+ response. Our findings demonstrate that 9,10‐PQ activation of human TRA1 is dependent on cysteine residues 621 and 665.

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“…Cigarette smoke extract induces expression of TRPA1 channels via HIF‐1α activation in A549 human alveolar adenocarcinoma cells (Nie et al ., ). The influence of sulfide on HIF‐1α activity and expression is still debatable.…”

Section: Putative Mechanisms Of Sulfide‐trpa1 Channel Interactionsmentioning

confidence: 97%

Effects of sulfide and polysulfides transmitted by direct or signal transduction‐mediated activation of TRPA1 channels

Pozsgai

Bátai

Pintér

2018

British J Pharmacology

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Hydrogen sulfide (H2S) is a gaseous mediator in various physiological and pathological processes, including neuroimmune modulation, metabolic pathways, cardiovascular system, tumour growth, inflammation and pain. Now the hydrogen polysulfides (H2Sn) have been recognised as signalling molecules modulating ion channels, transcription factors and protein kinases. Transient receptor potential (TRP) cation channels can be activated by mechanical, thermal or chemical triggers. Here, we review the current literature regarding the biological actions of sulfide and polysulfide compounds mediated by TRP channels with special emphasis on the role of TRPA1, best known as ion channels in nociceptors. However, the non‐neuronal TRPA1 channels should also be considered to play regulatory roles. Although sulfide and polysulfide effects in different pathological circumstances and TRPA1‐mediated processes have been investigated intensively, our review attempts to present the first comprehensive overview of the potential crosstalk between TRPA1 channels and sulfide‐activated signalling pathways.Linked ArticlesThis article is part of a themed section on Chemical Biology of Reactive Sulfur Species. To view the other articles in this section visit http://onlinelibrary.wiley.com/doi/10.1111/bph.v176.4/issuetoc

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Cigarette smoke extract (CSE) induces transient receptor potential ankyrin 1(TRPA1) expression via activation of HIF1αin A549 cells

Cited by 27 publications

References 35 publications

Complex Regulatory Role of the TRPA1 Receptor in Acute and Chronic Airway Inflammation Mouse Models

Complex Regulatory Role of the TRPA1 Receptor in Acute and Chronic Airway Inflammation Mouse Models

An environmental pollutant, 9,10‐phenanthrenequinone, activates human TRPA1 via critical cysteines 621 and 665

Effects of sulfide and polysulfides transmitted by direct or signal transduction‐mediated activation of TRPA1 channels

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