Inhibitory effects of nicotine derived from cigarette smoke on thymic stromal lymphopoietin production in epidermal keratinocytes

Dong, Jing; Segawa, Ryosuke; Mizuno, Natsumi; Hiratsuka, Masahiro; Hirasawa, Noriyasu

doi:10.1016/j.cellimm.2016.01.001

Cited by 14 publications

(8 citation statements)

References 46 publications

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“…The function of nicotine on cancer cells at the nAChR subtype level is valuable for cancer prevention and treatment ( Russo et al, 2011 ; Wu et al, 2011 ; Cardinale et al, 2012 ; Yang et al, 2013 ). In keratinocytes, α3β2-nAChR and α7-nAChR are necessary for nicotinergic chemokinesis, and α9-nAChR is critical for adhesion and motility ( Chernyavsky et al, 2004 ; Arredondo et al, 2006 ; Dong et al, 2016 ). Similarly, in breast epithelial cells α9-nAChR is responsible for nicotine-stimulated cell growth and malignant transformation ( Lee et al, 2010 ; Tu et al, 2011 ).…”

Section: Discussionmentioning

confidence: 99%

Alpha5 Nicotinic Acetylcholine Receptor Contributes to Nicotine-Induced Lung Cancer Development and Progression

Sun

Jia

2017

Front. Pharmacol.

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Nicotine and nicotinic acetylcholine receptors (nAChRs) are considered to be involved in lung cancer risk, onset and progression, but their precise physiological roles in these contexts remain unclear. Our previous studies suggested that α5-nAChR mediates nicotine-induced lung cancer cell proliferation, migration, and invasion in vitro. In this study, we aimed to determine the role of α5-nAChR in the development and progression of non-small cell lung cancer (NSCLC). Our microarray results reveal that knockdown of the CHRNA5 gene encoding α5-nAChR significantly modulates key pathways including the cell cycle, DNA replication, pathway in cancer. α5-nAChR knockdown in cultured A549 cells affected cell cycle distribution, apoptosis, and cyclin expression. In vivo, α5-nAChR silencing inhibited the growth of lung tumors, especially in the context of nicotine exposure. Importantly, α5-nAChR expression in patient tumors correlated with the primary T stage, N stage, and reduced survival time. These results reveal that α5-nAChR silencing inhibits the progression of nicotine-related NSCLC, making this receptor a potential pharmacological target for the treatment of nicotine-related lung carcinogenesis.

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Section: Discussionmentioning

confidence: 99%

Alpha5 Nicotinic Acetylcholine Receptor Contributes to Nicotine-Induced Lung Cancer Development and Progression

Sun

Jia

2017

Front. Pharmacol.

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“…However, in our experiment, the nAchR inhibitors did not show significant effects on keratinocytes (Figure 4). This could be due to either lower concentration or longer exposure (24 h) of keratinocytes to nAchR inhibitors, which were used in this study compared to the literature (47,48).…”

Section: Discussionmentioning

confidence: 99%

Protective Effects of Pinus halepensis Bark Extract and Nicotine on Cigarette Smoke-induced Oxidative Stress in Keratinocytes

Pavlou

Antoniadou

Peraki

et al. 2020

In Vivo

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Background/Aim: Cigarette smoke (CS) is a major environmental health threat. The oxidative stress induced by CS on keratinocytes and the possible protective effect of nicotine, its receptor inhibitors, and Pinus halepensis bark extract in relation to known antioxidants were investigated. Materials and Methods: Primary mouse keratinocytes were exposed to cigarette smoke in the presence and absence of Pinus halepensis bark extract (1 μg/ml), rutin (50 μΜ) and ascorbic acid (250 μΜ), nicotine (1 μM) with or without mecamylamine (5 μM) and α-bungarotoxin (0.1 μΜ). Keratinocyte viability and oxidative stress were evaluated by MTT and fluorescence assays. Results: Pinus halepensis bark extract decreased the oxidative stress and increased the viability of keratinocytes, and moreover, these effects were more pronounced compared to the mixture of rutin and Lascorbic acid. Nicotine significantly enhanced the viability potentiation of the beneficial effect induced by Pinus halepensis bark extract. Mecamylamine and α-bungarotoxin showed no specific effect. Conclusion: Pinus halepensis bark extract in combination with nicotine may successfully reverse skin damage induced by cigarette smoke. Cigarette smoke (CS) is a global problem of our society and according to the World Health Organization "the tobacco epidemic is one of the biggest public health threats the world has ever faced, killing more than 8 million people a year" (1). The Lancet Commission on pollution and health characterized CS as more dangerous than AIDS, tuberculosis, and malaria (2). CS is associated with cardiovascular diseases, higher risk of skin diseases, such as squamous cell carcinoma and atopic dermatitis, and is connected with decreased wound healing rate (3-7). The skin is the most important target for the harmful effect of CS pollution. Both solid and gas products of CS contain aniline, N-nitrosodimethylamine, benzopyrenes, acrolein, formaldehyde, N-nitrosopyrrolidine that are considered to be toxic, causing serious oxidative damage (8). CS produces reactive oxygen and nitrogen species oxidizing important biomolecules such as DNA, proteins and lipids leading to tissue injury which is translated to enhanced inflammatory phenomena (9-14). One of the main constituents of CS is nicotine; it is an agonist of acetylcholine and acts on the epidermis via the keratinocyte nicotinic acetylcholine receptors (nAChRs) (15). nAChRs are large (290 kDa) pentameric transmembrane complexes, which are ligand-gated ion channels (LGICs) permeable to Na, K and Ca ions (16, 17). Nicotine activity is doubtful as it has been shown to exert both toxic and beneficial effects; it has been reported as neurotoxic and neuroprotectant (18), toxic to muscles and lung epithelium (19, 20), beneficial in colitis (21), while its potential activity on mitochondria apparently requires further investigation (22). Concerning inflammatory and wound healing processes, the effect of nicotine is considered rather negative, while topical nAchR antagonists have been shown to improve these negativ...

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“…Inflammation contribute to systemic capillary leakage syndrome, tissue injury and fatal organ failure (1,2). Cholinergic agonist was useful for control of depression, Tourette's syndrome, Parkinson's disease, Crohn's disease and ulcerative colitis (9)(10)(11), indicating that α7 nAChR is crucial for inflammation regulation (30). Preserving cytoplasmic levels of inhibitor of NF-κB (IκB) was found to be essential for nicotine-mediated NF-κB inhibition (5,6).…”

Section: Discussionmentioning

confidence: 99%

“…Substantial evidence points to a critical role of nicotine in preventing nuclear translocation of the NF-κB complex (5,6), which demonstrated the inhibitory effects of nicotine on NF-κB activity (7,8). Although therapeutic use of nicotine has been documented in depression, Tourette's syndrome, Parkinson's disease, Crohn's disease and ulcerative colitis (9)(10)(11), the mechanisms of cholinergic anti-inflammation are still uncertain.…”

Section: Introductionmentioning

confidence: 99%

Nicotine induces TIPE2 upregulation and Stat3 phosphorylation contributes to cholinergic anti-inflammatory effect

Sui

et al. 2017

International Journal of Oncology

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Cholinergic anti-inflammatory pathway has therapeutic effect on inflammation-associated diseases. However, the exact mechanism of nicotine-mediated anti-inflammatory effect is still unclear. TIPE2, a new member of tumor necrosis factor-α-induced protein-8 family, is a negative regulator of immune homeostasis. However, the roles of TIPE2 in cholinergic anti-inflammatory effect are still uncertain. Here, we demonstrated that nicotine exerts its anti-inflammatory effect by TIPE2 upregulation and phosphorylated stat3 mediated the inhibition of NF-κB activation, which was supported by the following evidence: firstly, both nicotine and TIPE2 inhibit pro-inflammatory cytokine release via NF-κB inactivation. Secondly, nicotine upregulates TIPE2 expression via α7 nicotinic acetylcholine receptor. Moreover, the enhancement of stat3 phosphorylation and decrease of LPS-induced p65 translocation were achieved by nicotine treatment. Importantly, nicotine treatment augments the interaction of phosphorylated stat3 and p65, indicating that the inhibitory effect of nicotine on NF-κB activation was mediated with protein-protein interactions. Hence, this study revealed that TIPE2 upregulation and stat3 phosphorylation contribute to nicotine-mediated anti-inflammation effect, indicating that TIPE2 and stat3 might be potential molecules for dealing with inflammation-associated diseases.

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Inhibitory effects of nicotine derived from cigarette smoke on thymic stromal lymphopoietin production in epidermal keratinocytes

Cited by 14 publications

References 46 publications

Alpha5 Nicotinic Acetylcholine Receptor Contributes to Nicotine-Induced Lung Cancer Development and Progression

Alpha5 Nicotinic Acetylcholine Receptor Contributes to Nicotine-Induced Lung Cancer Development and Progression

Protective Effects of Pinus halepensis Bark Extract and Nicotine on Cigarette Smoke-induced Oxidative Stress in Keratinocytes

Nicotine induces TIPE2 upregulation and Stat3 phosphorylation contributes to cholinergic anti-inflammatory effect

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