Nicotine stimulation increases proliferation and matrix metalloproteinases-2 and -28 expression in human dental pulp cells

Rizzi, Manuela; Migliario, Mario; Rocchetti, Vincenzo; Renò, Filippo

doi:10.1016/j.lfs.2015.04.027

Cited by 9 publications

(8 citation statements)

References 40 publications

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“…When the mineralized matrix of a tooth is damaged, the pulp is exposed to a plethora of environmental stimuli. In human dental pulp cells, Manuela et al (97) showed that nicotine (0-50 mM) stimulated MMP2 and MMP28 gene expression extracted from impacted third molars of healthy patients. In addition, nicotine (5, 10, and 50 mM) can increase human dental pulp cell proliferation through nicotinic cholinergic receptors and downstream MAPK signaling pathways.…”

Section: Pro-inflammatory Effect Of Nicotine On Oral Diseasesmentioning

confidence: 99%

Nicotine in Inflammatory Diseases: Anti-Inflammatory and Pro-Inflammatory Effects

et al. 2022

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As an anti-inflammatory alkaloid, nicotine plays dual roles in treating diseases. Here we reviewed the anti-inflammatory and pro-inflammatory effects of nicotine on inflammatory diseases, including inflammatory bowel disease, arthritis, multiple sclerosis, sepsis, endotoxemia, myocarditis, oral/skin/muscle inflammation, etc., mainly concerning the administration methods, different models, therapeutic concentration and duration, and relevant organs and tissues. According to the data analysis from recent studies in the past 20 years, nicotine exerts much more anti-inflammatory effects than pro-inflammatory ones, especially in ulcerative colitis, arthritis, sepsis, and endotoxemia. On the other hand, in oral inflammation, nicotine promotes and aggravates some diseases such as periodontitis and gingivitis, especially when there are harmful microorganisms in the oral cavity. We also carefully analyzed the nicotine dosage to determine its safe and effective range. Furthermore, we summarized the molecular mechanism of nicotine in these inflammatory diseases through regulating immune cells, immune factors, and the vagus and acetylcholinergic anti-inflammatory pathways. By balancing the “beneficial” and “harmful” effects of nicotine, it is meaningful to explore the effective medical value of nicotine and open up new horizons for remedying acute and chronic inflammation in humans.

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Section: Pro-inflammatory Effect Of Nicotine On Oral Diseasesmentioning

confidence: 99%

Nicotine in Inflammatory Diseases: Anti-Inflammatory and Pro-Inflammatory Effects

et al. 2022

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“…Nicotine, a main constituent in many e-cigarettes, may have a pathogenic role in tooth loss due to its ability to reduce tooth mineralization through altered genetic signaling, 23 and activation of inflammatory pathways. 24 There is emerging evidence that suggests other components of e-cigarette promote oral inflammation and senescence of periodontal fibroblasts. 25 For example, propylene glycol, a major component of the e-liquid, can also decrease tooth integrity through altering calcium release and tooth mineralization.…”

Section: What Is Already Known On This Topicmentioning

confidence: 99%

Association of e-cigarette use with oral health: a population-based cross-sectional questionnaire study

Huilgol

Bhatt

Biligowda³

et al. 2018

Journal of Public Health

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“…Within the smaller set of proteins (i.e., those up-regulated only in α7KO), 3 proteins (S100A7, FGFR4, SERPINF2) were positive regulators of ERK1 and ERK2 cascades. ERK signaling has a potential role in cell proliferation and migration, which are characteristic effects of nicotine treatment in several cell types [28, 29] . Future investigations may study further the α7KO cell line in relation to ERK, cell migration/proliferation, and the α7 nAChR.…”

Section: Resultsmentioning

confidence: 99%

Isobaric Tag‐Based Protein Profiling of a Nicotine‐Treated Alpha7 Nicotinic Receptor‐Null Human Haploid Cell Line

Paulo

Gygi

2018

Proteomics

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Nicotinic acetylcholine receptors (nAChR), the primary cell surface targets of nicotine, have implications in various neurological disorders. Here we investigate the proteome-wide effects of nicotine on human haploid cell lines (wildtype HAP1 and α7KO-HAP1) to address differences in nicotine-induced protein abundance profiles between these cell lines. We performed an SPS-MS3-based TMT10-plex experiment arranged in a 2-3-2-3 design with two replicates for the untreated samples and three for the treated samples for each cell line. We quantified 8,775 proteins across all 10 samples, of which several hundred differed significantly in abundance. Comparing α7KO-HAP1 and HAP1wt cell lines revealed significant protein abundance alterations, however we also measured differences resulting from nicotine treatment in both cell lines. Among proteins with increased abundance levels due to nicotine treatment included those previously identified: APP, APLP2, and ITM2B. The magnitude of these changes was greater in HAP1wt compared to the α7KO-HAP1 cell line, implying a potential role of the α7 nAChR in HAP1 cells. Moreover, the data revealed that membrane proteins and proteins commonly associated with neurons were predominant among those with altered abundance. This study, which is the first TMT-based proteome profiling of HAP1 cells, defines further the effects of nicotine on non-neuronal cellular proteomes.

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Nicotine stimulation increases proliferation and matrix metalloproteinases-2 and -28 expression in human dental pulp cells

Cited by 9 publications

References 40 publications

Nicotine in Inflammatory Diseases: Anti-Inflammatory and Pro-Inflammatory Effects

Nicotine in Inflammatory Diseases: Anti-Inflammatory and Pro-Inflammatory Effects

Association of e-cigarette use with oral health: a population-based cross-sectional questionnaire study

Isobaric Tag‐Based Protein Profiling of a Nicotine‐Treated Alpha7 Nicotinic Receptor‐Null Human Haploid Cell Line

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