ArticleMedical molecular morphology2010
Nicotine induces upregulated expression of beta defensin-2 via the p38MAPK pathway in the HaCaT human keratinocyte cell line.
Article in Medical molecular morphology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed, 17 citations in OpenAlex.
- Potential Suppressive Effect of Nicotine on the Inflammatory Response in Oral Epithelial Cells: An In Vitro Study.International journal of environmental research and public health · 2021Article
- Activation of AMPKα2 in adipocytes is essential for nicotine-induced insulin resistance in vivo.Nature medicine · 2015Article
- Role of α7 nicotinic receptor in the immune system and intracellular signaling pathways.Central-European journal of immunology · 2015Review
- Cigarette smoke extract induces differential expression levels of beta-defensin peptides in human alveolar epithelial cells.Tobacco induced diseases · 2013Article
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9 authors at 1 institution in 1 country.
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Abstract
Human beta-defensins (hBDs), a group of antimicrobial peptides, are involved in the protective barrier of the oral epithelium. Nicotine induces periodontal and oral epithelial diseases. The purpose of the present study was to investigate the effect of nicotine on the expression pattern of hBD-2 in keratinocytes. HaCaT cells, a keratinocyte cell line, were incubated with 8, 15, 30, or 80 μM nicotine for 24 h. Expression of hBD-2 was observed by RT-PCR, qRTPCR, and ELISA assay. The cells were treated with inhibitors for intracellular pathways (p38MAP kinase, NF-κB, JNK, MAPK-ERK) and with nicotinic acetylcholine receptor (nAChR) inhibitors in a series of experiments. Data were analyzed using Student's t test. qRT-PCR revealed that the expression level of hBD-2 mRNA was significantly higher at 30 and 80 μM nicotine than the control without nicotine (P < 0.05). The 80 μM cell extraction contained significantly higher hBD-2 peptide levels than the control (P < 0.05). The p38MAP kinase inhibitor abolished the upregulated expression of hBD-2 by nicotine. Both nAChR inhibitors also abolished the upregulation of hBD-2 by nicotine. The present study demonstrated that nicotine causes upregulated expression of hBD-2 via the p38MAP kinase pathway in keratinocytes.
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