肿瘤坏死因子α
受体
肾上腺素能受体
细胞生物学
肿瘤坏死因子受体
癌症研究
肿瘤坏死因子α
β2肾上腺素能受体
化学
生物
内分泌学
内科学
医学
兴奋剂
作者
Linda K. Wijaya,Philip A. Stumbles,Peter D. Drummond
出处
期刊:Cytokine
[Elsevier]
日期:2020-01-01
卷期号:125: 154851-154851
被引量:10
标识
DOI:10.1016/j.cyto.2019.154851
摘要
Keratinocytes produce cytokines and nerve growth factor (NGF) as part of a repair response to injury, disease or stress, and express alpha1-adrenoceptors (α1-AR). The expression of these receptors is elevated in some inflammatory diseases and chronic pain conditions. In this study, we investigated whether inflammatory signalling affects α1-AR expression in keratinocytes in vitro. Tumor necrosis factor α (TNFα) was administered to human keratinocytes, after which the levels of other key pro-inflammatory cytokines and NGF were measured. The production of these cytokines and NGF increased in cells treated with TNFα compared to untreated cells. Furthermore, exposure to TNFα increased gene expression of the α1-AR subtype B in keratinocytes. Our results suggest that inflammatory cytokines released during injury stimulate α1-AR expression in keratinocytes. The up-regulation of α1-AR may amplify the adrenergic sensitivity of these cells to catecholamines released during sympathetic nervous system activation after injury which, in turn, could heighten the inflammatory response.
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