生物
尼古丁
烟碱乙酰胆碱受体
烟碱激动剂
细胞生物学
乙酰胆碱受体
烟碱拮抗剂
活性氧
受体
分子生物学
生物化学
神经科学
作者
Youichi Ohno,Daisuke Taura,Kentaro Okamoto,Haruka Fujita,Kyoko Honda-Kohmo,Koji Matsuo,Masakatsu Sone
出处
期刊:Stem Cells and Development
[Mary Ann Liebert]
日期:2023-03-02
卷期号:32 (9-10): 237-245
被引量:2
标识
DOI:10.1089/scd.2022.0258
摘要
The effects of smoking on fetal development and stem cell differentiation are not fully understood. Although nicotinic acetylcholine receptors (nAChRs) are expressed in many organs of the human body, their significance in human induced pluripotent stem cells (hiPSCs) remains unclear. After expression levels of nAChR subunits in hiPSCs were determined, the effects of the nAChR agonist, nicotine, on undifferentiated hiPSCs were evaluated using a Clariom S Array. We also determined the effect of nicotine alone and with a nAChR subunit antagonist on hiPSCs. nAChR α4, α7, and β4 subunits were strongly expressed in hiPSCs. cDNA microarray, gene ontology, and enrichment analyses showed that exposing hiPSCs to nicotine altered expression of genes associated with immune responses, neurological system, carcinogenesis, cell differentiation, and cell proliferation. Particularly affected was metallothionein, which acts to decrease reactive oxygen species (ROS). The nicotine-induced reduction of ROS in hiPSCs was canceled by an α4 subunit or nonselective nAChR antagonist. HiPSC proliferation was increased by nicotine, and this effect, too, was canceled by an α4 antagonist. In conclusion, nicotine reduces ROS and enhances cell proliferation through the α4 nAChR subunit in hiPSCs. These findings provide new insight into the significance of nAChRs on human stem cells and fertilized human ova.
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