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首页> 外文期刊>Life sciences >Nicotine-induced activation of soluble adenylyl cyclase participates in ion transport regulation in mouse tracheal epithelium.
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Nicotine-induced activation of soluble adenylyl cyclase participates in ion transport regulation in mouse tracheal epithelium.

机译：尼古丁诱导的可溶性腺苷酸环酶的活化参与小鼠气管上皮中的离子输送调控。

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Functional nicotinic acetylcholine receptors (nAChR) have been identified in airway epithelia and their location in the apical and basolateral membrane makes them targets for acetylcholine released from neuronal and non-neuronal sources. One function of nAChR in airway epithelia is their involvement in the regulation of transepithelial ion transport by activation of chloride and potassium channels. However, the mechanisms underlying this nicotine-induced activation of ion transport are not fully elucidated. Thus, the aim of this study was to investigate the involvement of adenylyl cyclases in the nicotine-induced ion current in mouse tracheal epithelium.To evaluate the nicotine-mediated changes of transepithelial ion transport processes electrophysiological Ussing chamber measurements were applied and nicotine-induced ion currents were recorded in the absence and presence of adenylyl cyclase inhibitors.The ion current changes induced by nicotine (100 μM, apical) were not altered in the presence of high doses of atropine (25 μM, apical and basolateral), underlining the involvement of nAChR. Experiments with the transmembrane adenylyl cyclase inhibitor 2'5'-dideoxyadenosine (50 μM, apical and basolateral) and the soluble adenylyl cyclase inhibitor KH7 (10 μM, apical and basolateral) both reduced the nicotine-mediated ion current to a similar extent. Yet, a statistically significant reduction was obtained only in the experiments with KH7.This study indicates that nicotine binding to nAChR in mouse tracheal epithelium activates transepithelial ion transport involving adenylyl cyclase activity. This might be important for novel therapeutic strategies targeting epithelial ion transport mediated by the non-neuronal cholinergic system.
机译：在气道上皮细胞上鉴定出函数烟碱乙酰胆碱受体（NACHR），它们在顶端和基石外膜中的位置使其成为从神经元和非神经元来源释放的乙酰胆碱的靶标。 NACHR在呼吸道上皮的一种功能是它们参与通过激活氯化物和钾通道的调节Transepithelial离子输送。然而，这种尼古丁诱导的离子输送活化的机制尚未完全阐明。因此，本研究的目的是研究腺苷酸环酶在小鼠气管上皮中尼古丁诱导的离子电流中的累积。如果评估尼古丁介导的尼古丁介导的尼古丁离子转运过程的变化，则施加电生理学杂志测量和尼古丁诱导的离子在没有腺苷酸环化酶抑制剂的情况下记录电流。尼古丁（100μm，顶端）诱导的离子电流变化在高剂量的阿托品（25μm，顶端和基石）的存在下，下划线NACHR。用跨膜腺苷酸环酶抑制剂2'5'-二氧化萘苷（50μm，顶端和基石）和可溶性腺苷酸环酶抑制剂KH7（10μm，顶端和基底间）的实验两者都将尼古丁介导的离子电流降低到相似程度上。然而，仅在KH7的实验中获得了统计学上显着的减少。本研究表明尼古丁与小鼠气管上皮中的NACHR结合，激活涉及腺苷酸环化酶活性的Transepelial离子转运。这对于靶向非神经元胆碱能系统介导的上皮离子输送的新疗法策略可能是重要的。

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