Interleukin-1 inhibits voltage-dependent P/Q-type Ca2+ channel associated with the inhibition of the rise of intracellular free Ca2+ concentration and catecholamine release in adrenal chromaffin cells
Interleukin-1 inhibits voltage-dependent P/Q-type Ca2+ channel associated with the inhibition of the rise of intracellular free Ca2+ concentration and catecholamine release in adrenal chromaffin cells
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DOI：
10.1016/j.bbagen.2004.04.012
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发表时间：
2004-08-04
影响因子：
3
通讯作者：
Dohi, T
中科院分区：
文献类型：
--
作者：
Morita, K;Miyasako, T;Dohi, T
在分离培养的牛肾上腺嗜铬细胞中检查白细胞介素 (IL) 对细胞内游离 Ca2+ 浓度 ([Ca2+]i) 升高和儿茶酚胺 (CA) 释放的影响。在正常和 Ca2+-蔗糖培养基中，IL-1α 和 IL-1β 均抑制乙酰胆碱 (ACh) 和过量 KCl 诱导的 [Ca2+]i 和 CA 释放的增加。 IL-1 受体拮抗剂 (IL-1RA) 预处理可阻断 IL-1α 的抑制作用。 IL-1α 可减少正常培养基中藜芦定诱导的 CA 释放，但在地尔硫卓存在下则不会。使用电压驱动 Ca2+ 通道 (VOCC) 的特异性阻断剂进行的分析表明，IL-1α 和 IL-1beta 特异性抑制 P/Q 型 Ca2+ 通道，以减少过量 KCl 引起的 [Ca2+]i 升高。 IL-1 不影响由缓激肽或咖啡因在 Ca2+ 剥夺培养基中或通过激活钙池操纵的 Ca2+ 通道 (SOC) 诱导的 [Ca2+]i 升高。 IL-1α 的抑制作用可被除草霉素 A、U0126 和 PD 98054 预处理阻断，但不能被 SB202190、SP 600125 或百日咳毒素 (PTX) 阻断。这些结果表明，IL-1 通过阻断电压操作的 P/O 型 Ca2+ 通道，抑制嗜铬细胞中刺激诱发的 [Ca2+]i 升高和 CA 释放。 IL-1 的抑制作用可能通过酪氨酸激酶和 MEK/ERK 途径介导。 (C) 2004 Elsevier B.V. 保留所有权利。
Effects of interleukin (IL) on intracellular free Ca2+ concentration ([Ca2+]i) rise and catecholamine (CA) release were examined in isolated, cultured bovine adrenal chromaffin cells. IL-1alpha and IL-1beta inhibited the rise of [Ca2+]i and CA release induced by acetylcholine (ACh) and excess KCl both in normal and in Ca2+-sucrose medium. Pretreatment by IL-1 receptor antagonist (IL-1RA) blocked the inhibitory actions of IL-1alpha. IL-1alpha reduced CA release induced by veratridine in normal medium but not in the presence of diltiazem. Analysis using specific blockers for voltage-operated Ca2+ channels (VOCC) revealed that IL-1alpha and IL-1beta specifically inhibited the P/Q-type Ca2+ channel to reduce [Ca2+]i rise induced by excess KCl. IL-1 did not affect [Ca2+]i rise induced either by bradykinin or caffeine in Ca2+-deprived medium or via activation of store-operated Ca2+ channel (SOC). The inhibitory effects of IL-1alpha were blocked by pretreatments with herbimycin A, U0126 and PD 98054, but not with SB202190, SP 600125 or pertussis toxin (PTX).These results demonstrated that IL-1 inhibits stimulation-evoked [Ca2+]i rise and CA release in chromaffin cells by blocking voltage-operated P/O-type Ca2+ channels. The inhibitory action of IL-1 may be mediated through the tyrosine kinase and MEK/ERK pathways. (C) 2004 Elsevier B.V. All rights reserved.