Regulation of SCN3B/scn3b by Interleukin 2 (IL-2): IL-2 modulates SCN3B/scn3b transcript expression and increases sodium current in myocardial cells.

Regulation of SCN3B/scn3b by Interleukin 2 (IL-2): IL-2 modulates SCN3B/scn3b transcript expression and increases sodium current in myocardial cells.
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白介素 2 (IL-2) 对 SCN3B/scn3b 的调节:IL-2 调节 SCN3B/scn3b 转录物表达并增加心肌细胞中的钠电流

DOI:
10.1186/s12872-015-0179-x
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发表时间:
2016-01-04
影响因子:
2.1
通讯作者:
Tu X
Tu X
中科院分区:
医学4区
文献类型:
--
作者:
Zhao Y;Sun Q;Zeng Z;Li Q;Zhou S;Zhou M;Xue Y;Cheng X;Xia Y;Wang Q;Tu X

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背景在心律失常的引发和维持中,炎症过程起着重要作用。 IL-2是一种促炎因子,与心律失常的发病相关,然而,IL-2如何影响心脏电生理仍不清楚。方法在本研究中,我们通过qRT-PCR观察IL-2对离子通道基因转录的影响,包括SCN2A、SCN3A、SCN4A、SCN5A、SCN9A、SCN10A、SCN1B、SCN2B、SCN3B、 KCNN1、KCNJ5、KCNE1、KCNE2、KCNE3、KCND3、KCNQ1、KCNA5、KCNH2 和 CACNA1C。通过Western blot检测和电生理学研究证明IL-2对SCN3B/scn3b翻译和钠电流的影响。结果结果显示Hela细胞中SCN3B的转录水平显着上调(与对照组相比,3.28倍,p = 0.022)。在HL-1细胞中验证了一致的结果(与对照组相比,3.73倍,p = 0.012)。电生理学研究结果表明,IL-2处理的细胞中钠电流密度显着增加,且IL-2对钠电流的影响与SCN3B无关(1.4倍,p = 0.023)。 Western blot分析显示IL-2导致HL-1细胞中p53和scn3b显着增加(p53为2.1倍,p = 0.021;scn3b为3.1倍,p = 0.023)。使用 qRT-PCR 分析在 HEK293 细胞中显示出一致的结果(P53 为 1.43 倍,p = 0.022;SCN3B 为 1.57 倍,p = 0.05)。 结论
BackgroundIn the initiation and maintenance of arrhythmia, inflammatory processes play an important role. IL-2 is a pro-inflammatory factor which is associated with the morbidity of arrhythmias, however, how IL-2 affects the cardiac electrophysiology is still unknown.MethodsIn the present study, we observed the effect of IL-2 by qRT-PCR on the transcription of ion channel genes including SCN2A, SCN3A, SCN4A, SCN5A, SCN9A, SCN10A, SCN1B, SCN2B, SCN3B, KCNN1, KCNJ5, KCNE1, KCNE2, KCNE3, KCND3, KCNQ1, KCNA5, KCNH2 and CACNA1C. Western blot assays and electrophysiological studies were performed to demonstrate the effect of IL-2 on the translation of SCN3B/scn3b and sodium currents.ResultsThe results showed that transcriptional level of SCN3B was up-regulated significantly in Hela cells (3.28-fold, p = 0.022 compared with the control group). Consistent results were verified in HL-1 cells (3.73-fold, p = 0.012 compared with the control group). The result of electrophysiological studies showed that sodium current density increased significantly in cells which treated by IL-2 and the effect of IL-2 on sodium currents was independent of SCN3B (1.4 folds, p = 0.023). Western blot analysis showed IL-2 lead to the significantly increasing of p53 and scn3b (2.1 folds, p = 0.021 for p53; 3.1 folds, p = 0.023 for scn3b) in HL-1 cells. Consistent results were showed in HEK293 cells using qRT-PCR analysis (1.43 folds for P53, p = 0.022; 1.57 folds for SCN3B, p = 0.05).Conclusions