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

• Published in: BMC cardiovascular disorders Vol. 16; no. 1; p. 1
• Main Authors: Zhao, Yuanyuan, Sun, Qiaobing, Zeng, Zhipeng, Li, Qianqian, Zhou, Shiyuan, Zhou, Mengchen, Xue, Yumei, Cheng, Xiang, Xia, Yunlong, Wang, Qing, Tu, Xin
• Format: Journal Article
• Language: English
• Published: England BioMed Central Ltd 04.01.2016; BioMed Central
• Subjects: Arrhythmia; Calcium Channels - drug effects; Calcium Channels - genetics; Cancer; Care and treatment; Chemotherapy; Complications and side effects; Gene Expression Regulation; Health aspects; HEK293 Cells; HeLa Cells; Humans; Influence; Interleukin-2; Interleukin-2 - pharmacology; Membrane Potentials - drug effects; Myocytes, Cardiac - drug effects; Myocytes, Cardiac - metabolism; Patch-Clamp Techniques; Potassium Channels, Voltage-Gated - drug effects; Potassium Channels, Voltage-Gated - genetics; Reverse Transcriptase Polymerase Chain Reaction; RNA, Messenger - drug effects; RNA, Messenger - metabolism; Sodium - metabolism; Voltage-Gated Sodium Channel beta-3 Subunit - drug effects; Voltage-Gated Sodium Channel beta-3 Subunit - genetics; Voltage-Gated Sodium Channels - drug effects; Voltage-Gated Sodium Channels - genetics; Illinois
• ISSN: 1471-2261; 1471-2261
• DOI: 10.1186/s12872-015-0179-x

In 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. In 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. The 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). The present study suggested that IL-2, may play role in the arrhythmia by regulating the expression of SCN3B and sodium current density.