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Blockage of K(Ca)3.1 and Kv1.3 channels of the B lymphocyte decreases the inflammatory monocyte chemotaxis

To investigate the effects of Ca(2+) activated potassium channel KCa3.1 and voltage-gated potassium channel Kv1.3 of B lymphocyte on inflammatory monocytes chemotaxis and the potential mechanisms. Thanswell test was used to detect the inflammatory monocyte (Ly-6C(hi)) chemotaxis caused by the B lymp...

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Bibliographic Details
Published in:International immunopharmacology 2016-02, Vol.31, p.266-271
Main Authors: Zhang, Shuangxia, Wang, Xianpei, Ju, Chenhui, Zhu, Lijie, Du, Yimei, Gao, Chuanyu
Format: Article
Language:English
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Summary:To investigate the effects of Ca(2+) activated potassium channel KCa3.1 and voltage-gated potassium channel Kv1.3 of B lymphocyte on inflammatory monocytes chemotaxis and the potential mechanisms. Thanswell test was used to detect the inflammatory monocyte (Ly-6C(hi)) chemotaxis caused by the B lymphocyte. Enzyme-linked immunosorbent assay (ELISA) was applied to detecting the C-C motif ligand 7 (CCL7) in cultured media. Cell counting kit-8 (CCK) was used to detect the proliferation of B lymphocytes after activation and blockage of both KCa3.1 and Kv1.3 channels. Western blot was used to detect the expression of phosphorylated extracellular signal-regulated kinase (P-ERK) of the B lymphocytes. When activated, B lymphocytes significantly proliferated. After application of KCa3.1 channel-specific inhibitor TRAM-34 and potent Kv1.3 channel inhibitor ShK, both B lymphocytes proliferation and Ly-6C(hi) monocyte chemotaxis were significantly inhibited. The expression of chemotaxis related factor CCL7 decreased remarkably. The opening of KCa3.1 and Kv1.3 channels promote B lymphocyte activation, proliferation and Ly-6C(hi) monocyte chemotaxis. The increase of CCL7 secretion by B lymphocyte may explain the pro migration effects.
ISSN:1878-1705
DOI:10.1016/j.intimp.2015.12.032