Journal of Capital Medical University ›› 2016, Vol. 37 ›› Issue (6): 725-730.doi: 10.3969/j.issn.1006-7795.2016.06.002

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Advanced glycation end products impair voltage-gated K+ channels in coronary vascular smooth muscle cells

Su Wen1, Li Hongwei1, Chen Hui1, Liu Huirong2, Huang Haixia2, Li Weiping1   

  1. 1. Department of Cardiology, Beijing Friendship Hospital, Capital Medical University, Beijing 100050, China;
    2. Department of Physiology and Pathophysiology, School of Basic Medical Sciences, Capital Medical University, Beijing 100069, China
  • Received:2016-10-03 Online:2016-12-21 Published:2016-12-16
  • Supported by:
    This study was supported by National Natural Science Foundation of China(30971240), Natural Science Foundation of Beijing (7122053),High-level Technical Talents Foundation in Beijing Health System (2013-3-060).

Abstract: Objective To investigate the role of advanced glycation end products (AGEs) in impairment of voltage-gated K+(Kv) channels in rat coronary vascular smooth muscle cells (VSMCs). Methods We isolated rat coronary VSMCs. The cells were incubated either in control medium, or medium with 100 μg/mL AGE-bovine serum albumin (AGE-BSA), or medium with 100 μg/mL AGE-BSA plus 100 μg/mL anti-receptor of AGEs immunoglobulin G (anti-RAGE IgG). Patch-clamp recording was used to assess the Kv currents. Western blotting and quantitative real-time PCR techniques were used to assess protein and mRNA expression of Kv 1.2 and Kv1.5. Results Incubation of VSMCs with AGE-BSA reduced Kv current density by 32.7% and decreased both protein and mRNA expression of Kv1.2 and Kv1.5 channels, whereas blocking AGE-BSA interacting with their receptors by preincubation with anti-RAGE IgG for 30 minutes prevented AGE-BSA-induced impairment of Kv channels.Conclusion AGEs impair Kv channels in coronary VSMCs by interacting with RAGE.

Key words: advanced glycation end products, voltage-gated K+ channels, coronary vascular smooth muscle cells, receptor of advanced glycation end products

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