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Role of canonical transient receptor potential channel-3 in acetylcholine-induced mouse airway smooth muscle cell proliferation

机译：典型瞬态受体电位通道-3在乙酰胆碱诱导的小鼠气道平滑肌细胞增殖中的作用

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Abstract Aims Canonical transient receptor potential channel-3 (TRPC3)-encoded Ca 2 + -permeable nonselective cation channel (NSCC) has been proven to be an important native constitutively active channel in airway smooth muscle cell (ASMC), which plays significant roles in physiological and pathological conditions by controlling Ca 2 + homeostasis in ASMC. Acetylcholine (ACh) is generally accepted as a contractile parasympathetic neurotransmitter in the airway. Recently studies have revealed the pathological role of ACh in airway remodeling, however, the mechanisms remain unclear. Here, we investigated the role of TRPC3 in ACh-induced ASMC proliferation. Materials and methods Primary mouse ASMCs were cultured with or without ACh treatment, then cell viability, TRPC3 expression, NSCC currents and [Ca 2 + ] i changes were examined by MTT assay, cell counting, Western blotting, standard whole-cell patch clamp recording and calcium imaging, respectively. Small interfering RNA (siRNA) technology was used to confirm the contribution of TRPC3 to ACh-induced ASMC proliferation. Key findings TRPC3 blocker Gd 3 + , antibody or siRNA largely inhibited ACh-induced up-regulation of TRPC3 protein, enhancement of NSCC currents, resting [Ca 2 + ] i and KCl-induced changes in [Ca 2 + ] i , eventually inhibiting ACh-induced ASMC proliferation. Significance Our data suggested ACh could induce ASMC proliferation, and TRPC3 may be involved in ACh-induced ASMC proliferation that occurs with airway remodeling.
机译：抽象宗旨典型瞬时受体电位通道-3（TRPC3）编码的Ca 2 +可透过的非选择性阳离子通道（NSCC）已被证明是在气道平滑肌细胞（ASMC）的重要天然组成型活性的信道，其在显著角色通过控制的Ca在ASMC 2和+体内平衡的生理和病理条件。乙酰胆碱（ACh）通常被接受为在气道可收缩副交感神经递质。最近的研究表明乙酰胆碱的气道重塑的病理作用，但机制尚不清楚。在这里，我们调查TRPC3的乙酰胆碱诱导ASMC增殖的作用。材料和方法原代小鼠主动脉平滑肌细胞在有或无乙酰胆碱的治疗，那么细胞活力，TRPC3表达，NSCC电流和的[Ca 2 +]通过MTT测定，细胞计数，Western印迹检查我的变化，标准的全细胞膜片钳记录中培养和钙成像，分别。小干扰RNA（siRNA）技术被用来确认TRPC3的乙酰胆碱诱导ASMC增殖的贡献。主要研究结果TRPC3阻滞剂的Gd 3 +，抗体或siRNA很大程度上抑制TRPC3蛋白，增强NSCC电流，休息的乙酰胆碱诱导的上调的[Ca 2 +] i的和KCl诱导的内[Ca 2 +] i的变化，最终抑制乙酰胆碱诱导ASMC增殖。意义我们的数据表明胆碱能诱导ASMC增殖，TRPC3可能参与与气道重塑发生乙酰胆碱诱导ASMC增殖。

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  • 来源
    《Life sciences》 |2017年第2017期|共10页
  • 作者

    Xiao-Xu Chen; Jia-Hua Zhang; Bin-Hua Pan; Hui-Li Ren; Xiu-Ling Feng; Jia-Ling Wang; Jun-Hua Xiao;

  • 作者单位

    Department of Pharmacology School of Basic Medicine Tongji Medical College Huazhong University;

    Center for Stem Cell Research and Application Union Hospital of Tongji Medical College Huazhong;

    Department of Pharmacology School of Basic Medicine Tongji Medical College Huazhong University;

    Department of Pharmacology School of Basic Medicine Tongji Medical College Huazhong University;

    Department of Pharmacology School of Basic Medicine Tongji Medical College Huazhong University;

    Department of Pharmacology School of Basic Medicine Tongji Medical College Huazhong University;

    Department of Pharmacology School of Basic Medicine Tongji Medical College Huazhong University;

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  • 原文格式 PDF
  • 正文语种 eng
  • 中图分类 医药、卫生;
  • 关键词

    TRPC3; Nonselective cation channel; Airway smooth muscle cell; Acetylcholine; Proliferation; Ca2+i;

    机译：TRPC3;非选择性阳离子通道;气道平滑肌细胞;乙酰胆碱;增殖;[CA2 +] i;

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