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首页> 外文期刊>Cell and Tissue Research >Melatonin modulates airway smooth muscle cell phenotype by targeting the STAT3/Akt/GSK-3 beta pathway in experimental asthma
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Melatonin modulates airway smooth muscle cell phenotype by targeting the STAT3/Akt/GSK-3 beta pathway in experimental asthma

机译：褪黑激素通过在实验性哮喘中靶向STAT3 / AKT / GSK-3β途径来调节气道平滑肌细胞表型

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摘要

Among the troika of clinicopathologic features of asthma, airway remodelling has gained sufficient attention for its contribution to progressive airway narrowing. Much effort has been directed at the management of airway smooth muscle cells (ASMCs), but few attempts have proven to prevent the progression of remodelling. Recently, accumulating data have shown the anti-inflammatory/anti-proliferative potency of melatonin (a crucial neurohormone involved in many physiological and pathological processes) in diverse cells. However, no evidence has confirmed its effect on ASMCs. The present study investigates the benefits of melatonin in asthma, with an emphasis on airway remodelling. The results indicated that melatonin significantly attenuated airway hyperresponsiveness (AHR), inflammation and remodelling in a house dust mite (HDM) model. Melatonin markedly alleviated goblet cell hyperplasia/metaplasia, collagen deposition and airway smooth muscle hyperplasia/hypertrophy, implying the achievement of remodelling remission. The data obtained in vitro further revealed that melatonin notably inhibited ASMCs proliferation, VEGF synthesis and cell migration induced by PDGF, which might depend on STAT3 signalling. Moreover, melatonin remarkably relieved ASMCs contraction and reversed ASMCs phenotype switching induced by TGF-beta, probably via the Akt/GSK-3 beta pathway. Altogether, our findings illustrated for the first time that melatonin improves asthmatic airway remodelling by balancing the phenotypic proportions of ASMCs, thus highlighting a novel purpose for melatonin as a potent option for the management of asthma.
机译：在哮喘的临床病理特征的三驾车中，气道重塑已经获得了对渐进气道缩小的贡献的充分重视。在气道平滑肌细胞（ASMCs）的管理中，努力已经致力于努力，但很少试图证明防止重塑进展。最近，积累数据显示了褪黑激素的抗炎/抗增殖性效力（在不同细胞中涉及许多生理和病理过程中的关键神经内核心）。但是，没有证据证实其对ASMC的影响。本研究调查了褪黑素在哮喘中的益处，重点是气道重塑。结果表明，褪黑素显着减弱了气道高反应性（AHR），炎症和房屋粉尘（HDM）模型中的重塑。褪黑激素显着​​缓解了脚蛋白细胞增生/细胞，胶原蛋白沉积和气道平滑肌增生/肥大，暗示了重塑缓解的成就。体外获得的数据进一步揭示了褪黑素鉴于PDGF诱导的AsMCS增殖，VEGF合成和细胞迁移，这可能取决于STAT3信号传导。此外，褪黑激素显着​​减轻了ASMCS收缩和由TGF-β诱导的ASMCS表型切换，可能通过AKT / GSK-3β途径诱导。通过平衡Asmcs的表型比例来说，我们的研究发现首次提高了褪黑激素改善了哮喘的气道重塑，从而突出了褪黑激素作为哮喘管理的有效选择的新目的。

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  • 来源
    《Cell and Tissue Research》 |2020年第1期|共14页
  • 作者

    Yu Qijun; Yu Xiaowei; Zhong Xiuhua; Ma Yuan; Wu Yan; Bian Tao; Huang Mao; Zeng Xiaoning;

  • 作者单位

    Nanjing Med Univ Dept Pulm &

    Crit Care Med Affiliated Hosp 1 300 Guangzhou Rd Nanjing 210029;

    Nanjing Med Univ Changzhou Peoples Hosp 2 Dept Pulm &

    Crit Care Med Changzhou 213003 Jiangsu;

    Nanjing Med Univ Dept Pulm &

    Crit Care Med Affiliated Hosp 1 300 Guangzhou Rd Nanjing 210029;

    Nanjing Med Univ Dept Pulm &

    Crit Care Med Affiliated Hosp 1 300 Guangzhou Rd Nanjing 210029;

    Nanjing Med Univ Dept Pulm &

    Crit Care Med Affiliated Wuxi Peoples Hosp 299 Qingyang Rd Wuxi;

    Nanjing Med Univ Dept Pulm &

    Crit Care Med Affiliated Wuxi Peoples Hosp 299 Qingyang Rd Wuxi;

    Nanjing Med Univ Dept Pulm &

    Crit Care Med Affiliated Hosp 1 300 Guangzhou Rd Nanjing 210029;

    Nanjing Med Univ Dept Pulm &

    Crit Care Med Affiliated Hosp 1 300 Guangzhou Rd Nanjing 210029;

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  • 原文格式 PDF
  • 正文语种 eng
  • 中图分类 细胞生物学;
  • 关键词

    Melatonin; Airway remodelling; STAT3; Akt; GSK-3 beta; House dust mite;

    机译：褪黑素;气道重塑;Stat3;AKT;GSK-3 Beta;房子尘螨;

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