Abstract：
OBJECTIVE: Epidemiological and clinical studies have shown that sharp changes in the ambient temperature are associated with the occurrence and development of Bell\'s palsy. However, the specific pathogenesis of peripheral facial paralysis remains nebulous. This study investigated the effect of cold stress on transient receptor potential cation channel subfamily V member 2 (TRPV2) secretion by Schwann cells and its role in Bell\'s palsy.
METHODS: Schwann cell morphology was observed using transmission electron microscopy (TEM). Cell proliferation, apoptosis and cell cycle were analysed using CCK8 and flow cytometry. ELISA, Reverse transcription-quantitative PCR, western blotting and immunocytochemical fluorescence staining were used to detect the effects of cold stress on TRPV2, neural cell adhesion molecule (NCAM) and nerve growth factor (NGF) expression in Schwann cells.
RESULTS: Cold stress resulted in a widening of the intercellular space, and the particles on the membrane showed different degrees of loss. Cold stress may cause Schwann cells to enter a cold dormant state. ELISA, RT-qPCR, western blotting and immunocytochemical fluorescences staining indicated that cold stress inhibited the expression of TRPV2, NCAM, and NGF.
CONCLUSIONS: Drastic temperature difference between cold and heat can downregulate TRPV2 and the secretome of Schwann cells. The imbalance of Schwann cell homeostasis under such stress may contribute to nerve signalling dysfunction leading to the development of facial paralysis.
METHODS: Schwann cell morphology was observed using transmission electron microscopy (TEM). Cell proliferation, apoptosis and cell cycle were analysed using CCK8 and flow cytometry. ELISA, Reverse transcription-quantitative PCR, western blotting and immunocytochemical fluorescence staining were used to detect the effects of cold stress on TRPV2, neural cell adhesion molecule (NCAM) and nerve growth factor (NGF) expression in Schwann cells.
RESULTS: Cold stress resulted in a widening of the intercellular space, and the particles on the membrane showed different degrees of loss. Cold stress may cause Schwann cells to enter a cold dormant state. ELISA, RT-qPCR, western blotting and immunocytochemical fluorescences staining indicated that cold stress inhibited the expression of TRPV2, NCAM, and NGF.
CONCLUSIONS: Drastic temperature difference between cold and heat can downregulate TRPV2 and the secretome of Schwann cells. The imbalance of Schwann cell homeostasis under such stress may contribute to nerve signalling dysfunction leading to the development of facial paralysis.
摘要：
目的：流行病学和临床研究表明，环境温度的急剧变化与贝尔麻痹的发生和发展有关。然而,周围性面瘫的具体发病机制仍然模糊不清。本研究探讨冷应激对雪旺氏细胞分泌瞬时受体电位阳离子通道亚家族V成员2(TRPV2)的影响及其在贝尔麻痹中的作用。
方法：使用透射电子显微镜（TEM）观察雪旺氏细胞形态。细胞增殖，使用CCK8和流式细胞术分析细胞凋亡和细胞周期。ELISA,逆转录-定量PCR,免疫印迹和免疫细胞化学荧光染色检测冷应激对雪旺氏细胞TRPV2、神经细胞黏附分子(NCAM)和神经生长因子(NGF)表达的影响。
结果：冷应力导致细胞间隙扩大，膜上的颗粒表现出不同程度的损失。冷应激可能导致雪旺氏细胞进入冷休眠状态。ELISA,RT-qPCR,免疫印迹和免疫细胞化学荧光染色显示冷应激抑制TRPV2、NCAM的表达,NGF。
结论：冷热之间的剧烈温差可以下调TRPV2和雪旺氏细胞的分泌组。在这种压力下，雪旺氏细胞稳态的失衡可能导致神经信号功能障碍，从而导致面瘫的发展。
方法：使用透射电子显微镜（TEM）观察雪旺氏细胞形态。细胞增殖，使用CCK8和流式细胞术分析细胞凋亡和细胞周期。ELISA,逆转录-定量PCR,免疫印迹和免疫细胞化学荧光染色检测冷应激对雪旺氏细胞TRPV2、神经细胞黏附分子(NCAM)和神经生长因子(NGF)表达的影响。
结果：冷应力导致细胞间隙扩大，膜上的颗粒表现出不同程度的损失。冷应激可能导致雪旺氏细胞进入冷休眠状态。ELISA,RT-qPCR,免疫印迹和免疫细胞化学荧光染色显示冷应激抑制TRPV2、NCAM的表达,NGF。
结论：冷热之间的剧烈温差可以下调TRPV2和雪旺氏细胞的分泌组。在这种压力下，雪旺氏细胞稳态的失衡可能导致神经信号功能障碍，从而导致面瘫的发展。
