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首页> 外文期刊>Cellular Physiology and Biochemistry >Melatonin Protects the Esophageal Epithelial Barrier by Suppressing the Transcription, Expression and Activity of Myosin Light Chain Kinase Through ERK1/2 Signal Transduction
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Melatonin Protects the Esophageal Epithelial Barrier by Suppressing the Transcription, Expression and Activity of Myosin Light Chain Kinase Through ERK1/2 Signal Transduction

机译：褪黑素通过抑制ERK1 / 2信号转导的肌球蛋白轻链激酶的转录，表达和活性，从而保护食管上皮屏障。

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biBackground/Aims /i/bDilated intercellular space (DIS) contributes to the pathophysiology of gastroesophageal reflux disease (GERD). Melatonin protects the esophageal mucosa; however, the mechanisms underlying that protection remain unclear. biMethods /i/bTransmission electron microscopy (TEM) was used to evaluate the intercellular spaces in the esophageal epithelium of GERD patients. The Het-1A monolayer barrier function was investigated by measuring transepithelial resistance (TER) and FITC-dextran paracellular permeation. The activity of MLCK was represented by MLC phosphorylation. The expression and phosphorylation of MLCK, MLC and ERK were examined by western blot analysis. biResults /i/bThe expression and activity of MLCK and ERK phosphorylation were increased in the esophageal epithelium. The increased expression and activity of MLCK was correlated with dilated intercellular spaces. Upon acid treatment, the Het-1A monolayer permeability was increased. When the Het-1A monolayer was pretreated with melatonin and PD98059 before the acid incubation, the permeability and the expression and phosphorylation of MLCK and ERK decreased. biConclusion /i/bMelatonin protects the esophageal epithelial barrier by suppressing the transcription, translation and activity of MLCK through ERK1/2 signal transduction. These findings provide a better understanding of the potential clinical application of melatonin in GERD treatment.
机译：背景/目标 扩张的细胞间隙（DIS）有助于胃食管反流病（GERD）的病理生理。褪黑素可保护食道粘膜;但是，保护的基本机制仍不清楚。 方法 使用透射电子显微镜（TEM）评估GERD患者食管上皮中的细胞间隙。 Het-1A单层屏障功能通过测量跨上皮抵抗性（TER）和FITC-右旋糖酐细胞旁渗透进行了研究。 MLCK的活性由MLC磷酸化表示。通过蛋白质印迹分析检测MLCK，MLC和ERK的表达和磷酸化。 结果 食管上皮中MLCK和ERK磷酸化的表达和活性均升高。 MLCK的表达和活性的增加与细胞间隙的扩大有关。经酸处理后，Het-1A单层渗透性增加。在酸孵育之前用褪黑素和PD98059对Het-1A单层进行预处理时，MLCK和ERK的渗透性以及表达和磷酸化降低。 结论 褪黑素通过ERK1 / 2信号转导抑制MLCK的转录，翻译和活性，从而保护食管上皮屏障。这些发现为褪黑激素在GERD治疗中的潜在临床应用提供了更好的理解。

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