异常下调的FENDRR由阿雷科林提高ROS和肌纤维细胞激活通过缓解miR-214/MFN2轴
Yi-Wen Liao1, Cheng-Chia Yu2, Chang-Wei Hsieh3
1Department of Medical Research, Chung Shan Medical University Hospital, Taichung 402, Taiwan; Institute of Oral Sciences, Chung Shan Medical University, Taichung 402, Taiwan.
International journal of biological macromolecules
|March 5, 2024
概括
长非编码RNAFENDRR在口腔下纤维化 (OSF) 中至关重要,通过调节miR-214和线粒素2抑制肌纤维细胞激活. 它的下调与阿雷科林暴露有关,促进OSF的进展.
科学领域:
- 分子生物学分子生物学
- 在瘤学瘤学.
- 纤维化研究 纤维化研究
背景情况:
- 长非编码RNAFENDRR具有抗纤维和抗癌作用.
- 它在先发性口腔膜纤维化 (OSF) 中的功能尚不清楚.
研究的目的:
- 调查FENDRR在口腔下粘膜纤维化 (OSF) 发展中的作用.
- 为了阐明FENDRR在肌纤维细胞转差中的分子机制.
主要方法:
- 在OSF组织和细胞中分析FENDRR表达.
- 对FENDRR.的过度表达和淘汰研究.
- 用RNA结合测定来确认FENDRR-miR-214的相互作用.
- 对于MFN2表达的西方涂抹.
- 评估反应性氧物种 (ROS) 水平.
主要成果:
- 在OSF标本和纤维化口腔粘膜纤维细胞 (fBMFs) 中,FENDRR的下调.
- 过度表达FENDRR抑制了肌纤维细胞的特征,而其下调促进了它们.
- FENDRR直接针对miR-214,抑制肌纤维细胞激活.
- 米托素2 (MFN2) 是miR-214的直接标;FENDRR与MFN2.2正相关.
- 影响FENDRR/miR-214轴的因素是胆诱导的ROS积累和肌纤维细胞转差.
结论:
- 在OSF中异常的FENDRR下调与慢性阿雷科林暴露有关.
- 这种下调促进ROS和肌纤维细胞激活通过miR-214介导的MFN2抑制.
- 通过抑制肌纤维细胞激活,FENDRR在OSF中起到瘤抑制作用.
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