长非编码RNAXIST通过miR-126-3p/EGFR轴促进糖尿病足的细胞增殖和迁移
Wangbing Hong1, Zhenfang Xiong2, Xin Wang1
1Medical Center of Burn plastic and wound repair, The 1st Affiliated Hospital, Jiangxi Medical College, Nanchang University, Nanchang, Jiangxi Province, China.
Diabetology & metabolic syndrome
|February 5, 2024
概括
糖尿病足 (DFU) 涉及长非编码RNA XIST的减少,这会损害细胞生长和迁移. 恢复miR-126-3p/EGFR轴可以改善DFU的愈合.
科学领域:
- 分子生物学分子生物学
- 生物化学 生物化学
- 细胞生物学 细胞生物学
背景情况:
- 糖尿病足 (DFU) 是一个重大的健康挑战,有效治疗方法有限.
- 长非编码RNA XIST (lncRNA XIST) 显示在各种疾病中具有保护作用,但其在DFU中的功能尚不清楚.
- 这项研究研究了lncRNA XIST在DFU的病变发生和生物机制中的作用.
研究的目的:
- 阐明 lncRNA XIST 在糖尿病足发作的作用.
- 了解DFU中涉及lncRNA XIST,microRNA-126-3p和表皮生长因子受体的分子相互作用.
- 确定改善DFU伤口愈合的潜在治疗点.
主要方法:
- 使用HE,马森三色和IHC染色对糖尿病鼠皮肤组织的分析.
- 基因和蛋白质表达分析通过RT-qPCR和西式涂抹.
- 细胞测定 (CCK-8,Transwell,伤口愈合) 来评估HaCaT细胞的增殖和迁移,并通过双 luciferase 测定进行相互作用验证.
主要成果:
- 在DFU组织和高葡萄糖诱导细胞中,lncRNA XIST和EGFR的下调,而miR-126-3p的上调.
- lncRNA XIST直接与miR-126-3p结合,miR-126-3p的目标是EGFR.
- 沉默lncRNA XIST通过上调miR-126-3p和降低EGFR来抑制细胞增殖和迁移,通过抑制miR-126-3p或EGFR过度表达来逆转效应.
结论:
- 减少的lncRNA XIST表达会通过抑制HaCaT细胞的增殖和迁移而加剧DFU.
- 在高葡萄糖条件下,miR-126-3p/EGFR轴是lncRNA XIST调节的关键通路.
- 针对lncRNA XIST/miR-126-3p/EGFR通路,有望提高DFU伤口愈合的速度.
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