SP1通过调节FGF7和PI3K/AKT通路促进高葡萄糖诱导的透镜上皮细胞活力,迁移和上皮-介质细胞过渡
Ledan Wang1, Xin Zhang1, Huijun Li1
1Department of Ophthalmology, Ophthalmology Center, Taizhou Hospital of Zhejiang Province, 150 Ximen Street, Linhai, 317000, China.
International ophthalmology
|July 5, 2024
概括
糖尿病白内障 (DC) 涉及特定蛋白1 (SP1) 激活纤维细胞生长因子7 (FGF7) 和PI3K/AKT通路. 这一过程在高葡萄糖条件下驱动细胞活力,迁移,入侵和上皮细胞-介质细胞过渡.
科学领域:
- 眼科医生 眼科 眼科
- 内分泌学 在内分泌学.
- 分子生物学分子生物学
背景情况:
- 糖尿病白内障 (DC) 是一种复杂的糖尿病并发症.
- 研究了特异性蛋白1 (SP1) 和纤维细胞生长因子7 (FGF7) 在DC中的作用.
研究的目的:
- 探索SP1和FGF7在糖尿病白内障发展中的参与.
- 阐明在DC中高葡萄糖诱导的细胞变化的基础上的分子机制.
主要方法:
- 使用SRA01/04细胞建立了高葡萄糖 (HG) 诱导的细胞模型.
- 使用MTT,Transwell和伤口愈合试验评估细胞活力,迁移,入侵和上皮-介质细胞过渡 (EMT).
- 分析了蛋白质和基因表达 (N-cadherin,E-cadherin,Collagen I,Fibronectin,SP1,FGF7) 通过Western blot和qRT-PCR;使用CHIP和双露西法酶试验研究了SP1-FGF7相互作用.
主要成果:
- 在DC患者和HG治疗细胞中,FGF7表达升高.
- HG促进了SRA01/04细胞活力,迁移,入侵和EMT;FGF7敲击逆转了这些效应.
- SP1激活了FGF7转录,加剧了HG诱导的损伤. SP1沉默抑制了HG效应,这些效应被FGF7上调调节所挽救. 此外,SP1还通过FGF7.7调节PI3K/AKT通路.
结论:
- SP1通过转录激活FGF7,有助于HG诱导的细胞活力,迁移,入侵和EMT.
- SP1-FGF7轴和PI3K/AKT通路是糖尿病白内障发病的关键调节者.
关键词:
电流 电流 电流 电流 电流 电流第七届国家财政基金HG HG 这是一个很大的问题.SP1 SP1 SP1 SP1 SP1 SP1 SP1 SP1 SP1 SP1 SP1 SP1 SP1 SP1 SP1 SP1 SP1 SP1 SP1 SP1 SP1 SP1 SP1 SP1 SP1 SP1 SP1 SP1 SP1 SP1 SP1 SP1 SP1 SP1 SP1 SP1 SP1 SP1 SP1 SP1 SP1 SP1 SP1 SP1 SP1 SP1 SP1 SP1 SP1 SP1 SP1 SP1 SP1 SP1 SP1 SP1 SP1 SP1细胞 SRA01/04 的细胞.更多相关视频
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