LncRNA HILPDA通过招募eIF4B来提高XPO1表达的调节来促进对比诱导的急性损伤
Haiyan Wei1, Tuersun Tilakezi1, Wei Feng1
1Second Department of Coronary Heart Disease, The First People's Hospital of Kashgar Prefecture, No. 120, Yingbin Avenue, Kashgar, Xinjiang Uyghur Autonomous Region 844000, P.R. China.
Toxicology research
|July 3, 2024
概括
长非编码RNAHILPDA (lnc-HILPDA) 通过增加XPO1表达和激活NF-κB通路来加速对比诱导的急性损伤 (CI-AKI). 低调 lnc-HILPDA 可能为CI-AKI提供治疗策略.
科学领域:
- 腎臟病學 (nephrology) 是一種醫學專業.
- 分子生物学分子生物学
- 生物化学 生化学
背景情况:
- 对比诱导的急性损伤 (CI-AKI) 是含的对比介质的严重并发症,与高死亡率有关.
- 长非编码RNAs (lncRNAs) 在CI-AKI病原发生中的作用仍然不完全理解.
- 本研究研究了lnc-HILPDA在CI-AKI的发展中的作用.
研究的目的:
- 阐明Inc-HILPDA在CI-AKI中的作用.
- 研究Inc-HILPDA影响CI-AKI的分子机制.
- 根据Inc-HILPDA功能,探索CI-AKI的潜在治疗点.
主要方法:
- CI-AKI模型是使用iopromide治疗建立的.
- 通过HE染色来评估脏病理;使用TUNEL标记和流动细胞计量来评估细胞亡.
- 细胞活力通过CCK-8试验确定;分子相互作用通过RIP和Co-IP试验得到证实.
主要成果:
- 在CI-AKI模型中,Lnc-HILPDA表达升高.
- 抑制lnc-HILPDA可以减少对比剂诱导的氧化应激和HK-2细胞的亡.
- 通过eIF4B相互作用,Lnc-HILPDA通过eIF4B相互作用上调XPO1,激活NF-κB通路;XPO1过度表达减弱了Inc-HILPDA下调的保护作用.
结论:
- Lnc-HILPDA通过eIF4B上调XPO1表达来促进CI-AKI的进展,随后激活NF-κB通路.
- 准Inc-HILPDA可能是预防或治疗CI-AKI的一种新疗法.
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