LncRNA HOTTIP通过招募DNMT1来表观遗传调节SP-C来促进LPS诱导的肺上皮细胞损伤
Shuang Li1, Shuangjia Li1, Zhanqun Gao1
1Department of Emergency The First Affiliated Hospital of Jiamusi University Jiamusi China.
Journal of cell communication and signaling
|March 28, 2024
概括
长非编码RNAHOTTIP通过DNMT1招募通过表观遗传沉默SP-C促进急性肺损伤. 针对HOTTIP可能为肺上皮细胞损伤提供治疗策略.
科学领域:
- 分子生物学分子生物学
- 细胞生物学 细胞生物学
- 遗传学 遗传学是一种遗传学.
背景情况:
- 急性肺损伤 (ALI) 是一种严重的疾病,治疗选择有限.
- 长非编码RNAs (lncRNAs) 越来越多地被认为是它们在细胞过程和疾病发病过程中的角色.
- 了解ALI背后的分子机制对于开发有效治疗方法至关重要.
研究的目的:
- 研究 lncRNA HOTTIP 在急性肺损伤 (ALI) 中的作用.
- 阐明HOTTIP影响ALI的潜在分子机制.
- 探索HOTTIP作为ALI的潜在治疗点.
主要方法:
- 定量实时PCR (qRT-PCR) 和西部斑点测试用于评估基因和蛋白质表达.
- 细胞计数套件-8 (CCK-8) 测试细胞活力和TUNEL染色用于细胞亡量化.
- 酶相关免疫吸收试验 (ELISA) 检测炎症因素,甲基化特定PCR (MSP) 检测DNA甲基化,以及RNA免疫沉试验 (RIP) 检测分子相互作用.
主要成果:
- 脂聚糖 (LPS) 在膜上皮细胞II型 (AECII) 中调高HOTTIP和调低SP-C.
- 在AEC II细胞中,HOTTIP knockdown降低了LPS诱导的亡和炎症性细胞因子分泌 (TNF-α,IL-1β,IL-6).
- 霍蒂普将DNA甲基转移酶1 (DNMT1) 引入了SP-C促进体,导致SP-C基因沉默并加剧LPS诱导的肺上皮细胞损伤.
结论:
- 霍蒂普通过招募DNMT1来表观遗传抑制SP-C表达,从而促进LPS诱导的肺上皮细胞损伤.
- 抑制SP-C逆转了HOTTIP或DNMT1敲击对LPS诱导的ALI的保护作用.
- 针对HOTTIP是一个有前途的急性肺损伤治疗策略.
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