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降低ER压力调节的长非编码RNA可以保护小鼠免受糖尿病和隔离的胰岛从细胞死亡

Mitsuo Kato¹, Maryam Abdollahi¹, Keiko Omori²

¹Department of Diabetes Complications and Metabolism, Arthur Riggs Diabetes & Metabolism Research Institute, Beckman Research Institute of City of Hope, 1500 E. Duarte Road, Duarte, CA 91010, USA.

Molecular therapy. Nucleic acids

|July 29, 2024

概括

针对长非编码RNA (lncRNA) lncMGC与GapmeR疗法显著降低了1型糖尿病小鼠模型中的血糖和小岛炎症,显示出治疗潜力.

科学领域:

内分泌学在内分泌学.
分子生物学分子生物学
免疫学免疫学免疫学

背景情况:

1型糖尿病 (T1D) 涉及胰腺小岛的破坏和功能障碍.
细胞内膜网膜 (ER) 的压力与T1D病变发生有关.
长非编码RNAs (lncRNAs) 是新兴的调节器在代谢疾病.

研究的目的:

研究ER压力调节的lncRNA lncMGC在T1D中的作用.
评估基于IncMGC的T1D治疗疗法.

主要方法:

使用IncMGC-Knockout (KO) 和链毒素 (STZ) 诱导的糖尿病小鼠模型.
在各种T1D小鼠模型 (NOD,阿基塔,人性化) 中使用针对 lncMGC 的反感性寡核酸 (GapmeR).
评估血糖水平 (BGLs),HbA1c,胰岛素和与ER压力和亡相关的基因表达.
在孤立的人类和老鼠小岛上进行了"体外"研究.

主要成果:

在糖尿病小鼠中,IncMGC-KO和GapmeR治疗显著降低了BGLs和HbA1c.
GapmeR 疗法减轻了胰岛炎和保护了小岛从细胞因子诱导的亡.
lncMGC和ER压力标志物 (CHOP) 在糖尿病岛屿上升调节,但在GapmeR治疗后降低.
在小岛中,GapmeR治疗调高了抗亡/抗ER压力基因和调低了亲亡基因.

结论:

lncMGC在T1D病原和ER压力中发挥作用.
通过GapmeR介导的lncMGC抑制是T1D的一种有前途的治疗策略.
这种方法保留了人类和老鼠小岛的生存能力,这表明了临床翻译的潜力.

关键词:

细胞灭亡 (apoptosis) 是一种死亡的过程.压力ERER压力ERER压力差距差距差距差距 MT:非编码RNA:长非编码RNA.线粒体中的线粒体.胰腺小岛是一个胰腺小岛.一个淘汰赛鼠标.在cMGC中,你会发现.这是一个微型RNA.第1类糖尿病 1型糖尿病

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