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长非编码RNAMir17hg通过抑制TGFβ受体2在心理压力下积极调节黑色素的产生

Jing Dong¹, Zan Peng¹, Minghan Chen¹

¹School of Traditional Chinese Pharmacy, China Pharmaceutical University, Nanjing, China.

The Journal of investigative dermatology

|September 14, 2023

概括

这项研究表明,长非编码RNA Mir17hg 调节黑色素发生,这是皮肤颜色的关键过程. 它在压力下降调节会影响黑色素细胞功能,为白风和其他脱色障碍提供潜在的治疗点.

科学领域:

皮肤病学皮肤病学
遗传学遗传学是一个
分子生物学分子生物学

背景情况:

Vitiligo 是一种与遗传学和心理压力相关的脱色障碍.
长非编码RNAs (lncRNAs) 在压力诱导的白风中的作用尚不清楚.
黑色素细胞的功能对于皮肤色素化至关重要.

研究的目的:

研究 lncRNAs 在与压力相关的白风病原发生中的作用.
为了确定参与压力下黑色素发生调节的特定 lncRNAs.
为了阐明 lncRNA介导的黑色素生成控制的分子机制.

主要方法:

在C57BL/6J小鼠的慢性克制压力模型中诱导黑色素细胞功能障碍.
RNA测序以识别差异表达的 lncRNAs.
在黑色素细胞和斑马鱼胚胎中进行过度表达和淘汰研究,以评估Mir17hg功能.
对下游信号通路 (TGFβ/SMAD,PI3K/AKT/mTOR) 的分析.

主要成果:

慢性压力抑制了小鼠的黑色素细胞功能.
在压力条件下,Mir17hg表达显著下调.
Mir17hg的过度表达促进了黑色素的产生,而 knockdown则抑制了它.
TGFβ受体2 (TGFβR2) 被确定为Mir17hg.的直接下游标.
Mir17hg通过TGFβ/SMAD和PI3K/AKT/mTOR通路调节黑色素的发生.

结论:

Mir17hg在黑色素发生过程中起着关键的调节作用.
Mir17hg介导的TGFβR2抑制是黑色素发生的一个关键机制.
Mir17hg代表了皮肤脱色障碍的潜在治疗标,如白风.

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