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会通过miRNA-mRNA-自轴加剧糖尿病病的进展

Xiaodan Zhang¹, Sira Jackson², Jianhao Liu³

¹Center for Endemic Disease Control, Chinese Center for Disease Control and Prevention, Harbin Medical University, Harbin, China; Key Lab of Etiology and Epidemiology, Education Bureau of Heilongjiang Province & Ministry of Health (23618504), Harbin, 150081, China; Heilongjiang Provincial Key Laboratory of Trace Elements and Human Health, Harbin, 150081, China.

Food and chemical toxicology : an international journal published for the British Industrial Biological Research Association

|April 5, 2024

概括

高暴露会通过破坏自和改变miRNA-mRNA相互作用,使糖尿病病 (DN) 恶化. 这些发现突出了与污染相关的DN进展的潜在治疗目标.

科学领域:

环境毒理学环境毒理学
分子生物学分子生物学
脏病理学脏病理学

背景情况:

糖尿病病 (DN) 的进展受环境因素的影响.
众所周知,暴露会加剧糖尿病患者的损伤.
引起的DN恶化的潜在机制仍未得到充分研究.

研究的目的:

在小鼠模型中研究暴露对DN进展的影响.
阐明分子机制,包括自和miRNA-mRNA相互作用,涉及诱导的DNA.
确定潜在的治疗目标,以减轻对DNA的影响.

主要方法:

建立一个暴露于 (10毫克/升和25毫克/升) DN小鼠模型.
评估纤维化和尿路微专蛋白 (mAlb) 水平.
转录组测序以分析基因表达和通路激活 (自).
生物信息分析 (in silico) 用于预测微RNA (miRNA) -mRNA相互作用.
双露西法酶记者测定以验证miRNA-mRNA结合.

主要成果:

在暴露于25 mg/L的DN小鼠中,纤维化和尿液mAlb水平显著增加.
在高暴露下,自相关途径的激活和Beclin1和p-ATG16L1/ATG16L1水平的增加.
确定特定的miRNA-mRNA相互作用 (let-7a-1-3p, let-7b-3p, let-7f-1-3p, miR-98-3p针对Cdc42,Mapk1,Rhoa),可能调解的作用.

结论:

高暴露会通过改变自而加剧糖尿病病的进展.
特定的miRNA-mRNA轴 (let-7家族/miR-98-3p准Cdc42,Mapk1,Rhoa) 都与该机制有关.
这些已识别的途径和相互作用代表了理解和治疗诱导DN的有希望的目标.

关键词:

亚是一种.自自是一种自的过程.糖尿病脏病糖尿病脏病微RNAs 是一个微型RNA.

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