Role of miR-451 in mediating cadmium induced head kidney injury in common carp via targeting cacna1ab through autophagy pathways*

文献类型： 外文期刊

第一作者： Luan, Peixian

作者： Luan, Peixian;Zhang, Xiaofeng;Hu, Guo;Luan, Peixian;Chen, Xiaoming;Zhang, Ziwei;Luan, Peixian;Zhang, Xiaofeng;Hu, Guo

作者机构：

关键词： Cadmium; Common carp; miR-451; Cacna1ab; Autophagy

期刊名称：AQUATIC TOXICOLOGY （ 影响因子：5.202； 五年影响因子：5.758 ）

ISSN： 0166-445X

年卷期： 2022 年 248 卷

页码：

收录情况： SCI

摘要： Cadmium (Cd) is a common environmental pollutant, which leads to Cd residue in aquatic animals. The Cd in aquatic animals will be enriched into the human body through the food chain and seriously harm human health. The research aims to investigate the molecular mechanism of Cd poisoning in common carps. Our previous studies have confirmed that 23 differentially expressed miRNAs were potential biomarkers for Cd exposure in common carp head kidney lymphocytes. Herein, based on the prediction of the website and previous studies, miR-451 and cacna1ab were selected and their targeting relationship was verified again by dual-luciferase. Subsequently, we established the miR-451 overexpression/knockdown models and miR-451 inhibitor, cacna1ab co-knockdown models in common carp head kidney lymphocytes respectively. Immunofluorescence staining, MDC staining, calcium staining, qRT-PCR (Quantitative Real-time PCR) and western blot were used to detect the levels of autophagy. Our results demonstrated that Cd significantly decreased the expression of miR451, miR-451 suppression thereby induced increased cacna1ab and the expression of ATG5, LC3-I, LC3-II and Beclin 1, while significantly inhibiting the expression of mTOR, P62 and Bcl-2, which indicated that autophagy was triggered. Moreover, the miR-451 knockdown group activated the expression of autophagy related factors as well as the Cd group. However, cacna1ab knockdown can reduce autophagy activation induced by miR-451 knockdown. Our results indicated that Cd induced autophagy in head kidney lymphocytes through the inhibition of miR-451 and the excitation of cacna1ab.

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