miR-8-3p regulates the antioxidant response and apoptosis in white shrimp, vannamei under ammonia-N stress

文献类型： 外文期刊

第一作者： Zhuo, Hongbiao

作者： Zhuo, Hongbiao;Zhang, Yuan;Fu, Shuo;Lin, Lanting;Li, Jinyan;Zhou, Xiaoxun;Wu, Guangbo;Guo, Chaoan;Liu, Jianyong;Zhuo, Hongbiao;Guo, Chaoan;Liu, Jianyong

作者机构：

关键词： Litopenaeus vannamei; Lva-miR-8-3p; Ammonia -N stress; Antioxidant response; Apoptosis

期刊名称：INTERNATIONAL JOURNAL OF BIOLOGICAL MACROMOLECULES （ 影响因子：7.7； 五年影响因子：7.7 ）

ISSN： 0141-8130

年卷期： 2024 年 274 卷

页码：

收录情况： SCI

摘要： Exposure to excess ammonia-N (NH3/NH4+) in aquaculture can disrupt physiological function in shrimp leading to enhanced oxidative stress and apoptosis, but little is known concerning the post-transcriptional regulation mechanism. In this study, the first miR-200 family member in crustacean was identified and characterized from Litopenaeus vannamei (designed as Lva-miR-8-3p). Lva-miR-8-3p was highly expressed in eyestalks, brainganglion, and gills. The expression of Lva-miR-8-3p in gills significantly decreased after ammonia-N stress, and LvamiR-8-3p was confirmed to target IKK beta 3'UTR for negatively regulating IKK beta/NF-kappa B pathway. Overexpression of miR-8-3p promoted the hemolymph ammonia-N accumulation, total hemocyte count (THC) decrease, and gills tissue damage, thus resulting in a decreased survival rate of ammonia-exposed shrimp. Besides, Lva-miR-8-3p silencing could enhance the antioxidant enzymes activities and reduce the oxidative damage, whereas overexpression of Lva-miR-8-3p exerted the opposite effects. Furthermore, Lva-miR-8-3p overexpression was found to aggravate ammonia-N induced apoptosis in gills. In primarily cultured hemocytes, the cell viability decreased, the ROS content and caspase-3 activity increased after agomiR-8-3p transfection, while antagomiR-8-3p transfection caused the opposite change except the cell viability. These findings indicate that Lva-miR-8-3p acts as a post-transcriptional regulator in ammonia-N induced antioxidant response and apoptosis by negatively regulating IKK beta/NF-kappa B pathway.

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