Ma Xiaoli, Wang Wen-Xiong
School of Energy and Environment and State Key Laboratory of Marine Pollution, City University of Hong Kong, Kowloon, Hong Kong, China.
Research Centre for the Oceans and Human Health, City University of Hong Kong Shenzhen Research Institute, Shenzhen 518057, China.
Int J Mol Sci. 2025 Feb 17;26(4):1703. doi: 10.3390/ijms26041703.
Migratory fish often encounter hypoxic zones during migration, which can lead to varying degrees of hypoxic stress. This issue has become increasingly severe due to human activities and climate change, which have resulted in the expansion of hypoxic zones in aquatic environments. However, there is limited research on how these species respond to hypoxic stress and subsequent recovery. In this study, we used , a well-recognized migratory and economically valuable fish species, as a model organism. Histological analysis revealed extensive neuronal damage during hypoxia exposure, with limited recovery observed even after 12 h of reoxygenation. Differential gene expression analysis highlighted progressive alterations in genes associated with stress response, neuroactive ligand interactions, and cellular repair mechanisms. Time-series analysis of differentially expressed genes (DEGs) identified critical expression profiles throughout the hypoxia-recovery process and revealed hub genes for each stage. Furthermore, dynamic changes in miRNA expression and proteomic profiles indicated active regulation of several key biological pathways, including MAPK, HIF-1, and ECM-receptor interactions. Through miRNA-mRNA-protein correlation analysis, we propose a model that predicts key regulatory pathways and critical miRNA-mRNA-protein interactions across the various stages of hypoxia-recovery in the brain of . This study presents the first integrated analysis of miRNA, mRNA, and protein throughout the entire hypoxia-recovery process in fish brains. The molecular interactions and regulatory pathways identified in this model could serve as valuable biomarkers for future research on hypoxia-recovery mechanisms in fish.
洄游鱼类在洄游过程中经常遇到缺氧区域，这可能导致不同程度的缺氧应激。由于人类活动和气候变化导致水生环境中缺氧区域的扩大，这个问题变得越来越严重。然而，关于这些物种如何应对缺氧应激及随后的恢复，研究还很有限。在本研究中，我们使用了一种公认的洄游且具有经济价值的鱼类作为模式生物。组织学分析显示，在缺氧暴露期间神经元有广泛损伤，即使在复氧12小时后恢复也有限。差异基因表达分析突出了与应激反应、神经活性配体相互作用和细胞修复机制相关的基因的渐进性改变。对差异表达基因（DEGs）的时间序列分析确定了整个缺氧-恢复过程中的关键表达谱，并揭示了每个阶段的枢纽基因。此外，miRNA表达和蛋白质组学图谱的动态变化表明了包括MAPK、HIF-1和ECM-受体相互作用在内的几个关键生物途径的活跃调控。通过miRNA-mRNA-蛋白质相关性分析，我们提出了一个模型，该模型预测了在洄游鱼类大脑缺氧-恢复的各个阶段的关键调控途径和关键的miRNA-mRNA-蛋白质相互作用。本研究首次对鱼类大脑整个缺氧-恢复过程中的miRNA、mRNA和蛋白质进行了综合分析。该模型中确定的分子相互作用和调控途径可为未来鱼类缺氧恢复机制的研究提供有价值的生物标志物。
