School of Biology and Basic Medical Sciences, Soochow University, 199 Renai Road, Suzhou, Jiangsu, PR China.
School of Biology and Basic Medical Sciences, Soochow University, 199 Renai Road, Suzhou, Jiangsu, PR China.
Fish Shellfish Immunol. 2019 Dec;95:659-669. doi: 10.1016/j.fsi.2019.11.014. Epub 2019 Nov 6.
Pikeperch (Sander lucioperca) is an economically important cool-water fish. In recent years, its cultivation has become threatened by higher temperatures in summer. We previously investigated the effects of heat stress on pikeperch liver under different temperatures, but the molecular mechanism of the heat-stress response is still unknown. This study applied consistent heat stress (29 °C, 0-48 h) to pikeperch juveniles, and a transcriptomic profile of pikeperch liver under heat stress (29 °C, 0 h) was performed by RNA-Seq. The antioxidant status, changes in liver histology, and antioxidant gene expression at different time points were examined. We identified 403 differentially expressed genes (DEGs), many of which were enriched in KEGG pathways, including protein processing in endoplasmic reticulum (ER), insulin signaling, and immune-related pathways. Among these, the most significant heat-stress-related pathway was protein processing in ER, indicating that this pathway is critical for the heat-stress response. After consistent heat stress at 29 °C, the total antioxidant capacity (T-AOC), the activities of total superoxide dismutase (T-SOD) and catalase (CAT), and the mRNA expression of manganese SOD (Mn-SOD), CAT, and glutathione peroxidase 1 and 7 (GPx1 and GPx7) in the treated groups showed the same trend of first increasing and then decreasing. Levels of malondialdehyde (MDA) content did not show significant differences between samples at 0 h and 3 h, but significantly increased by 6 h, and thereafter decreased. The liver tissue was normal at 0 h (29 °C); however, it suffered histological damage with increased duration of the heat stress. Above all, heat stress at 29 °C seemed to cause oxidative damage and dysfunction in pikeperch liver between 3 h and 48 h. The present results indicate that pikeperch have the capacity to defend against heat stress and maintain relative balance of oxidation-reduction reactions mainly through activating the antioxidant system, protein processing in ER, the insulin-signaling pathway, and immune-related pathways.
欧鲈（Sander lucioperca）是一种具有重要经济价值的冷水鱼类。近年来，其养殖受到夏季高温的威胁。我们之前研究了不同温度下热应激对欧鲈肝脏的影响，但热应激反应的分子机制尚不清楚。本研究采用持续热应激（29°C，0-48 h）处理欧鲈幼鱼，通过 RNA-Seq 对热应激（29°C，0 h）下欧鲈肝脏的转录组图谱进行了分析。检测了不同时间点的抗氧化状态、肝组织学变化和抗氧化基因表达。我们共鉴定到 403 个差异表达基因（DEGs），这些基因主要富集在蛋白质加工在内质网（ER）、胰岛素信号和免疫相关途径等 KEGG 通路中。其中，与热应激相关性最高的通路是 ER 中的蛋白质加工，表明该通路对热应激反应至关重要。在 29°C 持续热应激后，处理组的总抗氧化能力（T-AOC）、总超氧化物歧化酶（T-SOD）和过氧化氢酶（CAT）活性以及锰 SOD（Mn-SOD）、CAT 和谷胱甘肽过氧化物酶 1 和 7（GPx1 和 GPx7）的 mRNA 表达均呈现先升高后降低的相同趋势。0 h 和 3 h 时，丙二醛（MDA）含量在样本之间没有显著差异，但 6 h 时显著增加，此后降低。0 h（29°C）时肝脏组织正常，但随着热应激时间的延长，组织出现了组织学损伤。总之，29°C 的热应激似乎在 3 h 到 48 h 之间导致了欧鲈肝脏的氧化损伤和功能障碍。本研究结果表明，欧鲈具有抵御热应激的能力，并主要通过激活抗氧化系统、蛋白质加工在内质网、胰岛素信号通路和免疫相关途径来维持氧化还原反应的相对平衡。
