Journal
DEVELOPMENTAL AND COMPARATIVE IMMUNOLOGY
Volume 114, Issue -, Pages -Publisher
ELSEVIER SCI LTD
DOI: 10.1016/j.dci.2020.103844
Keywords
Litopenaeus vannamei; Cold shock; HSP70; Air exposure; Apoptosis
Categories
Funding
- National Key R&D Program of China [2019YFD0901601]
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The study reveals that HSP70 induced by cold shock can enhance the tolerance of shrimp to air exposure, inhibit the apoptosis pathway in cells, and decrease ROS content, cytochrome c expression, release from mitochondria, and caspase-3 activity in shrimp hemocytes.
Brief pretreatment of cold shock at 13 degrees C for 3 min proved to be an inducer of heat shock protein 70 (HSP70) and improved stress tolerance as a molecular chaperone. With the improvement of air exposure tolerance, HSP70 in shrimp hemocytes was upregulated in mRNA and protein levels after cold shock. Both HSP70 RNA interference (RNAi) gene knockdown and recombinant HSP70 (rHSP70) injection were successfully established in order to investigate the role of HSP70 in response to air exposure stress. Shrimp receiving rHSP70 showed an improved survival rate (80%) with no significant difference (p > 0.05) compared to cold shock treated shrimp (control, 90%) under air exposure, but the survival rate of HSP70-knockdown shrimp was significantly lower (62%, p < 0.05). Reactive oxygen species (ROS) content, relative expression of cytochrome c, caspase-3 activity, and apoptosis rate in hemocytes of HSP70 enriched shrimp (i.e., cold shock and rHSP70 injection) were significantly lower (p < 0.05) than HSP70-knockdown shrimp. Results suggested that HSP70 could be induced by cold shock and contributed to improve the tolerance of shrimp suffering air exposure by blocking the apoptosis pathway through scavenging intracellular ROS, inhibiting cytochrome c expression, inhibiting release from mitochondria, and inactivating caspase-3. This work updates the understanding of cold shock mechanism in water-free transportation of aquatic animals.
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