Suppression of miR-26a attenuates physiological disturbances arising from exposure of Nile tilapia () to ammonia.

MicroRNAs may affect stress responses because they act as rapid responders at the post-translation level. In this study, we found that miR-26a is abundantly expressed in the brain and gill tissues of tilapia. Expression of miR-26a in the brain decreased significantly with increasing ammonia concentrations using stem-loop qPCR. To analyze the function of miRNA , miR-26a was stably knocked down with an antagomir in tilapia. Following ammonia challenge, miR-26a antagomir treatment significantly suppressed blood ammonia/[Cl]/[K] concentration and the reactive oxygen species production, while it markedly enhanced glutamine accumulation and antioxidant enzyme activity in the brain of tilapia, indicating that miR-26a may be involved in the remission of physiological disturbances resulting from ammonia stress. We strongly conclude that there is a direct link between miR-26a and the responses to ammonia in tilapia. Furthermore, bioinformatics analysis and luciferase assays demonstrated that miR-26a regulates (heat shock protein 70) and (glutamine synthetase) expression by targeting their 3'-UTR and that the suppression of miR-26a could increase the intracellular level of and .