miR-194 Original DATA.xls

Hypothermia has been
reported to be effective in protecting the brain in various clinical
conditions, including resuscitation after cardiac arrest and complex
cardiovascular surgery, and is considered to be a promising therapy for stroke. The present study aimed to confirm a
pivotal role for miRNA-194-5p in
deep hypothermia circulation arrest. We
observed a decline in expression of miR-194-5p in the circulation of 21 aortic
dissection patients who underwent deep hypothermia circulatory arrest.
Subsequently, the specific expression, target, and function of miR-194-5p was
investigated using primary neuron culture, polymerase chain reaction, in situ
hybridization, and flow cytometry methods. Our results showed that miR-194-5p
expression was significantly downregulated in neurons subjected to hypothermia and
oxygen-glucose deprivation in
vitro. Cortical neurons transfected with
miR-194-5p mimic exhibited increased death due to oxygen-glucose deprivation.
MiR-194-5p mediated the regulation of neuronal death, which involves the
downregulation of the specific target protein SUMO2, which is a crucial protein
in ischemia tolerance. Collectively, these data highlight the unique role of
miR-194-5p in mediating the deep hypothermia circulation arrest response via the regulation of SUMO2. These
findings suggest that miR-194-5p could be a potential therapeutic target for
intervention in ischemic disease.