Introduction: We previously demonstrated that microRNAs (miRNA) play an important
role in Hypothermic Circulatory Arrest (DHCA)-associated neural injury. However, the specific
role of miRNAs in the pathogenesis of DHCA-induced neuron death is still unclear.
Material and Methods: Thus, in the present study, we investigated miR-29 expression and roles in
neuronal HT-22 cells with Oxygen-glucose Deprivation/reoxygenation (OGD/R). In this study, the
model of OGD/R was established using an airtight culture container and the anaeropack. Measurement
of Reactive Oxygen Species (ROS) production and Mitochondrial Membrane Potential
(MMP) was done using the probes of JC-1 and H2DCFDA. The microRNA (miRNA) profile in
hippocampal neurons from rat model of DHCA was determined by miRNA deep sequencing.
Results: We found that the expression of the miR-29 family (miR-29a/b/c) was significantly reduced
in model of DHCA and OGD/R. Overexpression of the miR-29 family inhibited the
OGD/R-induced elevation of ROS and reduction of MMP in HT-22 cells. In addition, administration
of the miR-29 family suppressed proteins of Keap1, Bax and PUMA and increased Nrf2 expression.
We further demonstrated that the miR-29 family targeted the PUMA by luciferase reporter
assay and Western blot analysis.
Conclusion: In conclusion, our data suggest that by targeting a pro-apoptotic BCL2 family member
PUMA, the miR-29 family might emerge as a strategy for protection against DHCA-mediated
neural cell injury.