Abstract
Background MicroRNAs (miRNA) have been identified to exert a wide range of biological functions
in acute kidney injury (AKI) after deep hypothermic circulatory arrest (DHCA). We
sought to investigate the renoprotection of miRNA-106b-5p in a rat model of DHCA by
targeting phosphatase and tensin homolog (PTEN).
Methods Overexpression of miRNA-106b-5p in vivo was conducted by directly injection of lentivirus
vectors containing pre-miRNA-106b-5p into the renal parenchyma of the animals under
the ultrasound guidance 7 days before DHCA. The vehicle or control lentivirus vectors
were given to the control group or the control vector group, respectively. Renal function
and apoptosis activity were evaluated by serum cystatin C, serum/tissue neutrophil
gelatinase-associated lipocalin (NGAL), and terminal deoxynucleotidyl transferase
dUTP nick-end labeling assay (TUNEL) at 24 hours after surgery. Expressions of miRNA-106b-5p,
PTEN, and caspase-3 in the kidney were evaluated by quantitative real-time polymerase
chain reaction and western blot analysis.
Results Transfection of pre-miRNA-106b-5p significantly enhanced the expression of miRNA-106b-5p
and dramatically downregulated the expressions of PTEN in the kidney compared with
the control group. Renal functions were markedly protected by pretreatment with pre-miRNA-106b-5p
as evidenced by decreases in serum cystatin C and serum/tissue neutrophil gelatinase-associated
lipocalin at 24 hours after surgery. The pre-miRNA-106b-5p group showed significantly
fewer apoptotic cells and lower levels of caspase-3 activation than the control group.
Conclusions Overexpression of miRNA-106b-5p attenuates kidney injuries after DHCA, possibly by
inhibition of PTEN.
Keywords
deep hypothermic circulatory arrest - phosphatase and tensin homolog - microRNAs
