Background:
MicroRNAs (miRNA) are known to play a key role in the etiology and
treatment of epilepsy through controlling the expression of gene. However, miR-125a-5p in the
epilepsy is little known. Epilepsy in rat models was induced by Pentylenetetrazol (PTZ) and miR-
125a-5p profiles in the hippocampus were investigated in our experiment. Also, the relationship
between miR-125a-5p and calmodulin-dependent protein kinase IV (CAMK4) was identified and
the related mechanism was also illustrated.
Methods:
The miR-125a-5p mRNA expression levels were evaluated by quantitative real time polymerase
chain reaction (qRT-PCR). Western Blot (WB) was used to analyze the CAMK4 protein
expression levels. Seizure score, latency and duration were determined based on a Racine scale.
The enzyme-linked immunosorbent assay (ELISA) was used to analyze the inflammatory factor
expression. The relationship between miR-125a-5p and CAMK4 was detected through dual luciferase
assay.
Results:
Downregulation of miR-125a-5p was observed in the hippocampus of PTZ-induced epilepsy
rats. The overexpression of miR-125a-5p attenuated seizure and decreased inflammatory factor
level in the hippocampus of PTZ-induced rats. The miR-125a-5p alleviated epileptic seizure
and inflammation in PTZ-induced rats by suppressing its target gene, CAMK4.
Conclusion:
miR-125a-5p may represent a novel therapeutic treatment for PTZ-induced epilepsy
by preventing the activation of CAMK4.
The relationship between calmodulin binding and phosphorylation of smooth muscle myosin kinase by the catalytic subunit of 3‘:5‘ cAMP-dependent protein kinase.
