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MicroRNA‑155 contributes to the occurrence of epilepsy through the PI3K/Akt/mTOR signaling pathway

Wei Duan1, Yan Chen2, Xiao-Rong Wang3

  • 1Department of Neurology, The Fifth Affiliated Hospital, Harbin Medical University, Harbin, Heilongjiang 150001, P.R. China.

International Journal of Molecular Medicine
|June 15, 2018
PubMed

Insights

MicroRNA-155 (miRNA-155) is elevated in temporal lobe epilepsy patients. This microRNA promotes epilepsy by inhibiting the PI3K/Akt/mTOR pathway, impacting key proteins involved in cell survival and death.

Area of Science:

  • Neuroscience
  • Molecular Biology
  • Genetics

Background:

  • Epilepsy is a neurological disorder characterized by recurrent seizures.
  • MicroRNAs play crucial roles in regulating gene expression and are implicated in various diseases, including epilepsy.
  • Understanding the molecular mechanisms underlying epilepsy is essential for developing effective treatments.

Purpose of the Study:

  • To investigate the role of microRNA-155 (miRNA-155) in the occurrence of temporal lobe epilepsy (TLE).
  • To elucidate the molecular mechanism by which miRNA-155 influences epilepsy.
  • To examine the relationship between miRNA-155, neurotrophic factors, and apoptosis in epilepsy.

Main Methods:

  • Reverse transcription-quantitative polymerase chain reaction (RT-qPCR) was used to measure miRNA-155 expression levels.
  • Western blot analysis was employed to assess the protein expression of brain-derived neurotrophic factor (BDNF), tropomyosin receptor kinase B (TrkB), caspase-3, tumor protein p53 (p53), apoptosis regulator BAX (Bax), phosphoinositide 3-kinase (PI3K), phosphorylated Akt (p-Akt), and phosphorylated mTOR (p-mTOR).
  • The effect of a PI3K inhibitor was evaluated in conjunction with miRNA-155.

Main Results:

  • Patients with temporal lobe epilepsy exhibited significantly higher miRNA-155 expression compared to healthy controls.
  • Overexpression of miRNA-155 led to decreased expression of BDNF and TrkB, increased caspase-3 activity, and elevated p53 and Bax protein levels.
  • miRNA-155 overexpression inhibited the PI3K/Akt/mTOR signaling pathway, evidenced by reduced PI3K, p-Akt, and p-mTOR protein expression.
  • Inhibition of PI3K exacerbated the effects of miRNA-155 on protein expression and apoptosis-related markers.

Conclusions:

  • MicroRNA-155 plays a significant role in the pathogenesis of epilepsy.
  • The PI3K/Akt/mTOR signaling pathway is a key mediator of miRNA-155's pro-epileptic effects.
  • Targeting miRNA-155 or the PI3K/Akt/mTOR pathway may offer therapeutic strategies for epilepsy.

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