MicroRNA-665 mediates propofol-induced cell apoptosis in human stem cell-derived neurons

Bioengineered. 2019 Dec;10(1):493-500. doi: 10.1080/21655979.2019.1682105.

Abstract

We aimed to evaluate the neurotoxicity and mechanisms of anesthetics propofol in hESC-derived neurons. Cell apoptosis in hESC-derived neurons' exposure to 4, 10 and 20 μg/mL propofol for 6 h was assessed using terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate in situ nick end labeling (TUNEL) staining and microRNA-665 (miR-665) expression was assessed using quantitative reverse transcription polymerase chain reaction (qRT-PCR). miR-665 was overexpressed and knocked down using a miR-665 mimic and anti-665 transfection, respectively. The results showed that hESCs exposed to propofol showed a dose-dependent cell apoptosis, followed by the upregulation of miR-665 expression. Overexpression of miR-665 increased propofol-induced apoptosis in hESC cells. And targeting miR-665 decreased propofol-induced cell apoptosis in hESC cells. These data suggest that propofol induces cell death in hESC-derived neurons and the propofol-induced cell apoptosis may occur via miR-665-dependent mechanism.

Keywords: Propofol; apoptosis; miR-665; neurotoxicity.

MeSH terms

  • Anesthetics, Intravenous / toxicity*
  • Animals
  • Apoptosis / drug effects*
  • Cells, Cultured
  • Humans
  • Mice
  • MicroRNAs / genetics
  • MicroRNAs / metabolism*
  • Neurons / cytology
  • Neurons / drug effects*
  • Neurons / metabolism
  • Propofol / toxicity*
  • Stem Cells / cytology
  • Stem Cells / drug effects*
  • Stem Cells / metabolism

Substances

  • Anesthetics, Intravenous
  • MicroRNAs
  • Propofol