MiR-99b regulates cerebral ischemia neuronal injury through targeting IGF1R

Dengbin Qi1, Wei Wang2, Ying Zhang3

  • 1Department of Neurology, Affiliated Hospital of Jining Medical University, YanZhou Branch, Jining, China.

Panminerva Medica
|April 29, 2020
PubMed
Abstract

Insights

MicroRNA-99b (miR-99b) enhances cell viability and reduces apoptosis in cerebral ischemia injury models. This protective effect is mediated by miR-99b targeting Insulin-like Growth Factor 1 Receptor (IGF1R).

Area of Science:

  • Neuroscience
  • Molecular Biology
  • Genetics

Background:

  • MicroRNA-99b (miR-99b) exhibits varied roles in human diseases.
  • The specific function of miR-99b in cerebral ischemia (CI) remains underexplored.

Purpose of the Study:

  • To investigate the role and mechanism of miR-99b in cerebral ischemia injury.
  • To determine if miR-99b affects neuronal viability and apoptosis in a CI model.

Main Methods:

  • Real-time quantitative PCR (RT-qPCR) for miR-99b and IGF1R expression.
  • Western blot for apoptosis-related proteins (Caspase-3, Bax, Bcl-2).
  • MTT assay for cell viability and dual-luciferase assay to confirm miR-99b targeting of IGF1R in an oxygen-glucose deprivation/reperfusion (OGD/R) model of SH-SY5Y cells.

Main Results:

  • miR-99b expression was upregulated in the OGD/R model.
  • Increased miR-99b enhanced SH-SY5Y cell viability and inhibited OGD/R-induced apoptosis.
  • IGF1R was identified as a direct target of miR-99b, with its expression decreasing under OGD/R conditions.

Conclusions:

  • miR-99b plays a protective role in cerebral ischemia injury.
  • The mechanism involves miR-99b targeting IGF1R, thereby promoting cell viability and suppressing apoptosis in neuronal cells under OGD/R conditions.

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