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Long non-coding RNA GAS5 promotes PC12 cells differentiation into Tuj1-positive neuron-like cells and induces cell

He-Yan Zhao1, Sheng-Tong Zhang1, Xiang Cheng1

  • 1Department of Human Anatomy, the Jiangsu Key Laboratory of Neuroregeneration, Medical School, Nantong University, Nantong, Jiangsu Province, China.

Neural Regeneration Research
|August 10, 2019
PubMed

Insights

The long non-coding RNA GAS5 promotes neuron-like differentiation in PC12 cells and suppresses proliferation. GAS5 enhances acetylcholine release, suggesting a beneficial role in nervous system recovery.

Area of Science:

  • Molecular Biology
  • Neuroscience
  • Genetics

Background:

  • Growth arrest-specific 5 (GAS5) is an anti-oncogene primarily studied in tumors.
  • Limited research exists on GAS5's role in nervous system diseases.

Purpose of the Study:

  • To investigate the function of the long non-coding RNA GAS5 in rat pheochromocytoma (PC12) cells.
  • To explore GAS5's impact on neuronal differentiation, cell cycle, apoptosis, and neurotransmitter expression.

Main Methods:

  • GAS5 overexpression via lentivirus transfection in PC12 cells.
  • Real-time PCR for GAS5 and C-myc expression.
  • 5-ethynyl-2'-deoxyuridine assay for cell cycle analysis.
  • Immunohistochemistry for neuronal markers (Tuj1, doublecortin, MAP2).
  • Flow cytometry for apoptosis detection.
  • Western blot for acetylcholine expression.

Main Results:

  • GAS5 overexpression promoted PC12 cell differentiation into Tuj1-positive neuron-like cells with extended processes.
  • GAS5 significantly suppressed cell proliferation and cell cycle progression.
  • GAS5 did not affect the apoptosis rate of PC12 cells.
  • GAS5 increased choline acetyltransferase expression and acetylcholine release.

Conclusions:

  • GAS5 promotes neuronal differentiation and cholinergic system function in PC12 cells.
  • GAS5 may be beneficial for neuronal recovery and the cholinergic nervous system.
  • Further research is warranted to explore GAS5's therapeutic potential in neurological disorders.
Keywords:
Alzheimer's diseasePC12 cellacetylcholinecell cyclecholine acetyltransferasegrowth arrest-specific 5nerve regenerationneural regenerationneuronproliferation

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