Growth factors stimulate expression of neuronal and glial miR-132

Neurosci Lett. 2011 Nov 21;505(3):242-7. doi: 10.1016/j.neulet.2011.10.025. Epub 2011 Oct 19.

Abstract

Brain-specific microRNAs (miRs) and brain-derived neurotrophic factor (BDNF) are both involved in synaptic function. We previously reported that upregulation of miR-132 is involved in BDNF-increased synaptic proteins, including glutamate receptors (NR2A, NR2B, and GluR1) in mature cortical neurons [7]. However, the potential role of other growth factors in miR-132 induction has not been clarified. Here, we examined the effect of growth factors including basic fibroblast growth factor (bFGF), insulin-like growth factor-1 (IGF-1), glial cell line-derived neurotrophic factor (GDNF), and epidermal growth factor (EGF), on expression of miR-132 and glutamate receptors in immature cortical neurons. We found that BDNF and bFGF upregulated levels of miR-132 in cortical cultures, though bFGF failed to increase glutamate receptors such as NR2A, NR2B, and GluR1. IGF-1, GDNF, and EGF did not have a positive influence on miR-132 and glutamate receptors in neuronal cultures. Furthermore, bFGF significantly upregulated miR-132 in cultured astroglial cells, while other growth factors failed to elicit such a response. It is possible that the growth factor-stimulated neuronal and glial action of miR-132 plays a critical role in brain function.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Analysis of Variance
  • Animals
  • Animals, Newborn
  • Butadienes / pharmacology
  • Cells, Cultured
  • Cerebral Cortex / cytology
  • Enzyme Inhibitors / pharmacology
  • Gene Expression Regulation / drug effects
  • Intercellular Signaling Peptides and Proteins / pharmacology*
  • MicroRNAs / genetics
  • MicroRNAs / metabolism*
  • Mitogen-Activated Protein Kinase Kinases / genetics
  • Mitogen-Activated Protein Kinase Kinases / metabolism
  • Neuroglia / drug effects*
  • Neurons / drug effects*
  • Nitriles / pharmacology
  • RNA, Messenger / metabolism
  • Rats
  • Receptors, N-Methyl-D-Aspartate / genetics
  • Receptors, N-Methyl-D-Aspartate / metabolism
  • Signal Transduction / drug effects
  • Signal Transduction / genetics

Substances

  • Butadienes
  • Enzyme Inhibitors
  • Intercellular Signaling Peptides and Proteins
  • MIRN132 microRNA, rat
  • MicroRNAs
  • Nitriles
  • RNA, Messenger
  • Receptors, N-Methyl-D-Aspartate
  • U 0126
  • Mitogen-Activated Protein Kinase Kinases