Real time RT-PCR shows correlation between retinoid-induced apoptosis and NGF-R mRNA levels

Biochem Biophys Res Commun. 2001 Dec 7;289(3):647-52. doi: 10.1006/bbrc.2001.6028.

Abstract

Neurotrophins and retinoic acid have a critical role in the differentiation and the survival of neurons. All-trans-, 9-cis-retinoic acid (10(-6) M) or NGF (50-100 ng/ml) induced morphologic differentiation and inhibited cell growth in SH-SY5Y neuroblastoma cells after 7 days of culture. Continuous treatment of undifferentiated cells with all-trans- or 9-cis-retinoic (10(-6) M) did not induce apoptosis, whereas NGF-differentiated cells showed dramatic apoptosis after 2 to 4 days of retinoic acid treatment as evidenced by TUNEL reaction and flow cytometry analysis following propidium iodide staining. Addition of Ro41-5253 blocked all-trans-retinoic-induced apoptosis, suggesting that the apoptotic signaling pathway was mediated by RARs. The effects of all-trans- or 9-cis-retinoic acid on the expression of NGF receptors was evaluated using real-time fluorescence reverse transcription-PCR. A slight transient increase in the expression of p75(NGFR) mRNA was observed by 2 to 4 h after retinoid treatment of undifferentiated cells, whereas a larger increase in the expression of both TrkA and p75(NGFR) mRNA up to threefold the basal level, was observed by 2 to 6 h after retinoid treatment of NGF-differentiated cells. Our results suggest that NGF-differentiated cells may be more susceptible to retinoid-induced apoptosis than undifferentiated cells.

Publication types

  • Comparative Study

MeSH terms

  • Alitretinoin
  • Animals
  • Apoptosis*
  • Cell Differentiation
  • Cell Division / drug effects
  • Flow Cytometry
  • Kinetics
  • Nerve Growth Factor / pharmacology
  • Neurites / drug effects
  • Neuroblastoma
  • Neurons / cytology
  • Neurons / drug effects
  • Neurons / metabolism*
  • RNA, Messenger / biosynthesis
  • Receptor, Nerve Growth Factor / biosynthesis*
  • Receptor, Nerve Growth Factor / genetics
  • Receptor, trkA / biosynthesis*
  • Receptor, trkA / genetics
  • Reverse Transcriptase Polymerase Chain Reaction
  • Transcriptional Activation
  • Tretinoin / pharmacology*
  • Tumor Cells, Cultured

Substances

  • RNA, Messenger
  • Receptor, Nerve Growth Factor
  • Alitretinoin
  • Tretinoin
  • Nerve Growth Factor
  • Receptor, trkA