The stimulation of rat astrocytes with phorbol-12-myristate-13-acetate increases the proenkephalin mRNA: involvement of proto-oncogenes

Brain Res Mol Brain Res. 1998 Mar 1;54(2):288-97. doi: 10.1016/s0169-328x(97)00344-6.

Abstract

The effect of phorbol-12-myristate-13-acetate (PMA) on the regulation of proenkephalin (proENK) mRNA level, ENKCRE-2 or AP-1 DNA binding activity, and the mRNA and protein levels of proto-oncogenes (c-fos, fra-1, and c-jun) in primary cultured rat astrocytes were studied. The proENK mRNA level was elevated at 4 h after the treatment of PMA (2.5 microM) without altering the intracellular proENK protein level, and this increase was attenuated by pre-treatment with cycloheximide (CHX; 15 microM), a protein synthesis inhibitor. Both AP-1 and ENKCRE-2 DNA binding activities were markedly increased at 1-4 h by PMA treatment and these PMA-induced responses were inhibited by pre-treatment with CHX, showing that the increase of proENK mRNA level was well correlated with the AP-1 and ENKCRE-2 DNA binding activities. In contrast, although the phospho-CREBP level was also increased by PMA at 0.5-1 h, the pre-treatment with CHX further increased the PMA-induced phospho-CREBP level. In addition, PMA caused the induction of c-fos, c-jun and fra-1 mRNA level and, especially, PMA-induced increase of fra-1 mRNA level was further enhanced by CHX treatment at 4 h. Furthermore, western immunoblot assay showed that PMA caused induction of c-Fos, Fra-1, and c-Jun protein levels. PMA-induced increases of proto-oncoproteins levels were also inhibited by CHX treatment. The results suggest that newly synthesized AP-1 proteins, such as c-Fos, Fra-1, and c-Jun may play important roles in the regulation of PMA-induced proENK gene expression in cultured rat astrocytes. Phospho-CREB protein appears not to be involved in the regulation of PMA-induced proENK gene expression.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Astrocytes / drug effects
  • Astrocytes / metabolism
  • Cells, Cultured
  • Cyclic AMP Response Element-Binding Protein / metabolism
  • Enkephalins / genetics*
  • Enzyme Activation
  • Nerve Tissue Proteins / genetics
  • Phosphorylation
  • Protein Kinase C / drug effects*
  • Protein Precursors / genetics*
  • Proto-Oncogene Proteins / genetics
  • Proto-Oncogenes / genetics*
  • RNA, Messenger / biosynthesis*
  • Rats
  • Rats, Sprague-Dawley
  • Stimulation, Chemical
  • Tetradecanoylphorbol Acetate / pharmacology*

Substances

  • Cyclic AMP Response Element-Binding Protein
  • Enkephalins
  • Nerve Tissue Proteins
  • Protein Precursors
  • Proto-Oncogene Proteins
  • RNA, Messenger
  • proenkephalin
  • Protein Kinase C
  • Tetradecanoylphorbol Acetate