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Phorbol myristate acetate enhances degradation of TRH receptor mRNA in a pituitary cell type-specific manner

M C Gershengorn1, C S Narayanan, J Fujimoto

  • 1Department of Medicine, Cornell University Medical College, New York Hospital, New York 10021.

Molecular and Cellular Neurosciences
|December 1, 1994
PubMed

Insights

Thyrotropin-releasing hormone (TRH) receptor mRNA degradation is regulated by protein kinase C activation in a cell-specific manner. This mechanism affects TRH-R mRNA levels in GH pituitary cells but not other cell types.

Area of Science:

  • Molecular Endocrinology
  • Gene Regulation
  • Cell Biology

Background:

  • Thyrotropin-releasing hormone (TRH) receptor (TRH-R) mRNA levels are controlled by gene transcription and mRNA degradation.
  • Understanding mRNA degradation mechanisms is crucial for comprehending TRH-R regulation.

Purpose of the Study:

  • To investigate the regulation of TRH-R mRNA degradation.
  • To determine the role of protein kinase C (PKC) in TRH-R mRNA stability.
  • To assess the cell-type specificity of TRH-R mRNA degradation regulation.

Main Methods:

  • Utilized stably transfected GH pituitary cells, AtT-20 pituitary cells, and nonpituitary cell lines expressing mouse TRH-R cDNA.
  • Employed the cytomegalovirus promoter for constitutive TRH-R expression, bypassing transcriptional regulation.
  • Administered phorbol 12-myristate 13-acetate (PMA), a PKC activator, and TRH to assess effects on TRH-R mRNA levels and degradation rates.

Main Results:

  • Phorbol 12-myristate 13-acetate (PMA) and TRH significantly decreased TRH-R mRNA levels in stably transfected GH pituitary cells.
  • This downregulation in GH cells was attributed to an increased rate of TRH-R mRNA degradation.
  • Neither TRH nor PMA affected TRH-R mRNA levels in stably transfected AtT-20 pituitary cells or nonpituitary cell lines, indicating cell-type specificity.

Conclusions:

  • Activation of protein kinase C enhances the degradation of TRH-R mRNA.
  • The regulation of TRH-R mRNA degradation by PKC is cell-type specific.
  • These findings provide insights into the post-transcriptional control of TRH receptor expression.

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