Thyrotropin-releasing hormone receptor activation does not elevate intracellular cyclic adenosine 3', 5'-monophosphate in cells expressing high levels of receptors

M. Heinflink, D. R. Nussenzveig, A. M. Friedman, M. C. Gershengorn

Research output: Contribution to journalArticle

11 Scopus citations

Abstract

Activation of TRH receptors (TRH-R) stimulates a signal transduction pathway that leads to the formation of two second messenger molecules, inositol 1, 4, 5-trisphosphate and 1, 2-diacylglycerol. It has been suggested that TRH may also cause an elevation of another second messenger, cAMP. As adenovirus-mediated gene transfer allows expression of TRH-R to high levels in a number of cell types, we tested again whether TRH-R activation might elevate intracellular cAMP in these more sensitive cell systems. In five cell lines, including three human lines, infection with a replication defective adenovirus that encodes the mouse TRH-R complementary DNA (AdCMVmTRHR) induced the expression of 0.2-2 million TRH-R/cell. AdCMVmTRHR-infected cells were activated by a maximally effective dose of TRH, and the levels of inositol phosphates and cAMP were measured. TRH stimulated the production of inositol phosphates from 5- to 9-fold in all cell types, but did not elevate cAMP in any cell type. These data confirm that TRH-R activation does not lead to an elevation of intracellular cAMP.

Original languageEnglish (US)
Pages (from-to)650-652
Number of pages3
JournalJournal of Clinical Endocrinology and Metabolism
Volume79
Issue number2
DOIs
StatePublished - Aug 1994

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ASJC Scopus subject areas

  • Endocrinology, Diabetes and Metabolism
  • Biochemistry
  • Endocrinology
  • Clinical Biochemistry
  • Biochemistry, medical

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