Phorbol myristate acetate enhances degradation of TRH receptor mRNA in a pituitary cell type-specific manner.
Regulation of the level of thyrotropin-releasing hormone (TRH) receptor (TRH-R) mRNA appears to involve both modulation of gene transcription and of mRNA degradation. To study regulation of TRH-R mRNA degradation and circumvent any physiological effect on transcription, we use cells stably transfected with mouse TRH-R cDNA under control of the constitutively active cytomegalovirus promoter. In stably transfected GH pituitary cells, we find that phorbol 12-myristate 13-acetate (PMA), like TRH, down-regulates TRH-R mRNA by increasing the rate of TRH-R mRNA degradation. In contrast, in stably transfected AtT-20 pituitary cells and in nonpituitary cell lines, neither TRH nor PMA decreased TRH-R mRNA levels. These findings are consistent with the idea that activation of protein kinase C leads to enhanced degradation of TRH-R mRNA in a cell-type-specific manner.
Gershengorn
M C
MC
Department of Medicine, Cornell University Medical College, New York Hospital, New York 10021.
Narayanan
C S
CS
Fujimoto
J
J
D000818:Animals; D002478:Cells, Cultured; D010902:Pituitary Gland / Q000166:cytology / Q000187:drug effects / Q000378:metabolism*; D012333:RNA, Messenger / Q000378:metabolism*; D051381:Rats; D018025:Receptors, Thyrotropin-Releasing Hormone / Q000235:genetics*; D013755:Tetradecanoylphorbol Acetate / Q000494:pharmacology*; D013973:Thyrotropin-Releasing Hormone / Q000494:pharmacology
D012333:RNA, Messenger; D018025:Receptors, Thyrotropin-Releasing Hormone; D013973:Thyrotropin-Releasing Hormone; D013755:Tetradecanoylphorbol Acetate