Thyrotropin-releasing hormone increases the levels of c-fos and beta-actin mRNA in GH3/B6 pituitary tumor cells.
The effects of thyrotropin-releasing hormone (TRH) on the mRNA levels of c-fos, N-myc, beta-actin and prolactin (PRL) were studied in GH3/B6 cells, a rat pituitary cell line. TRH has previously been shown to increase biosynthesis and release of PRL, and to stimulate PRL gene transcription (13,19) in these cells. All experiments were performed on quiescent serum-deprived cells, and under these conditions, addition of TRH stimulated PRL production but did not alter cellular proliferation. Simultaneously, TRH induced time- and concentration-dependent increases in c-fos and beta-actin mRNA levels, with peak responses at 30 min and 4 h, respectively, in a dose range from 1 nM to 100 nM. The TRH effects on N-myc mRNA levels were less consistent. Addition of serum to quiescent GH3/B6 cells induced (3-5 fold) increases in c-fos, beta-actin and PRL mRNAs which differed in magnitude and kinetics when compared to TRH stimulation. Serum did not alter N-myc mRNA levels. The TRH-induced increases in c-fos and beta-actin mRNA may play a role in the secretory response.
D000199:Actins / Q000235:genetics*; D000818:Animals; D002460:Cell Line; D046508:Culture Techniques / Q000379:methods; D005796:Genes / Q000187:drug effects*; D010911:Pituitary Neoplasms; D011519:Proto-Oncogenes / Q000187:drug effects*; D012333:RNA, Messenger / Q000187:drug effects / Q000235:genetics*; D051381:Rats; D013973:Thyrotropin-Releasing Hormone / Q000494:pharmacology*; D014158:Transcription, Genetic / Q000187:drug effects*
D000199:Actins; D012333:RNA, Messenger; D013973:Thyrotropin-Releasing Hormone