title: Characteristics of the prolactin stimulation of c-fos mRNA levels in mouse mammary gland explants.
abstract: The signal transduction pathway(s) for the prolactin (PRL) regulation of lactogenic processes in the mammary are not fully known. Recent studies indicate that the PRL occupancy of its receptor activates a tyrosine kinase (JAK-2), which is constitutively associated with the receptor. In the present studies, we have characterized the PRL stimulation of c-fos mRNA accumulation in mouse mammary gland explants that were precultured with insulin and cortisol for 36 hr. In time course studies, an initial effect (2-fold increase) of PRL was apparent after 15 min, a 4-fold increase occurred after 60 min, and a 2-fold increase was apparent after 2 hr. Dose-response experiments indicated an initial effect with 5 ng/ml PRL and a maximum effect with 500 ng/ml PRL. The accumulation of c-fos; mRNA in the cultured mammary tissues was also increased by human GH, recombinant bovine PRL, cycloheximide, and phorbol 12-myristate 13-acetate (TPA). The cycloheximide and PRL responses were additive, thus indicating that cycloheximide did not "superinduce" the PRL stimulation of c-fos mRNA accumulation. Downregulation of protein kinase C (PKC) by pretreating mammary tissues for 1 day with TPA did not affect the magnitude of the PRL stimulation of c-fos mRNA accumulation. The findings from these studies are consistent with c-fos playing a role in the PRL stimulation of lactogenic processes in the mammary gland. PRL had no effect on c-jun mRNA accumulation under any of the experimental conditions employed in the c-fos studies.
authors.affiliation: Department of Physiology, Wayne State University School of Medicine, Detroit, Michigan 48201, USA.
authors.forename: J A
authors.initials: JA
authors.lastname: Rillema
authors.forename: D L
authors.initials: DL
authors.lastname: Rowady
mesh_terms: D000199:Actins / Q000235:genetics; D000818:Animals; D002417:Cattle; D003513:Cycloheximide / Q000494:pharmacology; D018076:DNA, Complementary / Q000235:genetics; D005260:Female; D005786:Gene Expression Regulation / Q000187:drug effects*; D016762:Genes, fos / Q000187:drug effects*; D016758:Genes, jun / Q000235:genetics; D013006:Growth Hormone / Q000494:pharmacology; D006801:Humans; D006854:Hydrocortisone / Q000494:pharmacology; D007328:Insulin / Q000494:pharmacology; D008321:Mammary Glands, Animal / Q000166:cytology / Q000187:drug effects*; D051379:Mice; D009924:Organ Culture Techniques; D011247:Pregnancy; D011388:Prolactin / Q000494:pharmacology*; D011500:Protein Synthesis Inhibitors / Q000494:pharmacology; D012333:RNA, Messenger / Q000096:biosynthesis* / Q000235:genetics; D012756:Sheep; D015398:Signal Transduction / Q000187:drug effects; D013755:Tetradecanoylphorbol Acetate / Q000494:pharmacology
chemical_list: D000199:Actins; D018076:DNA, Complementary; D007328:Insulin; D011500:Protein Synthesis Inhibitors; D012333:RNA, Messenger; D011388:Prolactin; D013006:Growth Hormone; D003513:Cycloheximide; D013755:Tetradecanoylphorbol Acetate; D006854:Hydrocortisone