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Opposite Effect of Prolactin and Prostaglandin F₂ on the Expression of Luteal Genes as Revealed by Rat cDNA Expression Array

Department of Physiology and Biophysics, College of Medicine, University of Illinois at Chicago, Chicago, Illinois

It is well established that prolactin (PRL) sustains, while prostaglandin F₂ (PGF₂) curtails, progesterone production by the rat corpus luteum (CL). We have previously shown that the actions of both molecules converge on the 20-HSD gene and control its expression in a dramatically opposed manner. In this investigation, we have found twelve more genes that are inversely regulated by PRL and PGF₂. In addition to 20-HSD, PGF₂ stimulated and PRL inhibited PGF₂-receptor, phospholipase C₁ and TGFß₁ expression. In contrast PRL stimulated and PGF₂ inhibited the LH receptor, 11ß-HSD2, sterol carrier protein 2, mitochondrial glutathione S-transferase (GST), GSTµ₂, inhibitory DNA-binding proteins 1, 2, and 3, and calcium binding protein 2. We have also identified new target genes for PRL and PGF₂. PGF₂ stimulated the expression of genes involved in cell signaling such as cell adhesion kinase-ß, ERK3, FRA2, IL-2 receptor, and 14-3-3 proteins. PGF₂ also up-regulated the expression of the sodium channel ß₁, Na/K ATPase, annexin IV, GST7, and P450 reductase. In contrast PGF₂ inhibited the expression of two genes involved in cell cycle: cyclin D2 and retinoblastoma related protein (Rb2/p130). It also inhibited genes involved in estradiol (P-450_AROM) and cholesterol biosynthesis (HMG-CoA synthase), as well as genes involved in tissue remodeling: VEGF and TIMP3. PRL had a profound inhibitory effect on the expression of genes encoding the ADP-ribosylation factor 3, annexin V and c-jun, yet increased the expression of P450scc, 3ß-HSD, and SR-B1 (HDL-receptor), all genes involved in steroidogenesis. PRL also stimulated the expression of ß₂-microglobulin, TIMP2, cytochrome c oxidase IV, cathepsin H and L, and copper-zinc superoxide dismutase as well as elongation factor SIII, heat shock protein-60 and mitochondrial ATP synthase-D. In conclusion, this investigation has revealed a "yin-yang" relationship between PRL and PGF₂ in regulating certain critical genes in the rodent CL, and has demonstrated novel regulation by these factors of other important genes involved in luteal function.

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