Expression of Insulin-Like Growth Factor-I and Insulin-Like Growth Factor-Binding Protein-1 in the Rat Uterus during Decidualization*

Abstract

Decidualization of the uterus involves proliferation and differentiation of uterine cells. The effects of decidualization on uterine expression of insulin-like growth factor-I (IGF-I) and IGF-binding protein-1 (IGFBP-1) have been examined in the hypophysectomized-ovariectomized (hypox-ovx) rat and the pituitary-intact (ovx) rat. Decidualization was induced by uterine stimulation of animals treated with a combination of 17 beta-estradiol and progesterone. The patterns of change in uterine IGF-I mRNA and IGFBP-1 mRNA abundance were similar to hypox-ovx rats, hypox-ovx rats replaced with GH and T4, and ovx rats. The changes in IGF-I mRNA abundance were temporally related to 17 beta-estradiol injections. IGFBP-1 mRNA was undetectable early in the decidualization process and reached maximal levels on day 6. Mechanical separation of the deciduoma tissue from the underlying myometrium revealed that the deciduoma tissue was depleted in IGF-I mRNA, while the majority of the IGFBP-1 was located in the deciduoma tissue. The in situ hybridization technique was used to localize IGF-I and IGFBP-1 mRNA in the decidualized uterus. The majority of the IGF-I expression was localized to the outer stroma and smooth muscle cell layer, whereas IGFBP-1 mRNA was detected in uterine epithelial cells and stromal glands. These experiments demonstrated that uterine IGF-I and IGFBP-1 expression during the process of decidualization are pituitary independent. Furthermore, our observations support the hypothesis that the expression of IGFBP-1, a protein capable of inhibiting the mitogenic activity of IGF-I, in deciduoma tissue may inhibit paracrine IGF-1 actin and allow for the differentiation of stromal tissue.

Expression of the Estrogen and Progesterone Receptors and Insulin-like Growth Factor-I Genes in the Porcine Myometrium during Early Pregnancy.

“…This imply that the hormonal regulation of the myometrium is predominantly based on maternal steroid hormones. This is in accordance with studies on the pregnant rat uterus where IGF-I mRNA decreased in the decidualized tissue whereas the abundance in the myometrium was maintained [32].…”

Prostaglandin E2 Induces Fibroblast Growth Factor 9 via EP3-Dependent Protein Kinase Cδ and Elk-1 Signaling

“…When the cells reached confluence, they were subcultured in phenol red-free DMEM/F12 supplemented with 10% FBS and antibiotics until 70% confluence was reached. After serum starvation for 12 h, the cells were stimulated with PGE 2 (0.01 to 100 M) or vehicle for 0, 4,8,12, and 24 h. In a separate experiment, cells were treated with vehicle, 1 M PGE 2 , or 10 M sulprostone in the presence or absence of different inhibitors in serum-free, phenol red-free medium for 12 h. For the siRNA experiment, cells were cultured in a six-well plate and transfected with synthetic PKC␦, PKC␣, Elk-1, or control GFP siRNA according to procedures recommended by the manufacturer (Cell Signaling Technologies). Two sets of siRNA against PKC␦, designated duplex 1 (sense sequence, GAUGAAGGAGGCGCUCAGdTdT) and duplex 2 (sense sequence, GGCUGAGUUCUGGCUGGACdTdT) were used in this study.…”

“…Nonetheless, E 2 per se seldom exerts a growth-promoting effect. Instead, the mitogenic effect of E 2 is usually mediated by some peptide growth factors in an autocrine/paracrine manner (7,8,14,31). In addition, recent data indicate that overproduction of PGE 2 due to aberrant expression of COX-2 in endometriotic tissue and peritoneal macrophage may play critical roles in the survival and/or proliferation of endometriotic cells (28,42,49,50).…”

Expression of interleukin 1, interleukin 6 and tumour necrosis factor in mouse uterus during the peri-implantation period of pregnancy

“…Several recent findings suggest that some hormone-dependent changes may be due to local actions of polypeptide growth factors, such as epidermal growth factor and insulin-like growth factor 1 (DiAugustine et al, 1988;Murphy et al, 1988;Brigstock et al, 1989;Croze et al, 1990;Huet-Hudson et Nelson et al, 1991). These and related factors may function as autocrine or paracrine regulators of uterine cell proliferation and differentiation.…”