Abstract. Follistatin (FS) is produced and secreted from gonadotroph cells in pituitary gland as well as granulosa cells in the ovary. In the present study, we found that the FS promoter is activated by GnRH in the gonadotroph cell line, LbT2. Therefore, we examined the signal transduction pathways involved in the mechanism. The activation of the FS promoter by GnRH was inhibited by calphostin C, a protein kinase C inhibitor, and U0126, a MAP kinase kinase (MEK) inhibitor. Phosphorylation by protein kinase C of myristoylated alanine-rich C kinase substrate (MARCKS) in LbT2 cells was observed after 3-min treatment with GnRH and declined after 30 min. The subsequent activation of MAP kinase was also transient, and down-regulation of protein kinase C completely inhibited the MAP kinase activation by GnRH, suggesting that the transient activation of protein kinase C led to the transient activation of MAP kinase. Although phorbol 12-myristate 13-acetate treatment increased phosphorylation of MARCKS and activated MAP kinase, it did not activate the FS promoter. Genistein, a tyrosine kinase inhibitor, completely inhibited the GnRH-induced activation of the FS promoter, while no inhibition of the MAP kinase pathway was observed. These results suggest that the activations of both the protein kinase C and tyrosine kinase pathways are necessary for the activation of the FS promoter in gonadotroph cells. FOLLISTATIN (FS) was first identified from ovarian follicular fluid on the basis of its ability to suppress the secretion of follicle-stimulating hormone (FSH) from pituitary gonadotrophs [1][2][3][4]. FS is a monomeric glycoprotein structurally unrelated to inhibin [3]. FS binds to activin with high affinity [5] and inhibits the activity of activin to stimulate FSH secretion [6][7][8]. In ovary, the granulosa cells are responsible for producing and secreting FS in most species [9][10][11][12]. FS expression in granulosa cells is increased through both cyclic AMP and protein kinase C pathways [13][14][15][16][17]. In cultured rat granulosa cells, FSH and gonadotropin-releasing hormone (GnRH) increased FS protein production through the cyclic AMP and protein kinase C pathways, respectively. The expression of FS is not limited to the ovary, and FS is secreted within the pituitary gland, where it exerts autocrine/paracrine effect [18]. It has been reported that FS expression in gonadotrophs is regulated by GnRH at the steady state mRNA levels [18,19]. GnRH is a hypothalamic peptide and serves as a critical regulator for the synthesis and secretion of FSH [20,21]. FSH is composed of two noncovalently linked subunits, a and b. It is well known that the synthesis of the b-subunit (FSHb) is the rate-limiting step in the production of FSH [20]. Slow-frequency GnRH pulses increase FSHb mRNA through activation of the

Objective: To assess the factors influencing operative time and intraoperative blood loss in patients who had undergone laparoscopic myomectomy (LM). Methods: The study involved 374 patients who had undergone LM at our hospital between May 2009 and April 2011. We examined the relationships between operative time, intraoperative blood loss, maximum myoma diameter, number of resected myomas, and myoma growth patterns (5 groups: intramural, submucosal, subserosal, pedunculated subserosal, and intraligamentous). Results: There was a correlation between maximum myoma diameter, operative time (y = 0.73x + 51.51; r = 0.393), and intraoperative blood loss (y = 3.76x − 121.12; r = 0.456). Furthermore, the number of resected myomas was correlated with operative time (y = 5.06x + 81.71; r = 0.308) and intraoperative blood loss (y = 3.49x + 99.55; r = 0.049). There was a significant difference in operative time between pedunculated subserosal myomas and intraligamentous myomas, but there was no significant difference in intraoperative blood loss between myomas displaying different growth patterns. Conclusions: The maximum myoma diameter was a factor influencing operative time and intraoperative blood loss. In addition, the results suggested that operative time was influenced by the number of resected myomas and the growth patterns of myomas.

No abstract

No abstract