Follicle-Stimulating Hormone Stimulates Circulating Gonadotropin Surge-Attenuating/Inhibiting Factor Bioactivity in Cows1

Abstract

This study aimed to determine whether superovulation in cattle stimulates gonadotropin surge-attenuating/inhibiting factor (GnSAF/IF) bioactivity, as it does in humans. Blood samples were collected from cows (n = 7 per treatment) at -4, 8, 20, 32, 44, 56, and 68 h after injections of saline, eCG, or FSH. Equal volumes of plasma at each treatment and time point were pooled, and GnSAF/IF and inhibin bioactivities were measured using an established rat pituitary cell culture bioassay. Plasma from saline- and eCG-treated cows had little effect on GnRH-induced LH secretion (116.3 +/- 8.3%-81.6 +/- 6.0% of control), while plasma from FSH-treated cows produced a time-dependent suppression of GnRH-induced LH secretion, falling to 64.6 +/- 4.0% of the control value at 56 h after first FSH injection (p < 0.001). The GnSAF/IF bioactivity from the 56-h plasma eluted at pH 5.73 by pseudochromatofocusing-similar to the GnSAF/IF isoelectric point value of 5.81 determined using serum from superovulated women. Plasma from FSH-treated cows reduced basal FSH secretion more than plasma from eCG-treated cows (to 55.5 +/- 5.7% and 63.2 +/- 6.6% of the control value, respectively, p < 0.01) although immunoreactive inhibin concentrations were similar between the two groups. We conclude that FSH, but not eCG, treatment causes a time-dependent production of circulating GnSAF/IF bioactivity in cattle.

Effects of delaying the LH surge and altering LH secretion on plasma hormones and embryo production in heifers superstimulated with FSH

“…This is consistent with our previous data (Gosselin et al 2000) demonstrating that neither estradiol nor progesterone was correlated with LH pulsatility during superstimulation, a finding that was also confirmed by others (Takagi et al 2001). Other factors including (but not limited to) inhibin or the gonadotropin-surge inhibiting factor (Fowler and Price 1997), may be involved in the suppression of LH pulsatility during superstimulation. In the CIDR-7d group, the number of unovulated follicles increased and ovulation rate and embryo production decreased in animals with lower progesterone concentrations at the start of superstimulatory treatment.…”

FSH modulatory effect on human granulosa cells: a gene–protein candidate for gonadotrophin surge-attenuating factor

“…A line of evidence dating back to the late 1970s supports the existence of such a factor in humans as well as in other species (Ferraretti et al, 1983;Geiger et al, 1980;Koppenaal et al, 1992;Messinis et al, 1985Messinis et al, , 1986Templeton, 1989, 1991;Schenken and Hodgen, 1983;Sopelak and Hodgen, 1984). It has been suggested that FSH is the main hormone that stimulates the production of GnSAF (Fowler and Price, 1997;Messinis et al, , 1993Messinis et al, , 1994a. From a physiological point of view, it has been postulated that GnSAF, by antagonizing the stimulating effect of oestradiol on the pituitary, controls the amplitude of the LH surge and the coordination of the LH signal with follicular development and steroidogenesis in women and other mammals (Fowler et al, 2001(Fowler et al, , 2003Messinis et al, 1985Messinis et al, , 1998.…”

Purification of a candidate gonadotrophin surge‐inhibiting/attenuating factor (GnSIF/AF) showing MAPK as a possible target

“…Gonadotrophin surge‐inhibiting factor (GnSIF, also called gonadotrophin surge‐attenuating factor, GnSAF) has been known for over two decades, yet its molecular structure has still not been completely characterized. GnSIF/AF is an ovarian product, originating from the granulosa cells (Fowler et al, 2002), and its production is stimulated by follicle stimulating hormone (FSH) (Messinis et al, 1991; Fowler and Price, 1997). GnSIF/AF, in turn, inhibits the gonadotrophin‐releasing hormone (GnRH)‐induced pituitary luteinizing hormone (LH) secretion (Messinis and Templeton, 1991; Fowler et al, 2003) and antagonises the self‐priming effect of GnRH, both in vivo (Messinis and Templeton, 1991) and in vitro (Koppenaal et al, 1992; Fowler et al, 1994; Byrne et al, 1996; de Koning et al, 2001).…”