Evidence has accumulated that insertion of a foreign body into the uterine lumen (Spilman & Duby, 1972; Wilson, Cenedella, Butcher & Inskeep, 1972; Chaudhuri, 1973; Saksena & Harper, 1974; Saksena, Lau & Castracane, 1974) or its distension (Poyser, Horton, Thompson & Los, 1971) induces a significantly greater production of prostaglandin (PG) than in control uteri in several species including man (Batta, Mukerjee & Santhakumari, 1972). Likewise, the elevated levels of PG in the presence of an IUD and its effect on luteal regression (Spilman & Duby, 1972) and the antifertility effect induced by an IUD has been successfully reversed in rabbits by administering indomethacin (Saksena & Harper, 1974), an inhibitor of prostaglandin biosynthesis (Vane, 1971). All this evidence suggests that prostaglandins are involved in the mechanism of action of an IUD. We reported a preimplantation rise of uterine prostaglandin F (PGF) content and concentration in rabbits, rats and hamsters bearing
I. F. LAU, S. K. SAKSENA, and M. C. CHANG
I. F. LAU, S. K. SAKSENA, and M. C. CHANG
Prostaglandins (PGs) are known to exert profound physiological and pharmacological effects on the female reproductive system in women and in many other species (Weeks, 1972; Labhsetwar, 1974). Indomethacin and aspirin, inhibitors of prostaglandin biosynthesis, block PMSG-induced ovulation in immature (Armstrong & Grinwich, 1972; Orczyk & Behrman, 1972) and adult female rats (Tsafriri, Lindner, Zor & Lamprecht, 1972). In the rabbit, ovulation induced by HCG, LH or coitus was blocked by indomethacin (O'Grady, Caldwell, Auletta & Speroff, 1972). In mice, ovulation was blocked with indomethacin and the effect was reversed by injecting prostaglandins E2 or F2α (Saksena, Lau & Shaikh, 1974). All these studies provide indirect evidence that PGs are involved in the process of ovulation. A more direct approach, namely the specific binding of endogenous PGs by anti-PG sera raised in rabbits, was used in the present study. Attempts were also made to reverse the antiovulatory effect of
S. K. SAKSENA, I. F. LAU, and M. C. CHANG
Worcester Foundation for Experimental Biology, Shrewsbury, Massachusetts 01545, and Department of Biology, Boston University, Boston, Massachusetts 02215, U.S.A.
(Received 29th April 1974)
Recent studies implicate prostaglandins (PGs) of the E and F series in the release of anterior pituitary hormones (see Carlson, Barcikowski, & McCracken, 1973). Increases in serum levels of LH (Sato, Taya, Tyujo, Hirono & Igarashi, 1974) FSH and prolactin (Sato, Jyujo, Iesaka, Ishikawa & Igarashi, 1974) were observed following a single injection of PG E1, E2 or F2α in rats which were spayed and primed with oestrogen plus progesterone. Intrauterine insertion of a Silastic-PVP implant containing PGF2α has been shown to stimulate the release of LH in rats and hamsters (Saksena, Lau & Chang, 1974). Experiments in which PGs did not affect LH release have also been reported (Chamley & Christie, 1973). Here we report the results of the time sequence of LH
C. M. LUBICZ-NAWROCKI, NANCY I. F. LAU, and M. C. CHANG
Mouse and hamster spermatozoa from the cauda epididymidis were deposited into the female tract at various periods following ligation of the corpus epididymidis. It was found that the number of spermatozoa in the cauda epididymidis decreased sooner in the hamster than in the mouse but the initial decrease in fertilizing ability occurred much earlier in the mouse than in the hamster. The fertilizing life of spermatozoa in the cauda epididymidis is approximately 25 days in both species.
S. K. SAKSENA, I. F. LAU, A. BARTKE, and M. C. CHANG
Treatment of adult male rats with indomethacin, an inhibitor of prostaglandin (PG) synthesis, caused a significant decrease in LH and testosterone levels in the blood plasma and in the weight of the seminal vesicles, but the weight of the testes and ventral prostate, the levels of FSH in the plasma and fertility were not affected. The concentration of PGF in the blood plasma of the treated animals was reduced, even though measurable amounts of PGs were present in every group. The results of this study, together with the known effects of PG administration on LH release, suggest that the reduction of plasma LH levels in rats injected with indomethacin was due to decreased PG synthesis. It appears that PGs are normally involved in the regulation of LH release.
R. J. Wordinger, A. E. Moss, T. Lockard, D. Gray, I-F. C. Chang, and T. L. Jackson
Summary. Uterine samples were either rapidly frozen in liquid nitrogen or placed in Bouin's fixative. A commercial primary polyclonal antibody made in rabbits against human recombinant basic fibroblast growth factor (bFGF) was used. Western blot analysis indicated that the antibody was specific for bFGF and did not react with acidic FGF. The primary antibody was followed by either goat anti-rabbit immunoglobulin G (IgG) conjugated to the fluorescent phycobiliprotein tracer phycoerythrin or biotinylated goat anti-rabbit IgG and a biotin–avidin–peroxidase complex. Specificity controls using adjacent sections were carried out by (i) substituting normal rabbit sera for the primary antisera, (ii) omitting the primary antisera or (iii) extracting sections with NaCl (2 mol l−1) prior to the immunochemical procedures. No binding of the antibody was observed with any of the specificity control sections. The connective tissue stroma and the basal lamina associated with uterine glandular and surface epithelial layers were positive for bFGF. Localization was not observed within surface or glandular epithelial cells. The basal lamina and endothelial cells associated with blood vessels within the uterus and the smooth muscle cells of the myometrium were positive for bFGF. There were no differences in uterine localization patterns or intensity during the oestrous cycle or after ovariectomy and steroid hormone supplementation. These studies demonstrate the specific localization of bFGF within the mouse uterus.
Keywords: basic fibroblast growth factor; mouse