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K Olson1 , DH Townson1 *
Dept of An. & Nutr.Sci., Univ of New Hampshire, Durham, NH, USA 1
Prostaglandin F2 (PGF) is luteolytic, yet results in only transient regression of CL in the rat (Endocrinology 116:772-778). Here we have compared the ability of PGF and of prolactin (PRL) to induce in rat CL immune events thought to expedite luteolysis. Rats were ovulated with eCG–hCG and then hypophysectomized (D0). On D7-D12, half the rats received testosterone (T4) implants (aromatizable androgen) to enhance CL development and sensitivity to PGF/PRL; remaining rats were sham-operated. On D9-D11, the rats received 2X daily injections of saline (VEH, n=12), PGF (Lutalyse®, 250 µg; n=14), or PRL (312 µg; n=14). On D12, the rats were killed, blood was collected, and the ovaries prepared for immunostaining of intercellular adhesion molecule-1 (ICAM-1) and macrophages. Minimal staining of ICAM-1 and few macrophages (2-26 cells/high power field) were detected in CL of SAL- and PGF-treated rats, regardless of T4 treatment. In contrast, CL of PRL-treated rats (with/without T4) stained intensely for ICAM-1 and contained large numbers of macrophages (91 cells/hpf; p<.01). Luteal weight and plasma progestins (progesterone and 20a-dihydroprogesterone) indicated further immunologic/luteolytic effects of only PRL. For both luteal weight and plasma progestins, there was a significant treatment by T4 interaction (p<.01): CL of VEH- and PGF-treated rats were larger and produced more progestins in response to T4 than CL of PRL-treated rats. These results indicate that PRL, but not PGF, induces immune events in rat CL which compromise luteal function.[Supported by the UNH VP for Sponsored Research]
This abstract is being presented on Sunday, August 1 at 8:00 AM to 10:15 AM at CUB 2nd Floor Ballroom.