Abstract

Follistatin is a monomeric glycoprotein, expressed ubiquitously, and found in greatest levels in ovarian tissue. Our previous studies have demonstrated that ovarian venous follistatin levels are elevated at the same time as spontaneous luteolysis in merino ewes, but remain constant in circulating and uterine plasma across oestrous. It was hypothesized that the follistatin elevation may be part of functional luteolysis in the ovary. A cross-sectional study of ovarian venous follistatin during luteolysis was performed using merino ewes, which were synchronized with intravaginal sponges. Luteolysis was induced 10 days after oestrus using a PGF2α (IM) injection. Circulating (jugular and arterial), uterine venous and ovarian venous (luteinized and contralateral) blood samples were taken under general anaesthesia at times 0, 6, 12, 24, 36, 48 and >48 h (54–71 h) after the PGF2α injection. All samples were assayed for progesterone by RIA and follistatin using a specific follistatin antiserum (#204) in a competitive ELISA with rhFS-288 used as standard. Progesterone concentrations in the venous plasma from the luteinized ovaries plasma were significantly higher than those in the contralateral ovarian and circulating plasma. As expected progesterone concentrations began declining within 6 h and continued until 24 h after PGF2α. Mean circulating plasma follistatin concentrations were similar throughout the experiment with overall means of 9.9 ± 0.5 ng/mL. Both luteinized and contralateral ovarian venous plasma follistatin concentrations (11.8 ± 3.4 ng/mL) were not significantly different from circulating concentrations. However at 48 h ovarian venous follistatin concentrations were significantly elevated (22.5 ± 2.3 ng/mL) and remained elevated for at least 71 h (29.5 ± 7.9 ng/mL). This experiment confirms our previous work that both luteinized and contralateral ovarian venous follistatin concentrations do elevate concurrently with each other but that the elevation in follistatin is not directly related to functional luteolysis as induced by PGF2α.

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