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The study was conducted to determine gene expression of short form of leptin receptor (OB-Rs) using real time RT-PCR in distinct tissues of the central nervous system (medial basal hypothalamus, preoptic area, stalk median eminence), pituitary and reproductive tract (corpus luteum, ovarian stroma, endometrium, myometrium, and trophoblast) in pigs during luteal phase of the cycle and early gestation. The expression of OB-Rs mRNA in SME did not differ between analyzed stages of the cycle and pregnancy. In anterior pituitary, transcript levels were almost identical in mid- and late-luteal periods, but significantly decreased on 30-32 day of gestation when compared with day 14-16. In posterior pituitary, significantly higher expression was observed in two periods of pregnancy when compared with two stages of luteal phase. In corpus luteum the lowest expression was observed during days 10-12 of the cycle, whereas markedly higher levels were detected in late-luteal stage and gestation. In ovarian stroma the expression of Ob-Rs mRNA was markedly diminished during days 14-16 of the cycle when compared with days: 10-12 of the cycle and 30-32 of pregnancy. The expression of Ob-Rs mRNA in endometrium and myometrium reached the lowest levels on 30-32 day of pregnancy in comparison with earlier stage, 14-16 day. Summarizing, the expression of the short form of leptin receptor mRNA was found in majority of tested tissues including hypothalamus, pituitary and reproductive tract and their levels fluctuated depending on the phase (mid- and late-luteal) of the cycle and the day of pregnancy (early and late stage of implantation).
Soon after ovulation, the corpus luteum (CL) starts secreting progesterone (P4), a hormone necessary for implantation. The aim of the study was to evaluate whether P4 exerts an autocrine/paracrine action on luteal angiogenic activity and P4, prostaglandin E2 (PGE2) and NO production in the mare. Corpora hemorrhagica (CH) and mid-luteal phase CL (MCL) were cultured with (i) no hormone (Control); (ii) P4; (iii) a P4 precursor - pregnenolone; or (iv) a P4 antagonist - onapristone [10-4M;10-5M; all steroids]. NO production decreased in MCL, with respect to CH, when treated with P4 [10-4M] and pregnenolone [10-5M]. PGE2 increased from CH to MCL, and showed a tendency to rise in pregnenolone treated luteal tissues (10-4M; p=0.06). In the CH, P4 decreased with pregnenolone [10-4M] compared to control, P4 [10-5M], onapristone [10-4M;10-5M] and pregnenolone [10-5M](p<0.05). In the MCL, pregnenolone [10-5M] decreased (p<0.05) and P4 tended to decrease (p=0.06) bovine aortic endothelial cell (BAEC) mitogenesis. Onapristone [10-4M] increased BAEC proliferation with respect to P4 (p=0.01). Since there was no direct effect of treatments on BAEC, these data suggest that long-lasting effects of P4 and its precursor may inhibit angiogenic factor(s) production by equine MCL, preparing for CL functional and structural regression.
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