In vitro assessment of progesterone and prostaglandin e(2) production by the corpus luteum in cattle following pharmacological synchronization of estrus.

We studied the secretory function of the corpus luteum (CL) in cows following different estrus synchronization protocols. Estrus was synchronized using one (n=4) or two injections (n=5) of prostaglandin F(2alpha) (PGF(2alpha); dinoprost), two injections of different analogues of PGF(2alpha) (aPGF(2alpha)), luprostiol (n=5) and cloprostenol (n=5), at eleven-day intervals, a gestagen implant (norgestomet, n=5, for 10 days) or norgestomet together with a subsequent dinoprost injection on the day of implant removal (n=5). CL samples were collected by ovariectomy on Day 7-8 of the estrous cycle. Luteal strips were stimulated with LH (100 ng/ml) or prostaglandin E(2) (PGE(2), 10(-6)M) for 24 h in culture media. The progesterone (P(4)) and PGE(2) concentrations in the media were measured by enzyme immunoassay. In the control CL (spontaneous estrus; n=5), LH and PGE(2) stimulated P(4) and PGE(2) (P<0.001). The effects of both factors on P(4) were reduced in the CL following dinoprost- and cloprostenol-synchronized estrus (P<0.05) and were absent in the luprostiol-synchronized CL (P>0.05). In the norgestomet-synchronized CL, the stimulatory effects of LH and PGE(2) were higher compared with the CL synchronized by aPGF(2alpha) (P<0.05). Pharmacological manipulation of the estrous cycle using aPGF(2alpha) may cause lower P(4) secretion. Estrus synchronization inhibited CL sensitivity to luteotropic factors. Therefore, attention should be focused on the estrous synchronization method in both in vivo and in vitro studies of CL functions in cattle.

Lysophosphatic acid modulates prostaglandin secretion in the bovine uterus.

Lysophosphatidic acid (LPA) modulates prostaglandin (PG) synthesis via LPA receptor 3 (LPAR3) in the murine endometrium. The lack of functional LPAR3 in mice may lead to embryo mortality. In the present study, we examined the role of LPA in the bovine uterus. We confirmed that LPA is locally produced and released from the bovine endometrium. Moreover, there are enzymes involved in LPA synthesis (phospholipase (PL) D(2) and PLA2G1B) in the bovine endometrium during estrous cycle and early pregnancy. Expression of the receptor for LPA (LPAR1) was positively correlated with the expression of PGE(2) synthase (PGES) and negatively correlated with the expression of PGF(2alpha) synthase (aldose reductase with 20 alpha-hydroxysteroid dehydrogenase activity - PGFS) during early pregnancy. In vivo LPA induced P4 and PGE(2) secretion was inhibited by LPAR1 antagonist (Ki16425). The overall results indicate that LPA is locally produced and released from the bovine endometrium. Moreover, LPAR1 gene expression in the endometrium during the estrous cycle and early pregnancy indicates that LPA may play autocrine and/or paracrine roles in the bovine uterus. LPAR1 gene expression is positively correlated with the expression of the enzyme responsible for luteotropic PGE(2) production (PGES) in endometrium. In cow, LPA stimulates P4 and PGE(2) secretion. Thus, LPA in the bovine reproductive tract may indirectly (via endometrium) or directly support corpus luteum action via the increase of P4 synthesis and the increase of PGE(2)/PGF(2)(alpha) ratio. It suggests that LPA may serve as an important factor in the maintenance of early pregnancy in cow.