Noradrenaline and Adrenoreceptors Promote Prostaglandin F2α Generation in Lipopolysaccharide-Exposed Endometrial Epithelial Cells of Pigs ().

Severe kinds of uterine inflammation in animals cause reproductive and economic problems. Although there are changes in prostaglandin (PG) production and noradrenergic uterine innervation during endometritis, the role of noradrenaline (NA) and adrenoreceptors (ARs) in PGF2α formation is not yet fully understood. To recognize noradrenergic control of the PGF2α generation on the cellular level during endometritis, the action of NA as well as α1-, α2- and β-ARs on protein abundances of PGF synthase (PGFS) and PG 9-ketoreductase/carbonyl reductase (CBR1) in the lipopolysaccharide (LPS)-influenced pig endometrial epithelial cells and PGF2α release from these cells were studied. The epithelial cells were exposed to LPS and NA alone; LPS with NA; LPS with agonists of α1-, α2- and β-Ars; LPS with antagonists of β1-, β2- and β3-ARs with NA; and LPS with antagonists of β1-, β2- and β3-ARs in combinations with agonists of β1-, β2-, and β3-ARs for 24 h. PGFS and CBR1 protein abundances in cells were determined by Western blotting and PGF2α medium content by ELISA. LPS alone increased CBR1 protein abundance and PGF2α release by epithelial cells in reference to the control value. NA alone exerted a stimulatory effect on PGFS and CBR1 protein abundances and PGF2α secretion. After the exposure of cells to LPS with NA together, CBR1 protein abundance, as well as PGF2α release, was higher than in response to LPS and NA alone. PGFS protein abundance was increased by LPS with NA together compared to LPS action alone. In LPS-exposed endometrial epithelial cells, NA acting by β2- and β3-ARs leads to a rise in CBR1 protein abundance and PGF2α secretion. β2-ARs also participate in the NA excitatory effect on PGFS protein abundance. The NA effect on all the parameters tested is not mediated by α1- and α2-ARs. β2- and β3-ARs mediate the stimulatory effect of NA on PGF2α generation and secretion by the LPS-exposed pig endometrial epithelial cells. The results suggest that these cells may be a significant source of PGF2α under noradrenergic stimulation in the inflamed endometrium, and NA affects processes controlled by PGF2α during endometritis in an indirect manner.