Abstract
Endometritis frequently causes reproductive disruptions and economic losses in animals. Noradrenergic regulation of prostaglandin (PG)E2 generation in the endometrium under inflammatory conditions is not fully recognized. This study analyzed the significance of α1-, α2- and β-adrenoreceptors (ARs) in noradrenaline (NA)-influenced PG-endoperoxidase synthase-2 (PTGS-2), microsomal PTGE synthase-1 (mPTGES-1) and mPTGES-2 protein abundances, and PGE2 release by porcine Escherichia coli lipopolysaccharide (LPS)-treated endometrial epithelial cells.
Material and Methods
The cells were treated with 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, LPS with antagonists of β1-, β2- and β3-ARs in combinations with agonists of β1-, β2- and β3-ARs for 24 h. Enzyme abundances in cells were estimated by Western blotting, and the PGE2 concentration in a medium was determined by ELISA.
Results
In the studied cells, compared to the control value, LPS alone augmented PTGS-2 and mPTGES-1 protein abundances, while NA alone increased mPTGES-2 protein abundance. PGE2 release was enhanced by LPS and NA alone. In LPS-treated cells, PTGS-2 and mPTGES-1 protein abundances and PGE2 release in response to NA were higher than after using LPS and NA alone. In these cells, β(2, 3)-ARs are activated by NA to increase PTGS-2 and mPTGES-1 protein abundances and PGE2 secretion, and β1-ARs also contribute to a rise in mPTGES-1 protein abundance and PGE2 secretion. The NA stimulating effect on mPTGES-2 protein abundance takes place through β2-ARs. Adrenoreceptors α(1, 2) did not mediate the NA effect on the studied parameters.
Conclusion
In LPS-exposed endometrial epithelial cells, NA through β-ARs stimulates PGE2 formation and release. Results suggest the indirect influence of NA on processes modulated by PGE2 in the endometrium under inflammatory conditions.