Evidence for post-transcriptional regulation of Na,K-ATPase by prostaglandin E1

Abstract

The stimulatory effect of PGE 1 on the activity of the Na, K-ATPase in MDCK cells is associated with an increase in the rate of transcription of the Na, K-ATPase β1 subunit gene, and an increase in the rate of biosynthesis of the Na, K-ATPase [1]. In order to further define the molecular mechanisms, transient transfection and biosynthesis studies were conducted with Dibutyryl cAMP resistant (DB r ) MDCK cells, defective in cAMP dependent protein kinase, and PGE 1 Independent (PGE 1 Ind) MDCK cells with elevated intracellular cAMP. Transient transfection studies with the human Na, K-ATPase β1 promoter/luciferase construct, pHβ1-1141 Luc [2], showed that the stimulatory effect of PGE 1 and 8Br-cAMP on β1 subunit gene transcription is retained in the DB r and PGE 1 independent variants. However, the stimulatory effect of PGE 1 and 8Br-cAMP on Na, K-ATPase biosynthesis was lost in DB r (unlike PGE 1 Ind) variants. These results can be explained by a defect in posttranscriptional regulation.

Effect of prostaglandin E1 (PGE1) and sildenafil on serotonin metabolism and some oxidative damage markers in rat prostate gland and brain

“…This latter effect agrees with the studies conducted by Borsick & Taub (2006) who suggest that PGE1 exerts a stimulatory effect in the velocity of transcription and augments the velocity of synthesis of this enzyme. Oliw et al (1988) suggested a mechanism in which PGE1 stored in seminal vesicles is metabolised to 19-hidroxi-PGE1 (which is the main prostaglandin in humans and other primates), in the presence of NADPH.…”