Regulation of the Na,K-ATPase in MDCK cells by prostaglandin E1: a role for calcium as well as cAMP

Taub, Mary; Borsick, Maryanne; Geisel, Janet; Matlhagela, Keikantse; Rajkhowa, Trivikram; Allen, Cheryl

doi:10.1016/j.yexcr.2004.04.046

Cited by 19 publications

(59 citation statements)

References 41 publications

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“…In contrast, in DB r 3 cells only PGE 1 , PGE 2 and 16,16 dimethyl PGE 2 showed responses of this magnitude. The spectrum of prostaglandin responsiveness observed with DB r 3 cells at 100 ng/ml prostaglandin resembled the responsiveness previously observed with normal MDCK cells at a lower prostaglandin concentration (25 ng/ml) [24]. Thus these results are consistent with the hypothesis that DB r 3 cells have a higher K D values for prostaglandins.…”

Section: Effect Of Prostaglandins and 8br-camp On Transcriptionsupporting

confidence: 88%

“…Previously, we showed that the stimulatory effect of PGE 1 and 8Br-cAMP on Na, K-ATPase β1 subunit gene transcription is associated with an increase in the rate of biosynthesis of the Na, K-ATPase in MDCK cells [26], which is presumably responsible for the increased Na, KATPase activity observed under these conditions. Possibly, PGE 1 and 8Br-cAMP have similar affects on Na, K-ATPase biosynthesis in PGE 1 Ind Cl I, and DB r 3 cells.…”

Section: Effect Of Pge 1 and 8br-camp On The Biosynthesis Of The Na mentioning

confidence: 91%

“…Previously, we presented evidence indicating that PGE 1 stimulates β1 subunit gene transcription through its interaction with 2 different classes of prostaglandin receptors, including Gq coupled EP1 receptors, which activate Phospholipase C, and Gs coupled EP2 receptors which activate adenylate cyclase [25,26]. The PGE 2 analog 16,16-dimethyl-PGE 2 has a 10 fold higher affinity for EP1 than EP2 receptors [27], and thus may only activate EP2 receptors in normal MDCK cells at high prostaglandin concentrations.…”

Section: Effect Of Prostaglandins and 8br-camp On Transcriptionmentioning

confidence: 99%

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

Borsick

Rajkhowa

Taub

2006

Biochemical and Biophysical Research Communications

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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.

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Section: Effect Of Prostaglandins and 8br-camp On Transcriptionsupporting

confidence: 88%

Section: Effect Of Pge 1 and 8br-camp On The Biosynthesis Of The Na mentioning

confidence: 91%

Section: Effect Of Prostaglandins and 8br-camp On Transcriptionmentioning

confidence: 99%

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

Borsick

Rajkhowa

Taub

2006

Biochemical and Biophysical Research Communications

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“…Previously, we reported that PGE 1 , and 8-Bromocyclic AMP (8Br-cAMP) cause an increase in the Na,K-ATPase activity of MDCK cells [19], which was associated with an increase in the level of the Na,K-ATPase in this cell type [4]. The Na,K-ATPase is a protein which is composed of an α subunit with catalytic activity, as well as a β subunit, which facilitates the integration of the protein into the plasma membrane [20].…”

Section: Introductionmentioning

confidence: 96%

“…The renal prostaglandins produced in these various locales have a variety of affects on different types of renal cells, acting in both an autocrine and paracrine manner. PGE 2 in particular has profound effects on a number of the transport systems of the renal tubular epithelium [2,4], including the Na + /H + antiport system [5], the Na,K-ATPase [4] and the epithelial Na + channel [6,7]. The mechanisms by which prostaglandins affect transport systems are poorly understood, and the signaling pathways are to a large extent undefined.…”

Section: Introductionmentioning

confidence: 99%

Involvement of EP1 and EP2 receptors in the regulation of the Na,K-ATPase by prostaglandins in MDCK cells

Matlhagela

Taub

2006

Prostaglandins & Other Lipid Mediators

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Prostaglandins are key regulators of ion transport in the kidney. In MDCK cells, which model distal tubule cells, the transcription of the Na,K-ATPase β1 subunit is regulated by PGE 1 and PGE 2 . To identify the EP receptors that mediate transcriptional regulation, transient transfection studies are conducted using the human β1 promoter/luciferase construct, pHβ1-1141 Luc. The involvement of EP1 and EP2 receptors is indicated by studies with the EP1 selective agonist 17-phenyl trinor PGE 2 , and the EP2 selective agonist butaprost (which stimulate), as well as by studies with the antagonists SC-51089 (EP1 specific) and AH 6809 (EP1 and EP2 specific). Consistent with the involvement of Gs coupled EP2 receptors, is that the PGE 1 stimulation is inhibited by the PKAI expression vector (encoding the protein kinase A (PKA) inhibitory protein), as well as by the myristolated PKA inhibitory peptide PKI. In addition to this evidence (for the involvement of EP2 receptors), evidence for the involvement of EP1 receptors in the PGE 1 mediated stimulation of Na,KATPase β subunit gene transcription includes the stimulatory effect of 17-phenyl trinor PGE 2 , as well as the inhibitory effects of SC-51089. Also consistent with the involvement of Gq coupled EP1 receptors, the PGE 1 stimulation is inhibited by the PKCI vector (encoding the PKC inhibitory domain), the PKC inhibitor Go 6976, thapsigargin, as well as the calmodulin antagonists W7 and W13.

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Divergent signaling pathways mediate induction of Na,K-ATPase α1 and β1 subunit gene transcription by low potassium

2006

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Prolonged inhibition of Na,K-ATPase enzymatic activity by exposure of a variety of mammalian cells to low external K+ yields a subsequent adaptive up-regulation of Na,K-ATPase expression. The aim of this study was to examine the intracellular signal transduction system that is responsible for mediating increased Na,K-ATPase subunit gene expression in primary cultures of neonatal rat cardiac myocytes. In this work, we show long-term inhibition of Na,K-ATPase function with 0.6 mM K+ resulted in hypertrophy of cardiac myocytes and augmentation of Na,K-ATPase alpha1 and beta1 subunit gene expression. Transient transfection experiments in neonatal rat cardiac myocytes demonstrated that low K+ induction of alpha1 and beta1 gene transcription was dependent on intracellular Ca2+ and activation of calcineurin. Based on effects of pharmacological inhibitors, protein kinase A (PKA), extracellular signal-regulated kinase 1/2 (ERK1/2) and histone deacetylase were found to be unique downstream components in the low K+ signal transduction pathway leading to increased alpha1 subunit promoter activity. Similarly, low K+-induced beta1 subunit gene transcription was dependent on activation of protein kinase C (PKC), c-Jun-N-terminal kinase (JNK) and p38 mitogen-activated protein kinase (MAPK). These findings indicate that persistent inhibition of Na,K-ATPase activity with low external K+ activates overlapping and Na,K-ATPase subunit gene-specific signaling pathways in cardiac myocytes.

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Regulation of the Na,K-ATPase in MDCK cells by prostaglandin E1: a role for calcium as well as cAMP

Cited by 19 publications

References 41 publications

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

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

Involvement of EP1 and EP2 receptors in the regulation of the Na,K-ATPase by prostaglandins in MDCK cells

Divergent signaling pathways mediate induction of Na,K-ATPase α1 and β1 subunit gene transcription by low potassium

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