ArticleAmerican journal of physiology. Renal physiology2010
Regulation of renal proximal tubule Na-K-ATPase by prostaglandins.
Article in American journal of physiology. Renal physiology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 32 citations in OpenAlex.
- Na/K-ATPase in the renal proximal tubule cell: classic & novel roles in sodium handling.Frontiers in physiology · 2026Review
- Identified and potential internalization signals involved in trafficking and regulation of NaMolecular and cellular biochemistry · 2024Review
- Inherited Fanconi syndrome.World journal of pediatrics : WJP · 2023Review
- PPAR-α knockout leads to elevated blood pressure response to angiotensin II infusion associated with an increase in renal α-1 NaLife sciences · 2022Article
- Renal oncometabolite L-2-hydroxyglutarate imposes a block in kidney tubulogenesis: Evidence for an epigenetic basis for the L-2HG-induced impairment of differentiation.Frontiers in endocrinology · 2022Article
- Salt Inducible Kinase Signaling Networks: Implications for Acute Kidney Injury and Therapeutic Potential.International journal of molecular sciences · 2019Review
- Gene Level Regulation of Na,K-ATPase in the Renal Proximal Tubule Is Controlled by Two Independent but Interacting Regulatory Mechanisms Involving Salt Inducible Kinase 1 and CREB-Regulated Transcriptional Coactivators.International journal of molecular sciences · 2018Review
- Data on Na,K-ATPase in primary cultures of renal proximal tubule cells treated with catecholamines.Data in brief · 2016Article
- Group V Secretory Phospholipase A2 Is Involved in Tubular Integrity and Sodium Handling in the Kidney.PloS one · 2016Article
- Renal proximal tubule Na,K-ATPase is controlled by CREB-regulated transcriptional coactivators as well as salt-inducible kinase 1.Cellular signalling · 2015Article
- Identification of a VxP Targeting Signal in the Flagellar Na+ /K+ -ATPase.Traffic (Copenhagen, Denmark) · 2015Article
- Prostaglandin E2 increases proximal tubule fluid reabsorption, and modulates cultured proximal tubule cell responses via EP1 and EP4 receptors.Laboratory investigation; a journal of technical methods and pathology · 2015Article
- Transcriptional regulators of Na,K-ATPase subunits.Frontiers in cell and developmental biology · 2015Review
- Antagonism of the prostaglandin E2 EP1 receptor in MDCK cells increases growth through activation of Akt and the epidermal growth factor receptor.American journal of physiology. Renal physiology · 2014Article
- Atrial natriuretic peptide and renal dopaminergic system: a positive friendly relationship?BioMed research international · 2014Review
- MicroRNAs contribute to the maintenance of cell-type-specific physiological characteristics: miR-192 targets Na+/K+-ATPase β1.Nucleic acids research · 2013Article
- Targeting of renal proximal tubule Na,K-ATPase by salt-inducible kinase.Biochemical and biophysical research communications · 2010Review
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Prostaglandins (PGs) play a number of roles in the kidney, including regulation of salt and water reabsorption. In this report, evidence was obtained for stimulatory effects of PGs on Na-K-ATPase in primary cultures of rabbit renal proximal tubule (RPT) cells. The results of our real-time PCR studies indicate that in primary RPTs the effects of PGE(2), the major renal PG, are mediated by four classes of PGE (EP) receptors. The role of these EP receptors in the regulation of Na-K-ATPase was examined at the transcriptional level. Na-K-ATPase consists of a catalytic α-subunit encoded by the ATP1A1 gene, as well as a β-subunit encoded by the ATP1B1 gene. Transient transfection studies conducted with pHβ1-1141 Luc, a human ATP1B1 promoter/luciferase construct, indicate that both PGE(1) and PGE(2) are stimulatory. The evidence for the involvement of both the cAMP and Ca(2+) signaling pathways includes the inhibitory effects of the myristolylated PKA inhibitor PKI, the adenylate cyclase (AC) inhibitor SQ22536, and the PKC inhibitors Gö 6976 and Ro-32-0432 on the PGE(1) stimulation. Other effectors that similarly act through cAMP and PKC were also stimulatory to transcription, including norepinephrine and dopamine. In addition to its effects on transcription, a chronic incubation with PGE(1) was observed to result in an increase in Na-K-ATPase mRNA levels as well as an increase in Na-K-ATPase activity. An acute stimulatory effect of PGE(1) on Na-K-ATPase was observed and was associated with an increase in the level of Na-K-ATPase in the basolateral membrane.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.