ArticleAmerican journal of physiology. Renal physiology2008
Regulation of epithelial sodium transport by promyelocytic leukemia zinc finger protein.
Article in American journal of physiology. Renal physiology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 27 citations in OpenAlex.
- The glucocorticoid receptor is affected by its target ZBTB16 in a dissociated manner.The Journal of endocrinology · 2025Article
- Establishment of Murine Pregnancy Requires the Promyelocytic Leukemia Zinc Finger Transcription Factor.International journal of molecular sciences · 2024Article
- Enhanced ZBTB16 Levels by Progestin-Only Contraceptives Induces Decidualization and Inflammation.International journal of molecular sciences · 2023Article
- Aldosterone: Renal Action and Physiological Effects.Comprehensive Physiology · 2023Article
- Bioinformatics Analysis of ZBTB16 as a Prognostic Marker for Ewing's Sarcoma.BioMed research international · 2021Article
- The Promyelocytic Leukemia Zinc Finger Transcription Factor Is Critical for Human Endometrial Stromal Cell Decidualization.PLoS genetics · 2016Article
- Peroxisome Proliferator-Activated Receptor α Protects Renal Tubular Cells from Gentamicin-Induced Apoptosis via Upregulating NaMolecular medicine (Cambridge, Mass.) · 2016Article
- A corticosteroid-responsive transcription factor, promyelocytic leukemia zinc finger protein, mediates protection of the cochlea from acoustic trauma.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2011Article
- Regulation of sodium transport by ENaC in the kidney.Current opinion in nephrology and hypertension · 2010Review
- Targeting SGK1 in diabetes.Expert opinion on therapeutic targets · 2009Review
- The physiological impact of the serum and glucocorticoid-inducible kinase SGK1.Current opinion in nephrology and hypertension · 2009Review
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Aldosterone is the principal regulator of Na homeostasis, and thereby blood pressure. One of the main targets of aldosterone is the epithelial Na channel (ENaC) located in the apical membrane of target cells. Previous studies identified several genes involved in the regulation of ENaC such as SGK1; however, SGK1 knockout mice have only a mild salt-losing phenotype, indicating that further genes must be involved in the action of aldosterone. In our search for further aldosterone-regulated genes, we discovered that aldosterone, at physiological concentrations, induces the expression of the promyelocytic leukemia zinc finger protein (PLZF) in renal cortical collecting duct (CCD) cell lines that stably express mineralocorticoid receptors (MRs). This effect is rapid and does not require de novo protein synthesis, suggesting a direct action. Surprisingly, stable overexpression of human or mouse PLZF isoforms significantly decreased transepithelial Na transport in CCD cells while having no effect on the integrity of the monolayers. In parallel with the decline in Na transport, PLZF suppressed the mRNA levels of beta- and gamma-ENaC subunits. These observations suggest that PLZF is a negative regulator of ENaC in renal epithelial cells and might be part of a negative feedback loop that limits aldosterone's stimulatory effects on sodium reabsorption.
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Registered trials
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.