ArticleAmerican journal of physiology. Renal physiology2009
Biphasic regulation of ENaC by TGF-{alpha} and EGF in renal epithelial cells.
Article in American journal of physiology. Renal physiology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 38 citations in OpenAlex.
- Ribosomal s6 kinase is a mediator of aquaporin-2 S256 phosphorylation and membrane accumulation after EGFR inhibition with erlotinib.American journal of physiology. Renal physiology · 2025Article
- Cystin is required for maintaining fibrocystin (FPC) levels and safeguarding proteome integrity in mouse renal epithelial cells: A mechanistic connection between the kidney defects in cpk mice and human ARPKD.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2023Article
- Epidermal growth factor strongly affects epithelial NaScientific reports · 2021Article
- Role of Epidermal Growth Factor Receptor (EGFR) and Its Ligands in Kidney Inflammation and Damage.Mediators of inflammation · 2018Review
- Involvement of ENaC in the development of salt-sensitive hypertension.American journal of physiology. Renal physiology · 2017Review
- EGF Receptor Inhibition by Erlotinib Increases Aquaporin 2-Mediated Renal Water Reabsorption.Journal of the American Society of Nephrology : JASN · 2016Article
- Prolactin stimulates sodium and chloride ion channels in A6 renal epithelial cells.American journal of physiology. Renal physiology · 2015Article
- Roles of interstitial fluid pH in diabetes mellitus: Glycolysis and mitochondrial function.World journal of diabetes · 2015Review
- Impaired epithelial Na+ channel activity contributes to cystogenesis and development of autosomal recessive polycystic kidney disease in PCK rats.Pediatric research · 2015Article
- H-Ras mediates the inhibitory effect of epidermal growth factor on the epithelial Na+ channel.PloS one · 2015Article
- Role of Rho GDP dissociation inhibitor α in control of epithelial sodium channel (ENaC)-mediated sodium reabsorption.The Journal of biological chemistry · 2014Article
- Aldosterone sensitizes connecting tubule glomerular feedback via the aldosterone receptor GPR30.American journal of physiology. Renal physiology · 2014Article
- Estradiol activates epithelial sodium channels in rat alveolar cells through the G protein-coupled estrogen receptor.American journal of physiology. Lung cellular and molecular physiology · 2013Article
- The inhibitory effect of Gβγ and Gβ isoform specificity on ENaC activity.American journal of physiology. Renal physiology · 2013Article
- Epidermal growth factors in the kidney and relationship to hypertension.American journal of physiology. Renal physiology · 2013Review
- Deficiency of renal cortical EGF increases ENaC activity and contributes to salt-sensitive hypertension.Journal of the American Society of Nephrology : JASN · 2013Article
- ROS production as a common mechanism of ENaC regulation by EGF, insulin, and IGF-1.American journal of physiology. Cell physiology · 2013Article
- Erlotinib preserves renal function and prevents salt retention in doxorubicin treated nephrotic rats.PloS one · 2013Article
- Phosphatidylinositol phosphate-dependent regulation of Xenopus ENaC by MARCKS protein.American journal of physiology. Renal physiology · 2012Article
- Hypotonic stress upregulates β- and γ-ENaC expression through suppression of ERK by inducing MKP-1.American journal of physiology. Renal physiology · 2012Article
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
The epithelial sodium channel (ENaC) is regulated by epidermal growth factor (EGF). We investigate whether ENaC is regulated by another EGF receptor (EGFR) ligand, transforming growth factor-alpha (TGF-alpha). We show that chronic (24 h) treatment with TGF-alpha inhibits ENaC in Xenopus laevis kidney cells 20 times more strongly than EGF. By using single-channel measurements, we show that TGF-alpha significantly reduces the number of ENaC per patch. The open probability (P(o)) is unchanged by 24-h treatment with TGF-alpha. alpha-, beta-, and gamma-ENaC mRNA levels are significantly reduced by TGF-alpha or EGF. TGF-alpha or EGF reduces alpha- and gamma-ENaC proteins in the membrane; however, beta-ENaC is unchanged. TGF-alpha or EGF inhibits ENaC by activating EGFR since the EGFR inhibitor AG1478 blocks the effects of both. The MAPK 1/2 inhibitor U0126 also blocks the effect of TGF-alpha or EGF on ENaC, indicating that the MAPK1/2 pathway is involved in the TGF-alpha- or EGF-induced inhibition of ENaC. Interestingly, acute treatment (<1 h) with TGF-alpha or EGF does not inhibit ENaC current; it enhances ENaC activity by increasing P(o). Pretreatment of the cells with U0126 potentiates the acute TGF-alpha- or EGF-induced stimulation of ENaC. This TGF-alpha- or EGF-induced increase in sodium current is abolished by a phosphatidylinositol 3-kinase (PI-3 kinase) inhibitor, LY294002, suggesting that PI-3 kinase is involved in the activation of sodium transport. In conclusion, chronic treatment with TGF-alpha or EGF inhibits ENaC by decreasing the number of channels in the membrane transcriptionally through MAPK1/2 pathways, but acute treatment with TGF-alpha or EGF activates ENaC by increasing P(o) via PI-3 kinase.
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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.