ArticleBiochimica et biophysica acta2009
Epidermal growth factor activates Na(+/)H(+) exchanger in podocytes through a mechanism that involves Janus kinase and calmodulin.
Article in Biochimica et biophysica acta, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 48 citations in OpenAlex.
- ATP-mediated increase in HJournal of neurophysiology · 2024Article
- The SH2 domain and kinase activity of JAK2 target JAK2 to centrosome and regulate cell growth and centrosome amplification.PloS one · 2022Article
- Dynamic NaeLife · 2021Article
- Myocardial Impact of NHE1 Regulation by Sildenafil.Frontiers in cardiovascular medicine · 2021Review
- The NaThe Journal of physiology · 2019Article
- The multifunctional role of phospho-calmodulin in pathophysiological processes.The Biochemical journal · 2018Review
- Angiotensin II-induced podocyte apoptosis is mediated by endoplasmic reticulum stress/PKC-δ/p38 MAPK pathway activation and trough increased NaBMC nephrology · 2018Article
- Lysosome trafficking is necessary for EGF-driven invasion and is regulated by p38 MAPK and Na+/H+ exchangers.BMC cancer · 2017Article
- Absence of miR-146a in Podocytes Increases Risk of Diabetic Glomerulopathy via Up-regulation of ErbB4 and Notch-1.The Journal of biological chemistry · 2017Article
- EGF receptor deletion in podocytes attenuates diabetic nephropathy.Journal of the American Society of Nephrology : JASN · 2015Article
- Epidermal growth factor-induced proliferation of collecting duct cells from Oak Ridge polycystic kidney mice involves activation of Na+/H+ exchanger.American journal of physiology. Cell physiology · 2014Article
- Na+/H+ exchanger-1 reduces podocyte injury caused by endoplasmic reticulum stress via autophagy activation.Laboratory investigation; a journal of technical methods and pathology · 2014Article
- Down-regulation of the epithelial Na⁺ channel ENaC by Janus kinase 2.The Journal of membrane biology · 2014Article
- Signal transduction in podocytes--spotlight on receptor tyrosine kinases.Nature reviews. Nephrology · 2014Review
- Epidermal growth factor receptor inhibition with erlotinib partially prevents cisplatin-induced nephrotoxicity in rats.PloS one · 2014Article
- In scarcity and abundance: metabolic signals regulating cell growth.Physiology (Bethesda, Md.) · 2013Review
- Cucurbitacin I inhibits Rac1 activation in breast cancer cells by a reactive oxygen species-mediated mechanism and independently of Janus tyrosine kinase 2 and P-Rex1.Molecular pharmacology · 2013Article
- Roles of Na⁺/H⁺ exchanger type 1 and intracellular pH in angiotensin II-induced reactive oxygen species generation and podocyte apoptosis.Journal of pharmacological sciences · 2013Article
- Downregulation of the creatine transporter SLC6A8 by JAK2.The Journal of membrane biology · 2012Article
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Sodium-proton exchanger type 1 (NHE-1) is ubiquitously expressed, is activated by numerous growth factors, and plays significant roles in regulating intracellular pH and cellular volume, proliferation and cytoskeleton. Despite its importance, little is known about its regulation in renal glomerular podocytes. In the current work, we studied the regulation of NHE-1 activity by the epidermal growth factor receptor (EGFR) in cultured podocytes. RT-PCR demonstrated mRNAs for NHE-1 and NHE-2 in differentiated podocytes, as well as for EGFR subunits EGFR/ErbB1, Erb3, and ErbB4. EGF induced concentration-dependent increases in proton efflux in renal podocytes as assessed using a Cytosensor microphysiometer, were diminished in the presence of 5-(N-methyl-N-isobutyl) amiloride or in a sodium-free solution. Furthermore, pharmacological inhibitors of Janus kinase (Jak2) and calmodulin (CaM) attenuated EGF-induced NHE-1 activity. Co-immunoprecipitation studies determined that EGF induced formation of complexes between Jak2 and CaM, as well as between CaM and NHE-1. In addition, EGF increased levels of tyrosine phosphorylation of Jak2 and CaM. The EGFR kinase inhibitor, AG1478, blocked activation of NHE-1, but did not block EGF-induced phosphorylation of Jak2 or CaM. These results suggest that EGF induces NHE-1 activity in podocytes through two pathways: (1) EGF-->EGFR-->Jak2 activation (independent of EGFR tyrosine kinase activity)-->tyrosine phosphorylation of CaM-->CaM binding to NHE-1-->conformational change of NHE-1-->activation of NHE-1; and (2) EGF-->EGFR-->EGFR kinase activation-->association of CaM with NHE-1 (independent of Jak2)-->conformational change of NHE-1-->activation of NHE-1.
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