Increased SGK1 activity potentiates mineralocorticoid/NaCl-induced kidney injury
Serum and glucocorticoid-regulated kinase 1 (SGK1) stimulates aldosterone-dependent renal Na reabsorption and modulates blood pressure. In addition, genetic ablation or pharmacological inhibition of SGK1 limits the development of kidney inflammation and fibrosis in response to excess mineralocortico...
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Published in | American journal of physiology. Renal physiology Vol. 320; no. 4; pp. F628 - F643 |
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Main Authors | , , , , , , , , , , |
Format | Journal Article |
Language | English |
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American Physiological Society
01.04.2021
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Abstract | Serum and glucocorticoid-regulated kinase 1 (SGK1) stimulates aldosterone-dependent renal Na
reabsorption and modulates blood pressure. In addition, genetic ablation or pharmacological inhibition of SGK1 limits the development of kidney inflammation and fibrosis in response to excess mineralocorticoid signaling. In this work, we tested the hypothesis that a systemic increase in SGK1 activity would potentiate mineralocorticoid/salt-induced hypertension and kidney injury. To that end, we used a transgenic mouse model with increased SGK1 activity. Mineralocorticoid/salt-induced hypertension and kidney damage was induced by unilateral nephrectomy and treatment with deoxycorticosterone acetate and NaCl in the drinking water for 6 wk. Our results show that although SGK1 activation did not induce significantly higher blood pressure, it produced a mild increase in glomerular filtration rate, increased albuminuria, and exacerbated glomerular hypertrophy and fibrosis. Transcriptomic analysis showed that extracellular matrix- and immune response-related terms were enriched in the downregulated and upregulated genes, respectively, in transgenic mice. In conclusion, we propose that systemically increased SGK1 activity is a risk factor for the development of mineralocorticoid-dependent kidney injury in the context of low renal mass and independently of blood pressure.
Increased activity of the protein kinase serum and glucocorticoid-regulated kinase 1 may be a risk factor for accelerated renal damage. Serum and glucocorticoid-regulated kinase 1 expression could be a marker for the rapid progression toward chronic kidney disease and a potential therapeutic target to slow down the process. |
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AbstractList | Increased activity of protein kinase SGK1 may be a risk factor for accelerated renal damage. SGK1 expression could be a marker for rapid progression toward CKD and a potential therapeutic target to slow down the process.
Serum and glucocorticoid-regulated kinase 1 (SGK1) stimulates aldosterone-dependent renal Na
+
reabsorption and modulates blood pressure. In addition, genetic ablation or pharmacological inhibition of SGK1 limits the development of kidney inflammation and fibrosis in response to excess mineralocorticoid signaling. In this work, we tested the hypothesis that a systemic increase in SGK1 activity would potentiate mineralocorticoid/salt-induced hypertension and kidney injury. To that end, we used a transgenic mouse model with increased SGK1 activity. Mineralocorticoid/salt-induced hypertension and kidney damage was induced by unilateral nephrectomy and treatment with deoxycorticosterone acetate and NaCl in the drinking water for 6 wk. Our results show that although SGK1 activation did not induce significantly higher blood pressure, it produced a mild increase in glomerular filtration rate, increased albuminuria, and exacerbated glomerular hypertrophy and fibrosis. Transcriptomic analysis showed that extracellular matrix- and immune response-related terms were enriched in the downregulated and upregulated genes, respectively, in transgenic mice. In conclusion, we propose that systemically increased SGK1 activity is a risk factor for the development of mineralocorticoid-dependent kidney injury in the context of low renal mass and independently of blood pressure.
NEW & NOTEWORTHY Increased activity of the protein kinase serum and glucocorticoid-regulated kinase 1 may be a risk factor for accelerated renal damage. Serum and glucocorticoid-regulated kinase 1 expression could be a marker for the rapid progression toward chronic kidney disease and a potential therapeutic target to slow down the process. Serum and glucocorticoid-regulated kinase 1 (SGK1) stimulates aldosterone-dependent renal Na reabsorption and modulates blood pressure. In addition, genetic ablation or pharmacological inhibition of SGK1 limits the development of kidney inflammation and fibrosis in response to excess mineralocorticoid signaling. In this work, we tested the hypothesis that a systemic increase in SGK1 activity would potentiate mineralocorticoid/salt-induced hypertension and kidney injury. To that end, we used a transgenic mouse model with increased SGK1 activity. Mineralocorticoid/salt-induced hypertension and kidney damage was induced by unilateral nephrectomy and treatment with deoxycorticosterone acetate and NaCl in the drinking water for 6 wk. Our results show that although SGK1 activation did not induce significantly higher blood pressure, it produced a mild increase in glomerular filtration rate, increased albuminuria, and exacerbated glomerular hypertrophy and fibrosis. Transcriptomic analysis showed that extracellular matrix- and immune response-related terms were enriched in the downregulated and upregulated genes, respectively, in transgenic mice. In conclusion, we propose that systemically increased SGK1 activity is a risk factor for the development of mineralocorticoid-dependent kidney injury in the context of low renal mass and independently of blood pressure. Increased activity of the protein kinase serum and glucocorticoid-regulated kinase 1 may be a risk factor for accelerated renal damage. Serum and glucocorticoid-regulated kinase 1 expression could be a marker for the rapid progression toward chronic kidney disease and a potential therapeutic target to slow down the process. Serum and glucocorticoid-regulated kinase 1 (SGK1) stimulates aldosterone-dependent renal Na+ reabsorption and modulates blood pressure. In addition, genetic ablation or pharmacological inhibition of SGK1 limits the development of kidney inflammation and fibrosis in response to excess mineralocorticoid signaling. In this work, we tested the hypothesis that a systemic increase in SGK1 activity would potentiate mineralocorticoid/salt-induced hypertension and kidney injury. To that end, we used a transgenic mouse model with increased SGK1 activity. Mineralocorticoid/salt-induced hypertension and kidney damage was induced by unilateral nephrectomy and treatment with deoxycorticosterone acetate and NaCl in the drinking water for 6 wk. Our results show that although SGK1 activation did not induce significantly higher blood pressure, it produced a mild increase in glomerular filtration rate, increased albuminuria, and exacerbated glomerular hypertrophy and fibrosis. Transcriptomic analysis showed that extracellular matrix- and immune response-related terms were enriched in the downregulated and upregulated genes, respectively, in transgenic mice. In conclusion, we propose that systemically increased SGK1 activity is a risk factor for the development of mineralocorticoid-dependent kidney injury in the context of low renal mass and independently of blood pressure. |
Author | Velazquez-Garcia, Silvia Hernández, Guadalberto Alvarez de la Rosa, Diego Konu, Ozlen Vastola-Mascolo, Arianna Keskus, Ayse G Navarro-González, Juan F Rodríguez-Rodríguez, Ana E Porrini, Esteban Luis-Lima, Sergio Sierra-Ramos, Catalina |
Author_xml | – sequence: 1 givenname: Catalina surname: Sierra-Ramos fullname: Sierra-Ramos, Catalina organization: Departamento de Ciencias Médicas Básicas, Universidad de La Laguna, La Laguna, Tenerife, Spain – sequence: 2 givenname: Silvia surname: Velazquez-Garcia fullname: Velazquez-Garcia, Silvia organization: Instituto de Tecnologías Biomédicas, Universidad de La Laguna, La Laguna, Tenerife, Spain – sequence: 3 givenname: Ayse G surname: Keskus fullname: Keskus, Ayse G organization: Interdisciplinary Neuroscience Program, Bilkent University, Ankara, Turkey – sequence: 4 givenname: Arianna surname: Vastola-Mascolo fullname: Vastola-Mascolo, Arianna organization: Departamento de Ciencias Médicas Básicas, Universidad de La Laguna, La Laguna, Tenerife, Spain – sequence: 5 givenname: Ana E orcidid: 0000-0002-0803-864X surname: Rodríguez-Rodríguez fullname: Rodríguez-Rodríguez, Ana E organization: Departamento de Medicina Interna, Universidad de La Laguna, La Laguna, Tenerife, Spain – sequence: 6 givenname: Sergio surname: Luis-Lima fullname: Luis-Lima, Sergio organization: Departamento de Medicina Interna, Universidad de La Laguna, La Laguna, Tenerife, Spain – sequence: 7 givenname: Guadalberto surname: Hernández fullname: Hernández, Guadalberto organization: Instituto de Tecnologías Biomédicas, Universidad de La Laguna, La Laguna, Tenerife, Spain – sequence: 8 givenname: Juan F surname: Navarro-González fullname: Navarro-González, Juan F organization: Unidad de Investigación y Servicio de Nefrología, Hospital Universitario Nuestra Señora de Candelaria, Santa Cruz de Tenerife, Spain – sequence: 9 givenname: Esteban surname: Porrini fullname: Porrini, Esteban organization: Departamento de Medicina Interna, Universidad de La Laguna, La Laguna, Tenerife, Spain – sequence: 10 givenname: Ozlen surname: Konu fullname: Konu, Ozlen organization: UNAM-Institute of Materials Science and Nanotechnology, Ankara, Turkey – sequence: 11 givenname: Diego surname: Alvarez de la Rosa fullname: Alvarez de la Rosa, Diego organization: Instituto de Tecnologías Biomédicas, Universidad de La Laguna, La Laguna, Tenerife, Spain |
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Keywords | chronic kidney disease fibrosis mineralocorticoid receptor serum and glucocorticoid-regulated kinase 1 aldosterone |
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Snippet | Serum and glucocorticoid-regulated kinase 1 (SGK1) stimulates aldosterone-dependent renal Na
reabsorption and modulates blood pressure. In addition, genetic... Increased activity of protein kinase SGK1 may be a risk factor for accelerated renal damage. SGK1 expression could be a marker for rapid progression toward CKD... Serum and glucocorticoid-regulated kinase 1 (SGK1) stimulates aldosterone-dependent renal Na+ reabsorption and modulates blood pressure. In addition, genetic... |
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SubjectTerms | Acetic acid Acute Kidney Injury - chemically induced Acute Kidney Injury - metabolism Aldosterone Animals Blood pressure Blood Pressure - drug effects Drinking water Extracellular matrix Fibrosis Fibrosis - metabolism Fibrosis - pathology Glomerular filtration rate Glucocorticoids Hypertension Hypertrophy Immediate-Early Proteins - genetics Immune response Kidneys Mice Mineralocorticoids - pharmacology Nephrectomy Protein-Serine-Threonine Kinases - metabolism Reabsorption Risk factors Signal Transduction - drug effects Sodium chloride Sodium Chloride - metabolism Sodium Chloride - pharmacology Sodium Chloride, Dietary - pharmacology Transgenic mice |
Title | Increased SGK1 activity potentiates mineralocorticoid/NaCl-induced kidney injury |
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