Enhanced expression of the Epithelial Sodium Channel in neutrophils from hypertensive patients

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Abstract

© 2018 Elsevier B.V. Hypertension (HTN), i.e. abnormally high blood pressure, is a major risk factor for heart attack, stroke, and kidney failure. The Epithelial Sodium Channel (ENaC), one of the main transporters regulates blood pressure by tightly controlling the sodium reabsorption along the nephron. Recently, we have shown an α-ENaC overexpression in platelets from hypertensive patients compared to platelets from normotensive subjects, suggesting it makes a contribution to the activation state of platelets and the physiopathology of hypertension. However, the involvement of the α-ENaC localized in neutrophils to this disease remains unknown. Neutrophils are the first leukocytes to be recruited to an inflammatory site and are equipped with a strong ability to eliminate intra- or extracellular pathogens using reactive oxygen species or antibacterial proteins contained in their granules. Using the Western blotting (Wb), flow cytometry, and qRT-PCR approaches; we determined α-ENaC neutrophil overexpression at the protein and messenger RNA (mRNA) levels. By confocal and cytometry analysis, we determined the α-ENaC distribution and the heterogeneity of HTN neutrophils population, respectively. Immunoprecipitation and Wb assays demonstrated the presence of both α-ENaC and caveolin-1 phosphorylated forms, compared with neutrophils from healthy individuals. Although neutrophils from hypertensive subjects circulating in an activated state were exhibiting important oxidative stress and modifications registered by confocal, atomic force, and scanning electron microscope, they conserved their defense capabilities. The features described above for neutrophils from hypertensive patients could be attributed to α-ENaC overexpression, as its drug inhibition diminished their activation state modulating the actin cytoskeleton reorganization triggered during the activation process.
Original languageAmerican English
Pages (from-to)387-402
Number of pages346
JournalBiochimica et Biophysica Acta - Biomembranes
DOIs
StatePublished - 1 Feb 2019

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Epithelial Sodium Channels
Platelets
Neutrophils
Chemical activation
Blood pressure
Caveolin 1
Oxidative stress
Flow cytometry
Hypertension
Pathogens
Actins
Assays
Reactive Oxygen Species
Proteins
Electron microscopes
Sodium
Blood Platelets
Scanning
Western Blotting
Messenger RNA

Cite this

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title = "Enhanced expression of the Epithelial Sodium Channel in neutrophils from hypertensive patients",
abstract = "{\circledC} 2018 Elsevier B.V. Hypertension (HTN), i.e. abnormally high blood pressure, is a major risk factor for heart attack, stroke, and kidney failure. The Epithelial Sodium Channel (ENaC), one of the main transporters regulates blood pressure by tightly controlling the sodium reabsorption along the nephron. Recently, we have shown an α-ENaC overexpression in platelets from hypertensive patients compared to platelets from normotensive subjects, suggesting it makes a contribution to the activation state of platelets and the physiopathology of hypertension. However, the involvement of the α-ENaC localized in neutrophils to this disease remains unknown. Neutrophils are the first leukocytes to be recruited to an inflammatory site and are equipped with a strong ability to eliminate intra- or extracellular pathogens using reactive oxygen species or antibacterial proteins contained in their granules. Using the Western blotting (Wb), flow cytometry, and qRT-PCR approaches; we determined α-ENaC neutrophil overexpression at the protein and messenger RNA (mRNA) levels. By confocal and cytometry analysis, we determined the α-ENaC distribution and the heterogeneity of HTN neutrophils population, respectively. Immunoprecipitation and Wb assays demonstrated the presence of both α-ENaC and caveolin-1 phosphorylated forms, compared with neutrophils from healthy individuals. Although neutrophils from hypertensive subjects circulating in an activated state were exhibiting important oxidative stress and modifications registered by confocal, atomic force, and scanning electron microscope, they conserved their defense capabilities. The features described above for neutrophils from hypertensive patients could be attributed to α-ENaC overexpression, as its drug inhibition diminished their activation state modulating the actin cytoskeleton reorganization triggered during the activation process.",
author = "Erika Reus-Chavarr{\'i}a and Ivette Mart{\'i}nez-Vieyra and Cristina Salinas-Nolasco and Ch{\'a}vez-Pi{\~n}a, {Araceli Evangelina} and M{\'e}ndez-M{\'e}ndez, {Juan Vicente} and L{\'o}pez-Villegas, {Edgar Oliver} and Alejandro Sosa-Peinado and Doris Cerecedo",
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month = "2",
day = "1",
doi = "10.1016/j.bbamem.2018.11.003",
language = "American English",
pages = "387--402",
journal = "Biochimica et Biophysica Acta - Biomembranes",
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Enhanced expression of the Epithelial Sodium Channel in neutrophils from hypertensive patients. / Reus-Chavarría, Erika; Martínez-Vieyra, Ivette; Salinas-Nolasco, Cristina; Chávez-Piña, Araceli Evangelina; Méndez-Méndez, Juan Vicente; López-Villegas, Edgar Oliver; Sosa-Peinado, Alejandro; Cerecedo, Doris.

In: Biochimica et Biophysica Acta - Biomembranes, 01.02.2019, p. 387-402.

Research output: Contribution to journalArticleResearchpeer-review

TY - JOUR

T1 - Enhanced expression of the Epithelial Sodium Channel in neutrophils from hypertensive patients

AU - Reus-Chavarría, Erika

AU - Martínez-Vieyra, Ivette

AU - Salinas-Nolasco, Cristina

AU - Chávez-Piña, Araceli Evangelina

AU - Méndez-Méndez, Juan Vicente

AU - López-Villegas, Edgar Oliver

AU - Sosa-Peinado, Alejandro

AU - Cerecedo, Doris

PY - 2019/2/1

Y1 - 2019/2/1

N2 - © 2018 Elsevier B.V. Hypertension (HTN), i.e. abnormally high blood pressure, is a major risk factor for heart attack, stroke, and kidney failure. The Epithelial Sodium Channel (ENaC), one of the main transporters regulates blood pressure by tightly controlling the sodium reabsorption along the nephron. Recently, we have shown an α-ENaC overexpression in platelets from hypertensive patients compared to platelets from normotensive subjects, suggesting it makes a contribution to the activation state of platelets and the physiopathology of hypertension. However, the involvement of the α-ENaC localized in neutrophils to this disease remains unknown. Neutrophils are the first leukocytes to be recruited to an inflammatory site and are equipped with a strong ability to eliminate intra- or extracellular pathogens using reactive oxygen species or antibacterial proteins contained in their granules. Using the Western blotting (Wb), flow cytometry, and qRT-PCR approaches; we determined α-ENaC neutrophil overexpression at the protein and messenger RNA (mRNA) levels. By confocal and cytometry analysis, we determined the α-ENaC distribution and the heterogeneity of HTN neutrophils population, respectively. Immunoprecipitation and Wb assays demonstrated the presence of both α-ENaC and caveolin-1 phosphorylated forms, compared with neutrophils from healthy individuals. Although neutrophils from hypertensive subjects circulating in an activated state were exhibiting important oxidative stress and modifications registered by confocal, atomic force, and scanning electron microscope, they conserved their defense capabilities. The features described above for neutrophils from hypertensive patients could be attributed to α-ENaC overexpression, as its drug inhibition diminished their activation state modulating the actin cytoskeleton reorganization triggered during the activation process.

AB - © 2018 Elsevier B.V. Hypertension (HTN), i.e. abnormally high blood pressure, is a major risk factor for heart attack, stroke, and kidney failure. The Epithelial Sodium Channel (ENaC), one of the main transporters regulates blood pressure by tightly controlling the sodium reabsorption along the nephron. Recently, we have shown an α-ENaC overexpression in platelets from hypertensive patients compared to platelets from normotensive subjects, suggesting it makes a contribution to the activation state of platelets and the physiopathology of hypertension. However, the involvement of the α-ENaC localized in neutrophils to this disease remains unknown. Neutrophils are the first leukocytes to be recruited to an inflammatory site and are equipped with a strong ability to eliminate intra- or extracellular pathogens using reactive oxygen species or antibacterial proteins contained in their granules. Using the Western blotting (Wb), flow cytometry, and qRT-PCR approaches; we determined α-ENaC neutrophil overexpression at the protein and messenger RNA (mRNA) levels. By confocal and cytometry analysis, we determined the α-ENaC distribution and the heterogeneity of HTN neutrophils population, respectively. Immunoprecipitation and Wb assays demonstrated the presence of both α-ENaC and caveolin-1 phosphorylated forms, compared with neutrophils from healthy individuals. Although neutrophils from hypertensive subjects circulating in an activated state were exhibiting important oxidative stress and modifications registered by confocal, atomic force, and scanning electron microscope, they conserved their defense capabilities. The features described above for neutrophils from hypertensive patients could be attributed to α-ENaC overexpression, as its drug inhibition diminished their activation state modulating the actin cytoskeleton reorganization triggered during the activation process.

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