The expression of RAC1 and mineralocorticoid pathway-dependent genes are associated with different responses to salt intake

Alejandra Tapia-Castillo, Cristian A. Carvajal, Carmen Campino, Caroline Hill, Fidel Allende, Andrea Vecchiola, Carmen Carrasco, Rodrigo Bancalari, Carolina Valdivia, Carlos Lagos, Alejandro Martinez-Aguayo, Hernan Garcia, Marlene Aglony, Rene F. Baudrand, Alexis M. Kalergis, Luis F. Michea, Claudia A. Riedel, Carlos E. Fardella

Resultado de la investigación: Article

8 Citas (Scopus)

Resumen

Background Rac1 upregulation has been implicated in salt-sensitive hypertension as a modulator of mineralocorticoid receptor (MR) activity. Rac1 could affect the expression of oxidative stress markers, such as hemoxigenase-1 (HO- 1) or nuclear factor-B (NF-κB), and the expression of neutrophil gelatinaseassociated lipocalin (NGAL), a cytokine upregulated upon MR activation. aim We evaluated RAC1 expression in relation of high salt intake and association with MR, NGAL, HO-1, and NF-κB expression, mineralo- and glucocorticoids levels, and inflammatory parameters. subjects and methods We studied 147 adult subjects. A food survey identified the dietary sodium (Na) intake. RAC1 expression was considered high or low according to the value found in normotensive subjects with low salt intake. We determined the gene expression of RAC1, MR, NGAL, HO-1, NF-κB, and 18S, isolated from peripheral leukocytes. We measured aldosterone, cortisol, sodium, potassium excretion, metalloproteinase (MMP9 y MMP2), and C-reactive protein. results We identified 126 subjects with high Na-intake, 18 subjects had high, and 108 low-RAC1 expression. The subjects with high-RAC1 expression showed a significant increase in MR (P = 0.0002), NGAL (P < 0.0001) HO-1 (P = 0.0004), and NF-κB (P < 0.0001) gene expression. We demonstrated an association between RAC1 expression and MR (Rsp 0.64; P < 0.0001), NGAL (Rsp 0.48; P < 0.0001), HO-1 (Rsp 0.53; P < 0.0001), and NF-κB (Rsp0.52; P < 0.0001). We did not identify any association between RAC1 and clinical or biochemical variables. conclusions RAC1 expression was associated with an increase in MR, NGAL, NF-κB, and HO-1 expression, suggesting that RAC1 could be a mediator of cardiovascular damage induced by sodium, and may also useful to identify subjects with different responses to salt intake.

Idioma originalEnglish
Páginas (desde-hasta)722-728
Número de páginas7
PublicaciónAmerican Journal of Hypertension
Volumen28
N.º6
DOI
EstadoPublished - 1 ene 2015

Huella dactilar

Mineralocorticoid Receptors
Mineralocorticoids
Salts
Lipocalins
Neutrophils
Lipocalin 1
Genes
Sodium
Dietary Sodium
Gene Expression
Matrix Metalloproteinase 9
Aldosterone
C-Reactive Protein
Glucocorticoids
Hydrocortisone
Potassium
Oxidative Stress
Leukocytes
Up-Regulation
Cytokines

ASJC Scopus subject areas

  • Internal Medicine

Citar esto

Tapia-Castillo, A., Carvajal, C. A., Campino, C., Hill, C., Allende, F., Vecchiola, A., ... Fardella, C. E. (2015). The expression of RAC1 and mineralocorticoid pathway-dependent genes are associated with different responses to salt intake. American Journal of Hypertension, 28(6), 722-728. https://doi.org/10.1093/ajh/hpu224
Tapia-Castillo, Alejandra ; Carvajal, Cristian A. ; Campino, Carmen ; Hill, Caroline ; Allende, Fidel ; Vecchiola, Andrea ; Carrasco, Carmen ; Bancalari, Rodrigo ; Valdivia, Carolina ; Lagos, Carlos ; Martinez-Aguayo, Alejandro ; Garcia, Hernan ; Aglony, Marlene ; Baudrand, Rene F. ; Kalergis, Alexis M. ; Michea, Luis F. ; Riedel, Claudia A. ; Fardella, Carlos E. / The expression of RAC1 and mineralocorticoid pathway-dependent genes are associated with different responses to salt intake. En: American Journal of Hypertension. 2015 ; Vol. 28, N.º 6. pp. 722-728.
@article{dac20d04b2fe49ce9fa68e79e44533e9,
title = "The expression of RAC1 and mineralocorticoid pathway-dependent genes are associated with different responses to salt intake",
abstract = "Background Rac1 upregulation has been implicated in salt-sensitive hypertension as a modulator of mineralocorticoid receptor (MR) activity. Rac1 could affect the expression of oxidative stress markers, such as hemoxigenase-1 (HO- 1) or nuclear factor-B (NF-κB), and the expression of neutrophil gelatinaseassociated lipocalin (NGAL), a cytokine upregulated upon MR activation. aim We evaluated RAC1 expression in relation of high salt intake and association with MR, NGAL, HO-1, and NF-κB expression, mineralo- and glucocorticoids levels, and inflammatory parameters. subjects and methods We studied 147 adult subjects. A food survey identified the dietary sodium (Na) intake. RAC1 expression was considered high or low according to the value found in normotensive subjects with low salt intake. We determined the gene expression of RAC1, MR, NGAL, HO-1, NF-κB, and 18S, isolated from peripheral leukocytes. We measured aldosterone, cortisol, sodium, potassium excretion, metalloproteinase (MMP9 y MMP2), and C-reactive protein. results We identified 126 subjects with high Na-intake, 18 subjects had high, and 108 low-RAC1 expression. The subjects with high-RAC1 expression showed a significant increase in MR (P = 0.0002), NGAL (P < 0.0001) HO-1 (P = 0.0004), and NF-κB (P < 0.0001) gene expression. We demonstrated an association between RAC1 expression and MR (Rsp 0.64; P < 0.0001), NGAL (Rsp 0.48; P < 0.0001), HO-1 (Rsp 0.53; P < 0.0001), and NF-κB (Rsp0.52; P < 0.0001). We did not identify any association between RAC1 and clinical or biochemical variables. conclusions RAC1 expression was associated with an increase in MR, NGAL, NF-κB, and HO-1 expression, suggesting that RAC1 could be a mediator of cardiovascular damage induced by sodium, and may also useful to identify subjects with different responses to salt intake.",
keywords = "Blood pressure, Essential hypertension, Gene expression, Hypertension, PBMC, RAC1, Salt intake",
author = "Alejandra Tapia-Castillo and Carvajal, {Cristian A.} and Carmen Campino and Caroline Hill and Fidel Allende and Andrea Vecchiola and Carmen Carrasco and Rodrigo Bancalari and Carolina Valdivia and Carlos Lagos and Alejandro Martinez-Aguayo and Hernan Garcia and Marlene Aglony and Baudrand, {Rene F.} and Kalergis, {Alexis M.} and Michea, {Luis F.} and Riedel, {Claudia A.} and Fardella, {Carlos E.}",
year = "2015",
month = "1",
day = "1",
doi = "10.1093/ajh/hpu224",
language = "English",
volume = "28",
pages = "722--728",
journal = "American Journal of Hypertension",
issn = "0895-7061",
publisher = "Oxford University Press",
number = "6",

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Tapia-Castillo, A, Carvajal, CA, Campino, C, Hill, C, Allende, F, Vecchiola, A, Carrasco, C, Bancalari, R, Valdivia, C, Lagos, C, Martinez-Aguayo, A, Garcia, H, Aglony, M, Baudrand, RF, Kalergis, AM, Michea, LF, Riedel, CA & Fardella, CE 2015, 'The expression of RAC1 and mineralocorticoid pathway-dependent genes are associated with different responses to salt intake', American Journal of Hypertension, vol. 28, n.º 6, pp. 722-728. https://doi.org/10.1093/ajh/hpu224

The expression of RAC1 and mineralocorticoid pathway-dependent genes are associated with different responses to salt intake. / Tapia-Castillo, Alejandra; Carvajal, Cristian A.; Campino, Carmen; Hill, Caroline; Allende, Fidel; Vecchiola, Andrea; Carrasco, Carmen; Bancalari, Rodrigo; Valdivia, Carolina; Lagos, Carlos; Martinez-Aguayo, Alejandro; Garcia, Hernan; Aglony, Marlene; Baudrand, Rene F.; Kalergis, Alexis M.; Michea, Luis F.; Riedel, Claudia A.; Fardella, Carlos E.

En: American Journal of Hypertension, Vol. 28, N.º 6, 01.01.2015, p. 722-728.

Resultado de la investigación: Article

TY - JOUR

T1 - The expression of RAC1 and mineralocorticoid pathway-dependent genes are associated with different responses to salt intake

AU - Tapia-Castillo, Alejandra

AU - Carvajal, Cristian A.

AU - Campino, Carmen

AU - Hill, Caroline

AU - Allende, Fidel

AU - Vecchiola, Andrea

AU - Carrasco, Carmen

AU - Bancalari, Rodrigo

AU - Valdivia, Carolina

AU - Lagos, Carlos

AU - Martinez-Aguayo, Alejandro

AU - Garcia, Hernan

AU - Aglony, Marlene

AU - Baudrand, Rene F.

AU - Kalergis, Alexis M.

AU - Michea, Luis F.

AU - Riedel, Claudia A.

AU - Fardella, Carlos E.

PY - 2015/1/1

Y1 - 2015/1/1

N2 - Background Rac1 upregulation has been implicated in salt-sensitive hypertension as a modulator of mineralocorticoid receptor (MR) activity. Rac1 could affect the expression of oxidative stress markers, such as hemoxigenase-1 (HO- 1) or nuclear factor-B (NF-κB), and the expression of neutrophil gelatinaseassociated lipocalin (NGAL), a cytokine upregulated upon MR activation. aim We evaluated RAC1 expression in relation of high salt intake and association with MR, NGAL, HO-1, and NF-κB expression, mineralo- and glucocorticoids levels, and inflammatory parameters. subjects and methods We studied 147 adult subjects. A food survey identified the dietary sodium (Na) intake. RAC1 expression was considered high or low according to the value found in normotensive subjects with low salt intake. We determined the gene expression of RAC1, MR, NGAL, HO-1, NF-κB, and 18S, isolated from peripheral leukocytes. We measured aldosterone, cortisol, sodium, potassium excretion, metalloproteinase (MMP9 y MMP2), and C-reactive protein. results We identified 126 subjects with high Na-intake, 18 subjects had high, and 108 low-RAC1 expression. The subjects with high-RAC1 expression showed a significant increase in MR (P = 0.0002), NGAL (P < 0.0001) HO-1 (P = 0.0004), and NF-κB (P < 0.0001) gene expression. We demonstrated an association between RAC1 expression and MR (Rsp 0.64; P < 0.0001), NGAL (Rsp 0.48; P < 0.0001), HO-1 (Rsp 0.53; P < 0.0001), and NF-κB (Rsp0.52; P < 0.0001). We did not identify any association between RAC1 and clinical or biochemical variables. conclusions RAC1 expression was associated with an increase in MR, NGAL, NF-κB, and HO-1 expression, suggesting that RAC1 could be a mediator of cardiovascular damage induced by sodium, and may also useful to identify subjects with different responses to salt intake.

AB - Background Rac1 upregulation has been implicated in salt-sensitive hypertension as a modulator of mineralocorticoid receptor (MR) activity. Rac1 could affect the expression of oxidative stress markers, such as hemoxigenase-1 (HO- 1) or nuclear factor-B (NF-κB), and the expression of neutrophil gelatinaseassociated lipocalin (NGAL), a cytokine upregulated upon MR activation. aim We evaluated RAC1 expression in relation of high salt intake and association with MR, NGAL, HO-1, and NF-κB expression, mineralo- and glucocorticoids levels, and inflammatory parameters. subjects and methods We studied 147 adult subjects. A food survey identified the dietary sodium (Na) intake. RAC1 expression was considered high or low according to the value found in normotensive subjects with low salt intake. We determined the gene expression of RAC1, MR, NGAL, HO-1, NF-κB, and 18S, isolated from peripheral leukocytes. We measured aldosterone, cortisol, sodium, potassium excretion, metalloproteinase (MMP9 y MMP2), and C-reactive protein. results We identified 126 subjects with high Na-intake, 18 subjects had high, and 108 low-RAC1 expression. The subjects with high-RAC1 expression showed a significant increase in MR (P = 0.0002), NGAL (P < 0.0001) HO-1 (P = 0.0004), and NF-κB (P < 0.0001) gene expression. We demonstrated an association between RAC1 expression and MR (Rsp 0.64; P < 0.0001), NGAL (Rsp 0.48; P < 0.0001), HO-1 (Rsp 0.53; P < 0.0001), and NF-κB (Rsp0.52; P < 0.0001). We did not identify any association between RAC1 and clinical or biochemical variables. conclusions RAC1 expression was associated with an increase in MR, NGAL, NF-κB, and HO-1 expression, suggesting that RAC1 could be a mediator of cardiovascular damage induced by sodium, and may also useful to identify subjects with different responses to salt intake.

KW - Blood pressure

KW - Essential hypertension

KW - Gene expression

KW - Hypertension

KW - PBMC

KW - RAC1

KW - Salt intake

UR - http://www.scopus.com/inward/record.url?scp=84941568089&partnerID=8YFLogxK

U2 - 10.1093/ajh/hpu224

DO - 10.1093/ajh/hpu224

M3 - Article

C2 - 25430696

AN - SCOPUS:84941568089

VL - 28

SP - 722

EP - 728

JO - American Journal of Hypertension

JF - American Journal of Hypertension

SN - 0895-7061

IS - 6

ER -