The role of oxidative stress in the developmental origin of adult hypertension

Labib M. Ghulmiyyah, Maged Costantine, Huaizhi Yin, Esther Tamayo, Shannon Clark, Gary Hankins, George Saade, Monica Longo

Research output: Contribution to journalArticle

9 Citations (Scopus)

Abstract

Objective: To determine whether oxidative stress plays a role in the development of hypertension using a mouse model of fetal programming induced by endothelial nitric oxide synthase deficiency. Study Design: Homozygous nitric oxide synthase knockout and wild type mice were cross-bred producing maternal (endothelial nitric oxide synthase +pat/-mat) and paternal (endothelial nitric oxide synthase +mat/-pat) heterozygous offspring. RNA from liver and kidney tissues of female pups were obtained at 14 weeks of age. Relative expression of the heat shock protein-B6, peroxiredoxin-3, superoxide dismutase-1, peroxisome proliferator-activated receptor gamma, nitric oxide synthase-1 and -2 were determined. Results: In the kidneys, expression of nitric oxide synthase-2, peroxiredoxin-3, heat shock protein-B6, and superoxide dismutase-1 was up-regulated in endothelial nitric oxide synthase +pat/-mat but not in endothelial nitric oxide synthase +mat/-pat compared with wild type offspring. In the liver, there were no significant differences in the expression of nitric oxide synthase-1, nitric oxide synthase-2, peroxiredoxin, superoxide dismutase-1, or peroxisome proliferator-activated receptor gamma; however, heat shock protein-B6 was down-regulated in both heterozygotes offspring compared with wild type. Conclusion: The intrauterine environment alters oxidative pathways gene expression in the kidneys of offspring, which may be a mechanism in the development of adult hypertension.

Original languageEnglish (US)
JournalAmerican Journal of Obstetrics and Gynecology
Volume205
Issue number2
DOIs
StatePublished - Aug 2011

Fingerprint

Nitric Oxide Synthase Type III
Nitric Oxide Synthase
Oxidative Stress
Peroxiredoxin III
Hypertension
Heat-Shock Proteins
PPAR gamma
Kidney
Peroxiredoxins
Liver
Heterozygote
Fetal Development
Knockout Mice
Mothers
RNA
Gene Expression
Superoxide Dismutase-1

Keywords

  • fetal programming
  • gene expression
  • oxidative stress

ASJC Scopus subject areas

  • Obstetrics and Gynecology

Cite this

The role of oxidative stress in the developmental origin of adult hypertension. / Ghulmiyyah, Labib M.; Costantine, Maged; Yin, Huaizhi; Tamayo, Esther; Clark, Shannon; Hankins, Gary; Saade, George; Longo, Monica.

In: American Journal of Obstetrics and Gynecology, Vol. 205, No. 2, 08.2011.

Research output: Contribution to journalArticle

Ghulmiyyah, Labib M. ; Costantine, Maged ; Yin, Huaizhi ; Tamayo, Esther ; Clark, Shannon ; Hankins, Gary ; Saade, George ; Longo, Monica. / The role of oxidative stress in the developmental origin of adult hypertension. In: American Journal of Obstetrics and Gynecology. 2011 ; Vol. 205, No. 2.
@article{8fb55e121d904bd783b85fefa91fd464,
title = "The role of oxidative stress in the developmental origin of adult hypertension",
abstract = "Objective: To determine whether oxidative stress plays a role in the development of hypertension using a mouse model of fetal programming induced by endothelial nitric oxide synthase deficiency. Study Design: Homozygous nitric oxide synthase knockout and wild type mice were cross-bred producing maternal (endothelial nitric oxide synthase +pat/-mat) and paternal (endothelial nitric oxide synthase +mat/-pat) heterozygous offspring. RNA from liver and kidney tissues of female pups were obtained at 14 weeks of age. Relative expression of the heat shock protein-B6, peroxiredoxin-3, superoxide dismutase-1, peroxisome proliferator-activated receptor gamma, nitric oxide synthase-1 and -2 were determined. Results: In the kidneys, expression of nitric oxide synthase-2, peroxiredoxin-3, heat shock protein-B6, and superoxide dismutase-1 was up-regulated in endothelial nitric oxide synthase +pat/-mat but not in endothelial nitric oxide synthase +mat/-pat compared with wild type offspring. In the liver, there were no significant differences in the expression of nitric oxide synthase-1, nitric oxide synthase-2, peroxiredoxin, superoxide dismutase-1, or peroxisome proliferator-activated receptor gamma; however, heat shock protein-B6 was down-regulated in both heterozygotes offspring compared with wild type. Conclusion: The intrauterine environment alters oxidative pathways gene expression in the kidneys of offspring, which may be a mechanism in the development of adult hypertension.",
keywords = "fetal programming, gene expression, oxidative stress",
author = "Ghulmiyyah, {Labib M.} and Maged Costantine and Huaizhi Yin and Esther Tamayo and Shannon Clark and Gary Hankins and George Saade and Monica Longo",
year = "2011",
month = "8",
doi = "10.1016/j.ajog.2011.03.015",
language = "English (US)",
volume = "205",
journal = "American Journal of Obstetrics and Gynecology",
issn = "0002-9378",
publisher = "Mosby Inc.",
number = "2",

}

TY - JOUR

T1 - The role of oxidative stress in the developmental origin of adult hypertension

AU - Ghulmiyyah, Labib M.

AU - Costantine, Maged

AU - Yin, Huaizhi

AU - Tamayo, Esther

AU - Clark, Shannon

AU - Hankins, Gary

AU - Saade, George

AU - Longo, Monica

PY - 2011/8

Y1 - 2011/8

N2 - Objective: To determine whether oxidative stress plays a role in the development of hypertension using a mouse model of fetal programming induced by endothelial nitric oxide synthase deficiency. Study Design: Homozygous nitric oxide synthase knockout and wild type mice were cross-bred producing maternal (endothelial nitric oxide synthase +pat/-mat) and paternal (endothelial nitric oxide synthase +mat/-pat) heterozygous offspring. RNA from liver and kidney tissues of female pups were obtained at 14 weeks of age. Relative expression of the heat shock protein-B6, peroxiredoxin-3, superoxide dismutase-1, peroxisome proliferator-activated receptor gamma, nitric oxide synthase-1 and -2 were determined. Results: In the kidneys, expression of nitric oxide synthase-2, peroxiredoxin-3, heat shock protein-B6, and superoxide dismutase-1 was up-regulated in endothelial nitric oxide synthase +pat/-mat but not in endothelial nitric oxide synthase +mat/-pat compared with wild type offspring. In the liver, there were no significant differences in the expression of nitric oxide synthase-1, nitric oxide synthase-2, peroxiredoxin, superoxide dismutase-1, or peroxisome proliferator-activated receptor gamma; however, heat shock protein-B6 was down-regulated in both heterozygotes offspring compared with wild type. Conclusion: The intrauterine environment alters oxidative pathways gene expression in the kidneys of offspring, which may be a mechanism in the development of adult hypertension.

AB - Objective: To determine whether oxidative stress plays a role in the development of hypertension using a mouse model of fetal programming induced by endothelial nitric oxide synthase deficiency. Study Design: Homozygous nitric oxide synthase knockout and wild type mice were cross-bred producing maternal (endothelial nitric oxide synthase +pat/-mat) and paternal (endothelial nitric oxide synthase +mat/-pat) heterozygous offspring. RNA from liver and kidney tissues of female pups were obtained at 14 weeks of age. Relative expression of the heat shock protein-B6, peroxiredoxin-3, superoxide dismutase-1, peroxisome proliferator-activated receptor gamma, nitric oxide synthase-1 and -2 were determined. Results: In the kidneys, expression of nitric oxide synthase-2, peroxiredoxin-3, heat shock protein-B6, and superoxide dismutase-1 was up-regulated in endothelial nitric oxide synthase +pat/-mat but not in endothelial nitric oxide synthase +mat/-pat compared with wild type offspring. In the liver, there were no significant differences in the expression of nitric oxide synthase-1, nitric oxide synthase-2, peroxiredoxin, superoxide dismutase-1, or peroxisome proliferator-activated receptor gamma; however, heat shock protein-B6 was down-regulated in both heterozygotes offspring compared with wild type. Conclusion: The intrauterine environment alters oxidative pathways gene expression in the kidneys of offspring, which may be a mechanism in the development of adult hypertension.

KW - fetal programming

KW - gene expression

KW - oxidative stress

UR - http://www.scopus.com/inward/record.url?scp=79960929099&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=79960929099&partnerID=8YFLogxK

U2 - 10.1016/j.ajog.2011.03.015

DO - 10.1016/j.ajog.2011.03.015

M3 - Article

C2 - 21531372

AN - SCOPUS:79960929099

VL - 205

JO - American Journal of Obstetrics and Gynecology

JF - American Journal of Obstetrics and Gynecology

SN - 0002-9378

IS - 2

ER -